item_id	Regulator_ID	Target_ID	m6A_methylation_regulation	disease_ID	Drug_ID	PMID	summary
item1	REG00007	M6ATAR00356	Down	.	.	22575960	"Silencing the m(6)A methyltransferase significantly affects gene expression and alternative splicing patterns, resulting in modulation of the Cellular tumor antigen p53 (TP53/p53) (also known as TP53) signalling pathway and apoptosis. Modulation of p53 signalling through splicing is relevant to induction of apoptosis by silencing of METTL3."
item2	REG00005	M6ATAR00356	.	M6ADIS0128	.	23177736	"ALKBH5 as another mammalian demethylase that oxidatively reverses m(6)A in mRNA in vitro and in vivo. Alkbh5-deficient male mice have increased m(6)A in mRNA and are characterized by impaired fertility resulting from apoptosis that affects meiotic metaphase-stage spermatocytes. Identified in mouse testes 1,551 differentially expressed genes that cover broad functional categories and include spermatogenesis-related mRNAs involved in the Cellular tumor antigen p53 (TP53/p53) functional interaction network."
item3	REG00005	.	.	M6ADIS0020	.	23619745	A knockout of the Alkbh5 gene in mice resulted in impaired male fertility due to compromised spermatogenesis.
item4	REG00009	.	.	.	.	24407421	Morpholino-mediated knockdown targeting WTAP and/or METTL3 in zebrafish embryos caused tissue differentiation defects and increased apoptosis.
item5	REG00007	.	.	.	.	24407421	Morpholino-mediated knockdown targeting WTAP and/or METTL3 in zebrafish embryos caused tissue differentiation defects and increased apoptosis.
item6	REG00001	.	.	M6ADIS0080	.	25303482	"The content of m6A was highly associated with the risk of T2DM, and the increased mRNA expression of FTO is responsible for the reduction of m6A, which can further cause the complications of T2DM."
item7	REG00001	M6ATAR00414	Down	M6ADIS0083	.	25412662	FTO-dependent m6A demethylation functions as a novel regulatory mechanism of RNA processing and plays a critical role in the regulation of adipogenesis and obesity. FTO-dependent regulatory role of m6A and SRSF protein kinase 2 (SRPK2) in mRNA splicing and adipocyte differentiation. FTO controls exonic splicing of adipogenic regulatory factor RUNX1T1 by regulating m6A levels around splice sites and thereby modulates differentiation.
item8	REG00001	M6ATAR00338	Down	M6ADIS0083	.	25412662	FTO-dependent m6A demethylation functions as a novel regulatory mechanism of RNA processing and plays a critical role in the regulation of adipogenesis and obesity. FTO-dependent regulatory role of m6A and SRSF2 in mRNA splicing and adipocyte differentiation. FTO controls exonic splicing of adipogenic regulatory factor Protein CBFA2T1 (RUNX1T1) by regulating m6A levels around splice sites and thereby modulates differentiation.
item9	REG00007	M6ATAR00228	Up	.	.	25799998	The m(6)A mark acts as a key post-transcriptional modification that promotes the initiation of miRNA biogenesis. METTL3 depletion reduced the binding of Microprocessor complex subunit DGCR8 (DGCR8) to pri-miRNAs and resulted in the global reduction of mature miRNAs and concomitant accumulation of unprocessed pri-miRNAs.
item10	REG00001	.	.	M6ADIS0107	M6ADRUG0001	26078098	"A novel FTO-dependent function of m(6)A is involve in the hepatoprotective effects of betaine. betaine supplementation across adolescence could protect mice from high-fat-induced lipid accumulation NAFLD in the liver. Moreover, FTO-dependent m6A demethylation is affected by betaine. A novel FTO-dependent function of m(6)A may involve in the hepatoprotective effects of betaine."
item11	REG00001	M6ATAR00023	Up	.	.	26691922	"FTO senses branched-chain amino acids (BCAAs) and activates the nutrient sensitive kinase mechanistic target of Mammalian target of rapamycin complex 1 (mTORC1), which plays a key role in translation."
item12	REG00023	M6ATAR00274	Up	M6ADIS0058	.	26996300	YTHDC2 contributes to colon tumor metastasis by promoting translation of Hypoxia-inducible factor 1-alpha (HIF-1-Alpha/HIF1A) and that YTHDC2 is potentially a diagnostic marker and target gene for treating colon cancer patients.
item13	REG00005	M6ATAR00344	Up	M6ADIS0065	.	27001847	"Homeobox protein NANOG (NANOG) activity does not merely compensate for reduced O2 levels but significantly increases ALKBH5, JMJD2C, and TET1 activity in hypoxic breast cancer cells, leading to transcriptional and posttranscriptional changes in gene expression that promote the specification and/or maintenance of BCSCs. ALKBH5 overexpression decreased Homeobox protein NANOG (NANOG) mRNA methylation, increased NANOG levels, and increased the percentage of BCSCs,."
item14	REG00005	M6ATAR00344	Up	M6ADIS0065	.	27590511	ALKBH5 knockdown in MDA-MB-231 breast cancer cells significantly decreased metastasis from breast to lungs in immunodeficient mice. ALKBH5-mediated demethylation of N6-methyladenosine (m6A) in Homeobox protein NANOG (NANOG) mRNA leading to increased expression of NANOG.
item15	REG00006	M6ATAR00228	Up	M6ADIS0006	.	27774652	METTL14 interacts with the microprocessor protein Microprocessor complex subunit DGCR8 (DGCR8) and positively modulates the primary microRNA 126 process in an m6 A-dependent manner. microRNA 126 inhibits the repressing effect of METTL14 in Hepatocellular carcinoma metastasis.
item16	REG00007	.	.	M6ADIS0007	.	27856248	MIR33A can attenuate NSCLC cells proliferation via targeting to the 3'UTR of METTL3 mRNA.
item17	REG00001	M6ATAR00378	Down	M6ADIS0046	M6ADRUG0035	28017614	"FTO enhances leukemic oncogene-mediated cell transformation and leukemogenesis, and inhibits all-trans-retinoic acid (ATRA)-induced AML cell differentiation, through regulating expression of targets such as ASB2 and Retinoic acid receptor alpha (RARA) by reducing m6A levels in these mRNA transcripts."
item18	REG00001	M6ATAR00182	Down	M6ADIS0046	M6ADRUG0035	28017614	"FTO enhances leukemic oncogene-mediated cell transformation and leukemogenesis, and inhibits all-trans-retinoic acid (ATRA)-induced AML cell differentiation, through regulating expression of targets such as Ankyrin repeat and SOCS box protein 2 (ASB2) and RARA by reducing m6A levels in these mRNA transcripts."
item19	REG00008	.	.	M6ADIS0006	.	28104805	MIR145 modulates m6A levels by targeting the 3'-UTR of YTHDF2 mRNA in hepatocellular carcinoma cells.
item20	REG00001	.	.	M6ADIS0086	.	28176824	FTO-dependent demethylation of mRNA m6A methylation was involved in the regulation of skeletal muscle lipid accumulation by the AMPK signalling pathway.
item21	REG00007	M6ATAR00371	Up	M6ADIS0127	.	28297716	"Methylation at the 6 position of adenosine (m6A) in RNA is rapidly (within 2 min) and transiently induced at DNA damage sites in response to ultraviolet irradiation. This modification occurs on numerous poly(A)+ transcripts and is regulated by the methyltransferase METTL3 and the demethylase FTO. DNA DNA polymerase kappa (Pol Kappa/POLK), which has been implicated in both nucleotide excision repair and trans-lesion synthesis, required the catalytic activity of METTL3 for immediate localization to ultraviolet-induced DNA damage sites."
item22	REG00001	M6ATAR00371	Up	M6ADIS0127	.	28297716	"Methylation at the 6 position of adenosine (m6A) in RNA is rapidly (within 2 min) and transiently induced at DNA damage sites in response to ultraviolet irradiation. This modification occurs on numerous poly(A)+ transcripts and is regulated by the methyltransferase METTL3 and the demethylase FTO. DNA DNA polymerase kappa (Pol Kappa/POLK), which has been implicated in both nucleotide excision repair and trans-lesion synthesis, required the catalytic activity of METTL3 for immediate localization to ultraviolet-induced DNA damage sites."
item23	REG00005	M6ATAR00258	Up	M6ADIS0001	.	28344040	ALKBH5 and FOXM1-AS disrupted GSC tumorigenesis through the Forkhead box protein M1 (FOXM1) axis.
item24	REG00005	.	.	.	.	28484591	"A novel pathway in which m6A RNA, its associated enzymes, and DNA polymerase kappa constitute an early-response system that confers cellular resistance to ultraviolet irradiation, separate from the canonical nucleotide excision repair (NER) pathway that normally repairs UV-induced DNA damage."
item25	REG00001	M6ATAR00286	Down	M6ADIS0046	.	28486104	"1) Isocitrate dehydrogenase [NADP] cytoplasmic (IDH/IDH1) mutant cells, likely via a D2-HG-mediated competitive inhibition of the Alpha-KG-dependent RNA demethylase FTO, display significantly elevated RNA methylation; 2) Deregulated RNA methylation should be considered part of the pathogenesis of IDH-mutant tumors, which alongside with the well-characterized DNA and histone disturbances defines a ""hypermethylation triad""; 3) the effects of FTO expression on AML pathogenesis need to be interpreted in the context of IDH1/2 mutation since in this setting FTO activity is probably low, irrespective of its expression level."
item26	REG00023	.	.	M6ADIS0020	.	28809393	Ythdc2 knockout mice are infertile; males have significantly smaller testes and females have significantly smaller ovaries compared to those of littermates.
item27	REG00007	.	.	M6ADIS0020	.	28914256	"Combined deletion of Mettl3 and Mettl14 in advanced germ cells with Stra8-GFPCre disrupts spermiogenesis, whereas mice with single deletion of either Mettl3 or Mettl14 in advanced germ cells show normal spermatogenesis."
item28	REG00006	.	.	M6ADIS0020	.	28914256	"Combined deletion of Mettl3 and Mettl14 in advanced germ cells with Stra8-GFPCre disrupts spermiogenesis, whereas mice with single deletion of either Mettl3 or Mettl14 in advanced germ cells show normal spermatogenesis."
item29	REG00007	M6ATAR00375	Up	M6ADIS0046	.	28920958	"METTL3 depletion in human myeloid leukemia cell lines induces cell differentiation and apoptosis and delays leukemia progression in recipient mice in vivo. Single-nucleotide-resolution mapping of m6A coupled with ribosome profiling reveals that m6A promotes the translation of c-MYC, BCL2 and Mutated in multiple advanced cancers 1 (PTEN) mRNAs in the human acute myeloid leukemia MOLM-13 cell line. Moreover, loss of METTL3 leads to increased levels of phosphorylated AKT."
item30	REG00007	M6ATAR00341	Up	M6ADIS0046	.	28920958	"METTL3 depletion in human myeloid leukemia cell lines induces cell differentiation and apoptosis and delays leukemia progression in recipient mice in vivo. Single-nucleotide-resolution mapping of m6A coupled with ribosome profiling reveals that m6A promotes the translation of Myc proto-oncogene protein (MYC), BCL2 and PTEN mRNAs in the human acute myeloid leukemia MOLM-13 cell line. Moreover, loss of METTL3 leads to increased levels of phosphorylated AKT."
item31	REG00007	M6ATAR00196	Up	M6ADIS0046	.	28920958	"METTL3 depletion in human myeloid leukemia cell lines induces cell differentiation and apoptosis and delays leukemia progression in recipient mice in vivo. Single-nucleotide-resolution mapping of m6A coupled with ribosome profiling reveals that m6A promotes the translation of c-MYC, Apoptosis regulator Bcl-2 (BCL2) and PTEN mRNAs in the human acute myeloid leukemia MOLM-13 cell line. Moreover, loss of METTL3 leads to increased levels of phosphorylated AKT."
item32	REG00007	M6ATAR00175	Down	M6ADIS0046	.	28920958	"METTL3 depletion in human myeloid leukemia cell lines induces cell differentiation and apoptosis and delays leukemia progression in recipient mice in vivo. Single-nucleotide-resolution mapping of m6A coupled with ribosome profiling reveals that m6A promotes the translation of c-MYC, BCL2 and PTEN mRNAs in the human acute myeloid leukemia MOLM-13 cell line. Moreover, loss of METTL3 leads to increased levels of phosphorylated RAC-alpha serine/threonine-protein kinase (AKT1)."
item33	REG00007	M6ATAR00404	Up	M6ADIS0001	.	28991227	GBM tumors have elevated levels of METTL3 transcripts and silencing METTL3 in U87/TIC inhibited tumor growth in an intracranial orthotopic mouse model with prolonged mice survival. The exogenous overexpression of 3'UTR-less Transcription factor SOX-2 (SOX2) significantly alleviated the inhibition of neurosphere formation observed in METTL3 silenced GSCs.
item34	REG00017	M6ATAR00141	.	.	.	29125541	LncRNAs are involved in a plethora of cellular signaling pathways and actively regulate gene expression via a broad selection of molecular mechanisms. Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) could serve a role as a regulator of RNA processing or modification events through guiding METTL16 onto its RNA targets.
item35	REG00008	M6ATAR00451	Down	M6ADIS0061	.	29135329	"YTHDF2 knockdown significantly increases the total YAP expression, but inhibits TGF-beta/Smad signaling, indicating that YTHDF2 regulates EMT probably via Transcriptional coactivator YAP1 (YAP1) signaling. YTHDF2 is a new predictive biomarker of development of pancreatic cancer."
item36	REG00007	M6ATAR00401	Down	M6ADIS0006	.	29171881	METTL3 is frequently up-regulated in human HCC and contributes to HCC progression. METTL3 represses Suppressor of cytokine signaling 2 (SOCS2) expression in HCC through an m6A-YTHDF2-dependent mechanism.
item37	REG00008	M6ATAR00401	Down	M6ADIS0006	.	29171881	METTL3 is frequently up-regulated in human HCC and contributes to HCC progression. METTL3 represses Suppressor of cytokine signaling 2 (SOCS2) expression in HCC through an m6A-YTHDF2-dependent mechanism.
item38	REG00007	M6ATAR00319	Up	M6ADIS0065	.	29174803	"Ragulator complex protein LAMTOR5 (LAMTOR5/HBXIP) up-regulates METTL3 by suppressing let-7g, in which METTL3 increased HBXIP expression forming a positive feedback loop of HBXIP/let-7g/METTL3/HBXIP, leading to accelerated cell proliferation in breast cancer."
item39	REG00007	M6ATAR00139	Down	M6ADIS0065	.	29174803	"HBXIP up-regulates METTL3 by suppressing microRNA let-7g (MIRLET7G), in which METTL3 increased HBXIP expression forming a positive feedback loop of HBXIP/let-7g/METTL3/HBXIP, leading to accelerated cell proliferation in breast cancer."
item40	REG00007	M6ATAR00407	.	M6ADIS0046	.	29186125	"Genes regulated by METTL3 in this way are necessary for acute myeloid leukaemia. Two genes expressing the transcription factors SP1 and Transcription factor Sp2 (SP2), which have promoters occupied by METTL3."
item41	REG00007	M6ATAR00406	.	M6ADIS0046	.	29186125	"Genes regulated by METTL3 in this way are necessary for acute myeloid leukaemia. Two genes expressing the transcription factors Transcription factor Sp1 (SP1) and SP2, which have promoters occupied by METTL3."
item42	REG00007	M6ATAR00368	Down	M6ADIS0010	.	29221190	"Knockdown of METTL3 could obviously promote cell proliferation, migration and invasion function, and induce G0/G1 arrest,METTL3 acts as a novel marker for tumorigenesis, development and survival of RCC. Knockdown of METTL3 promoted changes in PI3-kinase subunit alpha (PI3k/PIK3CA)/AKT/mTOR markers' expression with a gain in p-PI3k, p-AKT, p-mTOR and p-p70, and a loss of p-4EBP1."
item43	REG00007	M6ATAR00175	Down	M6ADIS0010	.	29221190	"Knockdown of METTL3 could obviously promote cell proliferation, migration and invasion function, and induce G0/G1 arrest,METTL3 acts as a novel marker for tumorigenesis, development and survival of RCC. Knockdown of METTL3 promoted changes in pI3K/RAC-alpha serine/threonine-protein kinase (AKT1)/mTOR markers' expression with a gain in p-PI3k, p-AKT, p-mTOR and p-p70, and a loss of p-4EBP1."
item44	REG00007	M6ATAR00339	Down	M6ADIS0010	.	29221190	"Knockdown of METTL3 could obviously promote cell proliferation, migration and invasion function, and induce G0/G1 arrest,METTL3 acts as a novel marker for tumorigenesis, development and survival of RCC. Knockdown of METTL3 promoted changes in pI3K/AKT/Serine/threonine-protein kinase mTOR (MTOR) markers' expression with a gain in p-PI3k, p-AKT, p-mTOR and p-p70, and a loss of p-4EBP1."
item45	REG00007	M6ATAR00004	Down	M6ADIS0010	.	29221190	"Knockdown of METTL3 could obviously promote cell proliferation, migration and invasion function, and induce G0/G1 arrest,METTL3 acts as a novel marker for tumorigenesis, development and survival of RCC. Knockdown of METTL3 promoted changes in pI3K/AKT/mTOR markers' expression with a gain in p-PI3k, p-AKT, p-mTOR and p-P70, and a loss of p-4EBP1."
item46	REG00001	M6ATAR00215	Down	M6ADIS0001	M6ADRUG0066	29249359	"This work demonstrates anti-tumor effects of 2HG in inhibiting proliferation/survival of FTO-high cancer cells via targeting FTO/m6A/MYC/CCAAT/enhancer-binding protein alpha (CEBPA) signaling.High levels of FTO sensitize leukemia cells to R-2HG, whereas hyperactivation of MYC signaling confers resistance that can be reversed by the inhibition of MYC signaling. R-2HG also displays anti-tumor activity in glioma. High levels of FTO sensitize leukemic cells to R-2HG, whereas hyperactivation of MYC signaling confers resistance that can be reversed by the inhibition of MYC signaling."
item47	REG00001	M6ATAR00215	Down	M6ADIS0004	M6ADRUG0066	29249359	"This work demonstrates anti-tumor effects of 2HG in inhibiting proliferation/survival of FTO-high cancer cells via targeting FTO/m6A/MYC/CCAAT/enhancer-binding protein alpha (CEBPA) signaling.High levels of FTO sensitize leukemia cells to R-2HG, whereas hyperactivation of MYC signaling confers resistance that can be reversed by the inhibition of MYC signaling. R-2HG also displays anti-tumor activity in glioma. High levels of FTO sensitize leukemic cells to R-2HG, whereas hyperactivation of MYC signaling confers resistance that can be reversed by the inhibition of MYC signaling."
item48	REG00001	M6ATAR00341	Down	M6ADIS0001	M6ADRUG0066	29249359	"This work demonstrates anti-tumor effects of 2HG in inhibiting proliferation/survival of FTO-high cancer cells via targeting FTO/m6A/Myc proto-oncogene protein (MYC)/CEBPA signaling.High levels of FTO sensitize leukemia cells to R-2HG, whereas hyperactivation of MYC signaling confers resistance that can be reversed by the inhibition of MYC signaling. R-2HG also displays anti-tumor activity in glioma. High levels of FTO sensitize leukemic cells to R-2HG, whereas hyperactivation of MYC signaling confers resistance that can be reversed by the inhibition of MYC signaling."
item49	REG00001	M6ATAR00341	Down	M6ADIS0004	M6ADRUG0066	29249359	"This work demonstrates anti-tumor effects of 2HG in inhibiting proliferation/survival of FTO-high cancer cells via targeting FTO/m6A/Myc proto-oncogene protein (MYC)/CEBPA signaling.High levels of FTO sensitize leukemia cells to R-2HG, whereas hyperactivation of MYC signaling confers resistance that can be reversed by the inhibition of MYC signaling. R-2HG also displays anti-tumor activity in glioma. High levels of FTO sensitize leukemic cells to R-2HG, whereas hyperactivation of MYC signaling confers resistance that can be reversed by the inhibition of MYC signaling."
item50	REG00005	.	.	M6ADIS0020	.	29279410	ALKBH5-dependent m6A mainly controls mRNA fate in spermiogenesis.
item51	REG00006	M6ATAR00341	Up	M6ADIS0046	.	29290617	"METTL14 in normal myelopoiesis and AML pathogenesis, as featured by blocking myeloid differentiation and promoting self-renewal of normal HSPCs and LSCs/LICs. METTL14 exerts its oncogenic role by regulating its mRNA targets (e.g., MYB and Myc proto-oncogene protein (MYC)) through m6A modification, while the protein itself is negatively regulated by SPI1."
item52	REG00006	M6ATAR00340	Up	M6ADIS0046	.	29290617	"METTL14 in normal myelopoiesis and AML pathogenesis, as featured by blocking myeloid differentiation and promoting self-renewal of normal HSPCs and LSCs/LICs. METTL14 exerts its oncogenic role by regulating its mRNA targets (e.g., Transcriptional activator Myb (MYB) and MYC) through m6A modification, while the protein itself is negatively regulated by SPI1."
item53	REG00001	M6ATAR00246	Up	M6ADIS0030	.	29315835	The mRNA level of FTO is elevated in cervical squamous cell carcinoma (CSCC) tissues when compared with respective adjacent normal tissues.FTO enhances the chemo-radiotherapy resistance both in vitro and in vivo through regulating expression of beta-catenin by reducing m6A levels in its mRNA transcripts and in turn increases DNA excision repair protein ERCC-1 (ERCC1) activity.
item54	REG00001	M6ATAR00222	Up	M6ADIS0030	.	29315835	The mRNA level of FTO is elevated in cervical squamous cell carcinoma (CSCC) tissues when compared with respective adjacent normal tissues.FTO enhances the chemo-radiotherapy resistance both in vitro and in vivo through regulating expression of Catenin beta-1 (CTNNB1/Beta-catenin) by reducing m6A levels in its mRNA transcripts and in turn increases excision repair cross-complementation group 1 (ERCC1) activity.
item55	REG00005	M6ATAR00226	Down	.	.	29333169	"ATP-dependent RNA helicase DDX3X (DDX3X) interacted with ALKBH5, an RNA m6A demethylase.ATP domain of DDX3 and DSBH domain of ALKBH5 to be indispensable to their interaction with each other. Furthermore, DDX3 could modulate the demethylation of mRNAs."
item56	REG00007	.	.	M6ADIS0061	.	29345285	"METTL3 was associated with mitogen-activated protein kinase cascades, ubiquitin-dependent process and RNA splicing and regulation of cellular process, suggesting functional roles and targets of METTL3. METTL3 is a potent target for enhancing therapeutic efficacy in patients with pancreatic cancer."
item57	REG00023	M6ATAR00324	Up	.	.	29360036	Regulation of gene expression by YTHDC2-Meiosis-specific with coiled-coil domain protein (MEIOC) is an evolutionarily ancient strategy for controlling the germline transition into Mammalian meiosis.
item58	REG00008	.	Down	M6ADIS0057	.	29382422	YTHDF2 mRNA in gastric cancer was significantly higher than that in the normal tissues.Knockdown of YTHDF2 in MGC-803 cells inhibits cell proliferation and promotes apoptosis.
item59	REG00001	.	.	M6ADIS0018	.	29384212	"The decreased mRNA and protein expression levels of FTO are responsible for the increase in m6A in POI, which can further increase the risk of complications of POI. FACS was used to measure the levels of proliferation and apoptosis, and siRNA was used to establish FTO and ALKBH5 knockdown cell lines. The m6A content in the RNA from POI patients and POI mice was significantly higher than control groups and that POI was characterized by the content of m6A."
item60	REG00005	.	.	M6ADIS0018	.	29384212	"The decreased mRNA and protein expression levels of FTO are responsible for the increase in m6A in POI, which can further increase the risk of complications of POI. FACS was used to measure the levels of proliferation and apoptosis, and siRNA was used to establish FTO and ALKBH5 knockdown cell lines. The m6A content in the RNA from POI patients and POI mice was significantly higher than control groups and that POI was characterized by the content of m6A."
item61	REG00008	.	.	M6ADIS0068	.	29423080	YTHDF2 and miR-493-3p provide new insights into the carcinogenesis and new potential therapeutic targets for PCa.
item62	REG00012	M6ATAR00308	.	M6ADIS0008	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, FSCN1, Thymidine kinase, cytosolic (TK1), and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item63	REG00013	M6ATAR00308	.	M6ADIS0008	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, FSCN1, Thymidine kinase, cytosolic (TK1), and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item64	REG00014	M6ATAR00308	.	M6ADIS0008	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, FSCN1, Thymidine kinase, cytosolic (TK1), and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item65	REG00012	M6ATAR00308	.	M6ADIS0006	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, FSCN1, Thymidine kinase, cytosolic (TK1), and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item66	REG00013	M6ATAR00308	.	M6ADIS0006	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, FSCN1, Thymidine kinase, cytosolic (TK1), and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item67	REG00014	M6ATAR00308	.	M6ADIS0006	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, FSCN1, Thymidine kinase, cytosolic (TK1), and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item68	REG00012	M6ATAR00341	.	M6ADIS0008	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including Myc proto-oncogene protein (MYC), FSCN1, TK1, and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item69	REG00013	M6ATAR00341	.	M6ADIS0008	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including Myc proto-oncogene protein (MYC), FSCN1, TK1, and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item70	REG00014	M6ATAR00341	.	M6ADIS0008	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including Myc proto-oncogene protein (MYC), FSCN1, TK1, and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item71	REG00012	M6ATAR00341	.	M6ADIS0006	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including Myc proto-oncogene protein (MYC), FSCN1, TK1, and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item72	REG00013	M6ATAR00341	.	M6ADIS0006	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including Myc proto-oncogene protein (MYC), FSCN1, TK1, and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item73	REG00014	M6ATAR00341	.	M6ADIS0006	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including Myc proto-oncogene protein (MYC), FSCN1, TK1, and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item74	REG00012	M6ATAR00261	.	M6ADIS0008	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, Fascin (FSCN1), TK1, and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item75	REG00013	M6ATAR00261	.	M6ADIS0008	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, Fascin (FSCN1), TK1, and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item76	REG00014	M6ATAR00261	.	M6ADIS0008	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, Fascin (FSCN1), TK1, and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item77	REG00012	M6ATAR00261	.	M6ADIS0006	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, Fascin (FSCN1), TK1, and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item78	REG00013	M6ATAR00261	.	M6ADIS0006	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, Fascin (FSCN1), TK1, and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item79	REG00014	M6ATAR00261	.	M6ADIS0006	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, Fascin (FSCN1), TK1, and MARCKSL1, exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item80	REG00012	M6ATAR00337	.	M6ADIS0008	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, FSCN1, TK1, and MARCKS-related protein (MARCKSL1), exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item81	REG00013	M6ATAR00337	.	M6ADIS0008	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, FSCN1, TK1, and MARCKS-related protein (MARCKSL1), exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item82	REG00014	M6ATAR00337	.	M6ADIS0008	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, FSCN1, TK1, and MARCKS-related protein (MARCKSL1), exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item83	REG00012	M6ATAR00337	.	M6ADIS0006	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, FSCN1, TK1, and MARCKS-related protein (MARCKSL1), exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item84	REG00013	M6ATAR00337	.	M6ADIS0006	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, FSCN1, TK1, and MARCKS-related protein (MARCKSL1), exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item85	REG00014	M6ATAR00337	.	M6ADIS0006	.	29476152	"In contrast to the mRNA-decay-promoting function of YTH domain-containing family protein 2, IGF2BPs promote the stability and storage of their target mRNAs (for example, MYC) in an m6A-dependent manner under normal and stress conditions and therefore affect gene expression output. Four representative high confidence targets, including MYC, FSCN1, TK1, and MARCKS-related protein (MARCKSL1), exhibit strong binding with IGF2BPs around their m6A motifs in control cells. Knocking down of each individual IGF2BPs in Hela (cervical cancer) and HepG2 (liver cancer) cells significantly repressed MYC expression."
item86	REG00024	.	.	M6ADIS0059	M6ADRUG0048	29484125	The knockdown of YTHDF1 resulted in the suppression of cancer proliferation and sensitization to the exposure of anticancer drugs such as fluorouracil and oxaliplatin. m6A reader Ythdf1 plays a significant role in colorectal cancer progression. An oncogenic transcription factor MYC was associated with YTHDF1 in both expression and chromatin immunoprecipitation data.
item87	REG00024	.	.	M6ADIS0059	M6ADRUG0005	29484125	The knockdown of YTHDF1 resulted in the suppression of cancer proliferation and sensitization to the exposure of anticancer drugs such as fluorouracil and oxaliplatin. m6A reader Ythdf1 plays a significant role in colorectal cancer progression. An oncogenic transcription factor MYC was associated with YTHDF1 in both expression and chromatin immunoprecipitation data.
item88	REG00001	M6ATAR00216	Up	M6ADIS0107	.	29486327	"FTO increased the lipid accumulation in hepatocytes by increasing nuclear translocation of SREBP1c and SREBP1c maturation, thus improving the transcriptional activity of LD-associated protein Cell death activator CIDE-3 (CIDEC).The studies provide new mechanistic insight into nonalcoholic fatty liver disease (NAFLD) mediated by FTO."
item89	REG00001	M6ATAR00411	Up	M6ADIS0107	.	29486327	"FTO increased the lipid accumulation in hepatocytes by increasing nuclear translocation of Sterol regulatory element-binding protein 1 (SREBF1) and SREBP1c maturation, thus improving the transcriptional activity of LD-associated protein CIDEC.The studies provide new mechanistic insight into nonalcoholic fatty liver disease (NAFLD) mediated by FTO."
item90	REG00007	M6ATAR00342	Down	M6ADIS0106	.	29502358	"Knocked down METTL3 and demonstrated that METTL3 depletion decreased the expression of inflammatory cytokines and the phosphorylation of IKK-alpha/beta, p65 and IKappa-B-alpha in the NF-Kappa-B signalling pathway as well as p38, ERK and JNK in the MAPK signalling pathway in LPS-induced HDPCs. METTL3 inhibits the LPS-induced inflammatory response of HDPCs by regulating alternative splicing of Myeloid differentiation primary response protein MyD88 (MYD88)."
item91	REG00007	.	.	.	M6ADRUG0067	29680375	"m6A modification on RNA was significantly increased in arsenite-transformed cells and this modification was synergistically regulated by METTL3, METTL14, WTAP and FTO. Demonstrated the significant role of m6A in the prevention of tumor occurrence and progression induced by arsenite."
item92	REG00006	.	.	.	M6ADRUG0067	29680375	"m6A modification on RNA was significantly increased in arsenite-transformed cells and this modification was synergistically regulated by METTL3, METTL14, WTAP and FTO. Demonstrated the significant role of m6A in the prevention of tumor occurrence and progression induced by arsenite."
item93	REG00009	.	.	.	M6ADRUG0067	29680375	"m6A modification on RNA was significantly increased in arsenite-transformed cells and this modification was synergistically regulated by METTL3, METTL14, WTAP and FTO. Demonstrated the significant role of m6A in the prevention of tumor occurrence and progression induced by arsenite."
item94	REG00001	.	.	.	M6ADRUG0067	29680375	"m6A modification on RNA was significantly increased in arsenite-transformed cells and this modification was synergistically regulated by METTL3, METTL14, WTAP and FTO. Demonstrated the significant role of m6A in the prevention of tumor occurrence and progression induced by arsenite."
item95	REG00001	M6ATAR00205	Up	M6ADIS0083	M6ADRUG0025	29795461	m6A-dependent Cyclin-A2 (CCNA2) and CDK2 expressions mediated by FTO and YTHDF2 contributed to EGCG-induced adipogenesis inhibition.
item96	REG00008	M6ATAR00205	Down	M6ADIS0083	M6ADRUG0025	29795461	m6A-dependent Cyclin-A2 (CCNA2) and CDK2 expressions mediated by FTO and YTHDF2 contributed to EGCG-induced adipogenesis inhibition.
item97	REG00001	M6ATAR00210	Up	M6ADIS0083	M6ADRUG0025	29795461	m6A-dependent CCNA2 and Cyclin-dependent kinase 2 (CDK2) expressions mediated by FTO and YTHDF2 contributed to EGCG-induced adipogenesis inhibition.
item98	REG00008	M6ATAR00210	Down	M6ADIS0083	M6ADRUG0025	29795461	m6A-dependent CCNA2 and Cyclin-dependent kinase 2 (CDK2) expressions mediated by FTO and YTHDF2 contributed to EGCG-induced adipogenesis inhibition.
item99	REG00001	M6ATAR00343	Up	M6ADIS0007	.	29842885	"FTO enhanced Myeloid zinc finger 1 (MZF1) expression by reducing m6A levels and mRNA stability in MZF1 mRNA transcript, leading to oncogenic functions. The functional importance of FTO in the tumor progression of LUSC and provides a potential therapeutic target for LUSC treatment."
item100	REG00009	.	.	M6ADIS0083	.	29866655	"WTAP, coupled with METTL3 and METTL14, is increased and distributed in nucleus by the induction of adipogenesis dependently on RNA in vitro Knockdown of each of these three proteins leads to cell cycle arrest and impaired adipogenesis associated with suppression of cyclin A2 upregulation during MCE, whose knockdown also impairs adipogenesis."
item101	REG00007	.	.	M6ADIS0083	.	29866655	"WTAP, coupled with METTL3 and METTL14, is increased and distributed in nucleus by the induction of adipogenesis dependently on RNA in vitro Knockdown of each of these three proteins leads to cell cycle arrest and impaired adipogenesis associated with suppression of cyclin A2 upregulation during MCE, whose knockdown also impairs adipogenesis."
item102	REG00006	.	.	M6ADIS0083	.	29866655	"WTAP, coupled with METTL3 and METTL14, is increased and distributed in nucleus by the induction of adipogenesis dependently on RNA in vitro Knockdown of each of these three proteins leads to cell cycle arrest and impaired adipogenesis associated with suppression of cyclin A2 upregulation during MCE, whose knockdown also impairs adipogenesis."
item103	REG00001	.	.	M6ADIS0095	M6ADRUG0047	29875633	"MA2, which is a highly selective inhibitor of FTO, has a protective effect and improves the viability of HEI-OC1 cells after cisplatin treatment, and they provide new insights into potential therapeutic targets for the amelioration of cisplatin-induced ototoxicity."
item104	REG00007	.	.	M6ADIS0021	.	29879109	"METTL3 depletion-induced loss of m6A modification causes extended RNA half-lives and aberrant splicing events, consequently leading to dysregulation of transcriptome-wide gene expression and premature CGC death.Mettl3 in mouse nervous system causes severe developmental defects in the brain."
item105	REG00005	M6ATAR00437	Up	M6ADIS0007	.	29904125	Deregulated Ubiquitin-conjugating enzyme E2 C (UBE2C)-autophagy repression axis drives NSCLC progression which renders varieties of potential molecular targets in cancer therapy of NSCLC. UBE2C is repressed post-transcriptionally via tumor suppressor miR-381 and epitranscriptionally stabilized with maintenance of lower m6A level within its mature RNAs due to the upregulation of m6A demethylase ALKBH5 in NSCLC.
item106	.	M6ATAR00059	.	M6ADIS0057	.	29973643	Down-regulation of hsa_circ_0066779 (circPVRL3) could promote the proliferation in gastric carcinoma and have potential to encode protein.
item107	REG00007	M6ATAR00341	Up	M6ADIS0046	.	29978784	"METTL3 level was slightly increased in AML-M5 patients,and its expression was significantly higher in immature cells than in mature monocytes.METTL3 acts as an oncogene in MOLM13 cells by upregulating Myc proto-oncogene protein (MYC) expression."
item108	REG00001	.	.	M6ADIS0093	M6ADRUG0067	29982692	Targeting the m6A demethylase FTO in the prevention or intervention against arsenite-related neurodegenerative diseases.
item109	REG00001	.	.	M6ADIS0101	.	29997116	FTO-dependent cardiac m6A methylome in cardiac contraction during heart failure and provides a novel mechanistic insight into the therapeutic mechanisms of FTO.
item110	REG00005	M6ATAR00082	Up	M6ADIS0061	.	30032148	ALKBH5 inhibits pancreatic cancer motility by demethylating lncRNA KCNK15 and WISP2 antisense RNA 1 (KCNK15-AS1).
item111	REG00008	M6ATAR00423	Down	M6ADIS0077	.	30065315	"Knocking down one of YTHDF2's key targets, T-cell acute lymphocytic leukemia protein 1 (TAL1) mRNA, partially rescued the phenotype.the function of YTHDF2 in adult stem cell maintenance and identifies its important role in regulating HSC ex vivo expansion."
item112	REG00001	M6ATAR00259	.	M6ADIS0080	.	30137347	"Glucose Is Involved in the Dynamic Regulation of m6A in Patients with Type 2 Diabetes. High-glucose stimulation enhances FTO expression, which leads to decreased m6A, and the lower m6A induces methyltransferase upregulation; FTO then triggers the mRNA expression of Forkhead box protein O1 (FOXO1), FASN, G6PC, and DGAT2, and these four genes were correlated with glucose and lipid metabolism."
item113	REG00001	M6ATAR00250	.	M6ADIS0080	.	30137347	"Glucose Is Involved in the Dynamic Regulation of m6A in Patients With Type 2 Diabetes.high-glucose stimulation enhances FTO expression, which leads to decreased m6A, and the lower m6A induces methyltransferase upregulation; FTO then triggers the mRNA expression of FOXO1, Fatty acid synthase (FASN), G6PC, and DGAT2, and these four genes were correlated with glucose and lipid metabolism."
item114	REG00001	M6ATAR00263	.	M6ADIS0080	.	30137347	"Glucose Is Involved in the Dynamic Regulation of m6A in Patients With Type 2 Diabetes.high-glucose stimulation enhances FTO expression, which leads to decreased m6A, and the lower m6A induces methyltransferase upregulation; FTO then triggers the mRNA expression of FOXO1, FASN, Glucose-6-phosphatase catalytic subunit 1 (G6PC/G6PC1), and DGAT2, and these four genes were correlated with glucose and lipid metabolism."
item115	REG00001	M6ATAR00227	.	M6ADIS0080	.	30137347	"Glucose Is Involved in the Dynamic Regulation of m6A in Patients With Type 2 Diabetes.high-glucose stimulation enhances FTO expression, which leads to decreased m6A, and the lower m6A induces methyltransferase upregulation; FTO then triggers the mRNA expression of FOXO1, FASN, G6PC, and Diacylglycerol O-acyltransferase 2 (DGAT2), and these four genes were correlated with glucose and lipid metabolism."
item116	REG00008	.	.	M6ADIS0077	.	30150673	YTHDF2 deletion uniquely affects the homeostasis of HSPCs.
item117	REG00007	M6ATAR00366	Up	M6ADIS0067	.	30154548	About 70% of endometrial tumours exhibit reductions in m6A methylation that are probably due to either this METTL14 mutation or reduced expression of METTL3. Reductions in m6A methylation lead to decreased expression of the negative AKT regulator PHLPP-like (PHLPP2) and increased expression of the positive AKT regulator mTORC2. these results reveal reduced m6A mRNA methylation as an oncogenic mechanism in endometrial cancer and identify m6A methylation as a regulator of AKT signalling.
item118	REG00006	M6ATAR00366	Up	M6ADIS0067	.	30154548	About 70% of endometrial tumours exhibit reductions in m6A methylation that are probably due to either this METTL14 mutation or reduced expression of METTL3. Reductions in m6A methylation lead to decreased expression of the negative AKT regulator PHLPP-like (PHLPP2) and increased expression of the positive AKT regulator mTORC2. these results reveal reduced m6A mRNA methylation as an oncogenic mechanism in endometrial cancer and identify m6A methylation as a regulator of AKT signalling.
item119	REG00007	M6ATAR00005	Down	M6ADIS0067	.	30154548	About 70% of endometrial tumours exhibit reductions in m6A methylation that are probably due to either this METTL14 mutation or reduced expression of METTL3. Reductions in m6A methylation lead to decreased expression of the negative AKT regulator PHLPP2 and increased expression of the positive AKT regulator Mammalian target of rapamycin complex 2 (mTORC2). these results reveal reduced m6A mRNA methylation as an oncogenic mechanism in endometrial cancer and identify m6A methylation as a regulator of AKT signalling.
item120	REG00006	M6ATAR00005	Down	M6ADIS0067	.	30154548	About 70% of endometrial tumours exhibit reductions in m6A methylation that are probably due to either this METTL14 mutation or reduced expression of METTL3. Reductions in m6A methylation lead to decreased expression of the negative AKT regulator PHLPP2 and increased expression of the positive AKT regulator Mammalian target of rapamycin complex 2 (mTORC2). these results reveal reduced m6A mRNA methylation as an oncogenic mechanism in endometrial cancer and identify m6A methylation as a regulator of AKT signalling.
item121	REG00007	M6ATAR00443	Up	M6ADIS0066	.	30249526	METTL3 promoted epithelial-mesenchymal transition (EMT) by upregulating the receptor tyrosine kinase Tyrosine-protein kinase receptor UFO (AXL) and that METTL3 serves as a novel prognostic and/or therapeutic target of interest in ovarian cancer.
item122	REG00008	M6ATAR00205	Down	M6ADIS0083	.	30305247	"FTO knockdown markedly decreased the expression of Cyclin-A2 (CCNA2) and CDK2, crucial cell cycle regulators, leading to delayed entry of MDI-induced cells into G2 phase. m6A-binding protein YTHDF2 recognized and decayed methylated mRNAs of CCNA2 and CDK2, leading to decreased protein expression, thereby prolonging cell cycle progression and suppressing adipogenesis. The adipocyte life cycle, including proliferation and adipogenesis, has become a potential target for many bioactive compounds and drugs for the prevention and treatment of obesity."
item123	REG00001	M6ATAR00205	.	M6ADIS0083	.	30305247	"FTO knockdown markedly decreased the expression of Cyclin-A2 (CCNA2) and CDK2, crucial cell cycle regulators, leading to delayed entry of MDI-induced cells into G2 phase. m6A-binding protein YTHDF2 recognized and decayed methylated mRNAs of CCNA2 and CDK2, leading to decreased protein expression, thereby prolonging cell cycle progression and suppressing adipogenesis. The adipocyte life cycle, including proliferation and adipogenesis, has become a potential target for many bioactive compounds and drugs for the prevention and treatment of obesity."
item124	REG00008	M6ATAR00210	Down	M6ADIS0083	.	30305247	"FTO knockdown markedly decreased the expression of CCNA2 and Cyclin-dependent kinase 2 (CDK2), crucial cell cycle regulators, leading to delayed entry of MDI-induced cells into G2 phase. m6A-binding protein YTHDF2 recognized and decayed methylated mRNAs of CCNA2 and CDK2, leading to decreased protein expression, thereby prolonging cell cycle progression and suppressing adipogenesis. The adipocyte life cycle, including proliferation and adipogenesis, has become a potential target for many bioactive compounds and drugs for the prevention and treatment of obesity."
item125	REG00001	M6ATAR00210	.	M6ADIS0083	.	30305247	"FTO knockdown markedly decreased the expression of CCNA2 and Cyclin-dependent kinase 2 (CDK2), crucial cell cycle regulators, leading to delayed entry of MDI-induced cells into G2 phase. m6A-binding protein YTHDF2 recognized and decayed methylated mRNAs of CCNA2 and CDK2, leading to decreased protein expression, thereby prolonging cell cycle progression and suppressing adipogenesis. The adipocyte life cycle, including proliferation and adipogenesis, has become a potential target for many bioactive compounds and drugs for the prevention and treatment of obesity."
item126	REG00006	M6ATAR00241	Up	M6ADIS0002	.	30306128	"METTL14 and ALKBH5 determine the m6A status of target genes by controlling each other's expression and by inhibiting m6A reader YTHDF3 (YTH N 6-methyladenosine RNA binding protein 3), which blocks RNA demethylase activity. ALKBH5/METTL14 constitute a positive feedback loop with RNA stability factor ELAV-like protein 1 (HuR/ELAVL1) to regulate the stability of target transcripts. This study unveils a previously undefined role for m6A in cancer and shows that the collaboration among writers-erasers-readers sets up the m6A threshold to ensure the stability of progrowth/proliferation-specific genes, and protumorigenic stimulus."
item127	REG00005	M6ATAR00241	Up	M6ADIS0002	.	30306128	"METTL14 and ALKBH5 determine the m6A status of target genes by controlling each other's expression and by inhibiting m6A reader YTHDF3 (YTH N 6-methyladenosine RNA binding protein 3), which blocks RNA demethylase activity. ALKBH5/METTL14 constitute a positive feedback loop with RNA stability factor ELAV-like protein 1 (HuR/ELAVL1) to regulate the stability of target transcripts. This study unveils a previously undefined role for m6A in cancer and shows that the collaboration among writers-erasers-readers sets up the m6A threshold to ensure the stability of progrowth/proliferation-specific genes, and protumorigenic stimulus."
item128	.	M6ATAR00006	.	M6ADIS0006	.	30361504	"N6-methyladenosine (m6A) motif was identified in the 353-357 region of YAP 3'UTR, and this m6A modification was essential for the interaction between miR-582-3p and YAP 3'UTR. And targeting Circ_104075 provides new strategies in HCC diagnosis and therapy."
item129	REG00012	M6ATAR00461	Up	M6ADIS0002	.	30371874	IGF2BP1 promotes Serum response factor (SRF) and SRF target genes at the post-transcriptional level suggesting it as a post-transcriptional enhancer of SRF itself as well as SRF-dependent gene expression in cancer cells.
item130	REG00008	M6ATAR00237	Down	M6ADIS0006	.	30423408	YTHDF2 acts as a tumor suppressor to repress cell proliferation and growth via destabilizing the Epidermal growth factor receptor (EGFR) mRNA in HCC.
item131	REG00007	M6ATAR00376	Up	M6ADIS0115	.	30429466	"Knockout of Mettl3 reduces the translation efficiency of MSCs lineage allocator Parathyroid hormone 1 receptor (PTH1R), and disrupts the PTH-induced osteogenic and adipogenic responses in vivo."
item132	REG00006	M6ATAR00290	Down	M6ADIS0078	.	30463905	"Responses to nonmicrobial dsDNA in uninfected cells, which shape host immunity and contribute to autoimmune disease, are regulated by enzymes controlling m6A epitranscriptomic changes. While METTL14 depletion reduced virus reproduction and stimulated dsDNA- or HCMV-induced Interferon beta (IFNB1) mRNA accumulation, ALKBH5 depletion had the opposite effect."
item133	REG00006	M6ATAR00290	Down	M6ADIS0044	.	30463905	"Responses to nonmicrobial dsDNA in uninfected cells, which shape host immunity and contribute to autoimmune disease, are regulated by enzymes controlling m6A epitranscriptomic changes. While METTL14 depletion reduced virus reproduction and stimulated dsDNA- or HCMV-induced Interferon beta (IFNB1) mRNA accumulation, ALKBH5 depletion had the opposite effect."
item134	REG00005	M6ATAR00290	Up	M6ADIS0078	.	30463905	"Responses to nonmicrobial dsDNA in uninfected cells, which shape host immunity and contribute to autoimmune disease, are regulated by enzymes controlling m6A epitranscriptomic changes. While METTL14 depletion reduced virus reproduction and stimulated dsDNA- or HCMV-induced Interferon beta (IFNB1) mRNA accumulation, ALKBH5 depletion had the opposite effect."
item135	REG00005	M6ATAR00290	Up	M6ADIS0044	.	30463905	"Responses to nonmicrobial dsDNA in uninfected cells, which shape host immunity and contribute to autoimmune disease, are regulated by enzymes controlling m6A epitranscriptomic changes. While METTL14 depletion reduced virus reproduction and stimulated dsDNA- or HCMV-induced Interferon beta (IFNB1) mRNA accumulation, ALKBH5 depletion had the opposite effect."
item136	REG00007	M6ATAR00456	Down	M6ADIS0054	.	30518868	"m6A modifications maintained the low expression level of ZNF750 in NPC. Knocking down METTL3 stimulated endogenous Zinc finger protein 750 (ZNF750) expression, and vice versa."
item137	REG00007	M6ATAR00356	Up	M6ADIS0058	.	30578766	"The produced p53 R273H mutant protein resulted in acquired multidrug resistance in colon cancer cells. Either silencing METTL3 expression by using small interfering RNA (siRNA) or inhibiting RNA methylation with neplanocin A suppressed m6A formation in Cellular tumor antigen p53 (TP53/p53) pre-mRNA, and substantially increased the level of phosphorylated p53 protein (Ser15) and its function in cells heterozygously carrying the R273H mutation, thereby re-sensitizing these cells to anticancer drugs."
item138	REG00007	.	.	M6ADIS0100	.	30586742	"Inhibition of METTL3 completely abrogated the ability of cardiomyocytes to undergo hypertrophy when stimulated to grow, whereas increased expression of the m6A RNA methylase METTL3 was sufficient to promote cardiomyocyte hypertrophy both in vitro and in vivo."
item139	REG00001	.	.	M6ADIS0057	.	30637548	"Aberrant expression of demethylase genes, FTO and ALKBH1, has a distinct prognostic value in Gastric cancer patients, indicating that FTO and ALKBH1 play vital roles in GC progression and metastasis."
item140	REG00001	M6ATAR00373	Up	M6ADIS0010	.	30648791	"FTO plays a critical anti-tumorigenic role in Clear Cell Renal Cell Carcinoma.Restored expression of FTO, through reducing m6A levels in mRNA transcripts of its critical target gene PPAR-gamma coactivator 1-alpha (PGC-1a/PPARGC1A), increases mitochondrial content, ROS production and oxidative damage, with the most important effect of repressed tumour growth."
item141	REG00007	M6ATAR00172	Up	M6ADIS0070	.	30659266	"AF4/FMR2 family member 4 (AFF4), two key regulators of NF-Kappa-B pathway (IKBKB and RELA) and MYC were further identified as direct targets of METTL3-mediated m6A modification.overexpression of METTL3 significantly promoted Bladder cancer cell growth and invasion."
item142	REG00007	M6ATAR00292	Up	M6ADIS0070	.	30659266	"AF4/FMR2 family member 4 (AFF4), two key regulators of NF-Kappa-B pathway (Inhibitor of nuclear factor kappa-B kinase subunit beta (IKBKB) and RELA) and MYC were further identified as direct targets of METTL3-mediated m6A modification.overexpression of METTL3 significantly promoted Bladder cancer cell growth and invasion."
item143	REG00007	M6ATAR00425	Up	M6ADIS0070	.	30659266	"AF4/FMR2 family member 4 (AFF4), two key regulators of NF-Kappa-B pathway (IKBKB and Transcription factor p65 (RELA)) and MYC were further identified as direct targets of METTL3-mediated m6A modification.overexpression of METTL3 significantly promoted Bladder cancer cell growth and invasion."
item144	REG00007	M6ATAR00341	Up	M6ADIS0070	.	30659266	"AF4/FMR2 family member 4 (AFF4), two key regulators of NF-Kappa-B pathway (IKBKB and RELA) and Myc proto-oncogene protein (MYC) were further identified as direct targets of METTL3-mediated m6A modification.overexpression of METTL3 significantly promoted Bladder cancer cell growth and invasion."
item145	REG00001	M6ATAR00341	Up	M6ADIS0061	.	30719115	"FTO has been indicated to interact with Myc proto-oncogene protein (MYC) proto-oncogene, bHLH transcription factor and to enhance its stability by decreasing its m6A level.the aforementioned observations indicate a novel mechanism for the regulation of pancreatic cancer cells by FTO."
item146	REG00007	M6ATAR00334	Up	M6ADIS0029	.	30762711	METTL3 is upregulated in human melanoma and plays a role in invasion/migration through MMP2. METTL3 overexpression promotes accumulation of 72 kDa type IV collagenase (MMP2) and N-cadherin in melanoma cells.
item147	REG00007	M6ATAR00202	Up	M6ADIS0029	.	30762711	METTL3 is upregulated in human melanoma and plays a role in invasion/migration through MMP2. METTL3 overexpression promotes accumulation of MMP2 and Cadherin-2 (CDH2/N-cadherin) in melanoma cells.
item148	.	M6ATAR00341	.	M6ADIS0002	.	30766746	"In this review, we discuss the specific roles of m6A ""writers"", ""erasers"", and ""readers"" in normal physiology and how their altered expression promotes tumorigenesis. We also describe the potential of exploiting the aberrant expression of these enzymes for cancer diagnosis, prognosis, and the development of novel therapies. The abnormal expression of m6A regulatory enzymes affects m6A abundance and consequently dysregulates the expression of tumor suppressor genes and oncogenes, including Myc proto-oncogene protein (MYC), SOCS2, ADAM19, and PTEN."
item149	.	M6ATAR00401	.	M6ADIS0002	.	30766746	"In this review, we discuss the specific roles of m6A ""writers"", ""erasers"", and ""readers"" in normal physiology and how their altered expression promotes tumorigenesis. We also describe the potential of exploiting the aberrant expression of these enzymes for cancer diagnosis, prognosis, and the development of novel therapies. The abnormal expression of m6A regulatory enzymes affects m6A abundance and consequently dysregulates the expression of tumor suppressor genes and oncogenes, including MYC, Suppressor of cytokine signaling 2 (SOCS2), ADAM19, and PTEN."
item150	.	M6ATAR00171	.	M6ADIS0002	.	30766746	"In this review, we discuss the specific roles of m6A ""writers"", ""erasers"", and ""readers"" in normal physiology and how their altered expression promotes tumorigenesis. We also describe the potential of exploiting the aberrant expression of these enzymes for cancer diagnosis, prognosis, and the development of novel therapies. The abnormal expression of m6A regulatory enzymes affects m6A abundance and consequently dysregulates the expression of tumor suppressor genes and oncogenes, including MYC, SOCS2, Meltrin-beta (ADAM19), and PTEN."
item151	.	M6ATAR00375	.	M6ADIS0002	.	30766746	"In this review, we discuss the specific roles of m6A ""writers"", ""erasers"", and ""readers"" in normal physiology and how their altered expression promotes tumorigenesis. We also describe the potential of exploiting the aberrant expression of these enzymes for cancer diagnosis, prognosis, and the development of novel therapies. The abnormal expression of m6A regulatory enzymes affects m6A abundance and consequently dysregulates the expression of tumor suppressor genes and oncogenes, including MYC, SOCS2, ADAM19, and Mutated in multiple advanced cancers 1 (PTEN)."
item152	REG00007	M6ATAR00368	Up	M6ADIS0007	.	30774445	"MiR-600 inhibited lung cancer via down-regulating METTL3 expression, and knockdown of METTL3 was used as a novel strategy for lung cancer therapy. The PI3-kinase subunit alpha (PI3k/PIK3CA)/Akt pathway is implicated in cell growth and survival and we also observed that knockdown of METTL3 changed the expression and phosphorylation of proteins of PI3K signaling pathway members."
item153	REG00007	.	.	M6ADIS0001	.	30781903	METTL3 plays a vital role in many steps of RNA processing and orchestrates successful execution of oncogenic pathways in Glioma.
item154	.	M6ATAR00274	.	M6ADIS0125	.	30824325	"Lnc-Dpf3 directly bound to Hypoxia-inducible factor 1-alpha (HIF-1-Alpha/HIF1A) and suppressed HIF-1-alpha-dependent transcription of the glycolytic gene Ldha, thus inhibiting DC glycolytic metabolism and migratory capacity. CCR7-inducible lnc-Dpf3 in coupling epigenetic and metabolic pathways to feedback-control DC migration and inflammatory responses."
item155	REG00001	M6ATAR00349	Up	M6ADIS0088	.	30835997	"Decreased m6A in dopaminergic cells by overexpressing a nucleic acid demethylase, FTO, or by m6A inhibitor. m6A reduction could induce the expression of Glutamate receptor ionotropic, NMDA 1 (NMDAR1/GRIN1), and elevate oxidative stress and Ca2+ influx, resulting in dopaminergic neuron apoptosis. m6A modification plays a vital role in the death of dopaminergic neuron, which provides a novel view of mRNA methylation to understand the epigenetic regulation of Parkinson's disease."
item156	REG00025	.	.	M6ADIS0009	.	30866959	"Abundance of m6A and expression of VIRMA/YTHDF3 were different among Testicular Germ Cell Tumors subtypes, with higher levels in SEs, suggesting a contribution to SE phenotype maintenance."
item157	REG00015	.	Up	M6ADIS0009	.	30866959	"Abundance of m6A and expression of VIRMA/YTHDF3 were different among Testicular Germ Cell Tumors subtypes, with higher levels in SEs, suggesting a contribution to SE phenotype maintenance."
item158	REG00007	M6ATAR00426	Down	M6ADIS0096	.	30870073	"METTL3 methylates Transcription factor EB (TFEB), a master regulator of lysosomal biogenesis and autophagy genes, at two m6A residues in the 3'-UTR, which promotes the association of the RNA-binding protein HNRNPD with TFEB pre-mRNA and subsequently decreases the expression levels of TFEB. METTL3-ALKBH5 and autophagy, providing insight into the functional importance of the reversible mRNA m6A methylation and its modulators in ischemic heart disease."
item159	REG00005	M6ATAR00426	Up	M6ADIS0096	.	30870073	"METTL3 methylates Transcription factor EB (TFEB), a master regulator of lysosomal biogenesis and autophagy genes, at two m6A residues in the 3'-UTR, which promotes the association of the RNA-binding protein HNRNPD with TFEB pre-mRNA and subsequently decreases the expression levels of TFEB. METTL3-ALKBH5 and autophagy, providing insight into the functional importance of the reversible mRNA m6A methylation and its modulators in ischemic heart disease."
item160	REG00007	.	.	M6ADIS0010	.	30877265	"It is plausible that VHL-HIF-METTL3/14 pathways are involved in the m6A regulation in clear cell renal cell carcinoma cells, and PI3K-mTOR as well as p53 signaling pathways are possible downstream targets of m6A in ccRCC."
item161	REG00006	.	.	M6ADIS0010	.	30877265	"It is plausible that VHL-HIF-METTL3/14 pathways are involved in the m6A regulation in clear cell renal cell carcinoma cells, and PI3K-mTOR as well as p53 signaling pathways are possible downstream targets of m6A in ccRCC."
item162	REG00007	M6ATAR00196	Up	M6ADIS0057	.	30886897	"Down-regulation of METTL3 inhibits the proliferation and mobility of human gastric cancer cells and leads to inactivation of the AKT signaling pathway, suggesting that METTL3 is a potential target for the treatment of human gastric cancer. METTL3 knockdown decreased Apoptosis regulator Bcl-2 (BCL2) and increased Bax and active Caspase-3 in gastric cancer cells, which suggested the apoptotic pathway was activated. METTL3 led to inactivation of the AKT signaling pathway in human gastric cancer cells, including decreased phosphorylation levels of AKT and expression of down-stream effectors p70S6K and Cyclin D1."
item163	REG00007	M6ATAR00195	Down	M6ADIS0057	.	30886897	"Down-regulation of METTL3 inhibits the proliferation and mobility of human gastric cancer cells and leads to inactivation of the AKT signaling pathway, suggesting that METTL3 is a potential target for the treatment of human gastric cancer. METTL3 knockdown decreased Bcl2 and increased Apoptosis regulator BAX (BAX) and active Caspase-3 in gastric cancer cells, which suggested the apoptotic pathway was activated. METTL3 led to inactivation of the AKT signaling pathway in human gastric cancer cells, including decreased phosphorylation levels of AKT and expression of down-stream effectors p70S6K and Cyclin D1."
item164	REG00007	M6ATAR00203	Down	M6ADIS0057	.	30886897	"Down-regulation of METTL3 inhibits the proliferation and mobility of human gastric cancer cells and leads to inactivation of the AKT signaling pathway, suggesting that METTL3 is a potential target for the treatment of human gastric cancer. METTL3 knockdown decreased Bcl2 and increased Bax and active Caspase-3 (CASP3) in gastric cancer cells, which suggested the apoptotic pathway was activated. METTL3 led to inactivation of the AKT signaling pathway in human gastric cancer cells, including decreased phosphorylation levels of AKT and expression of down-stream effectors p70S6K and Cyclin D1."
item165	REG00007	M6ATAR00175	Up	M6ADIS0057	.	30886897	"Down-regulation of METTL3 inhibits the proliferation and mobility of human gastric cancer cells and leads to inactivation of the AKT signaling pathway, suggesting that METTL3 is a potential target for the treatment of human gastric cancer. METTL3 knockdown decreased Bcl2 and increased Bax and active Caspase-3 in gastric cancer cells, which suggested the apoptotic pathway was activated. METTL3 led to inactivation of the AKT signaling pathway in human gastric cancer cells, including decreased phosphorylation levels of RAC-alpha serine/threonine-protein kinase (AKT1) and expression of down-stream effectors p70S6K and Cyclin D1."
item166	REG00007	M6ATAR00313	Up	M6ADIS0057	.	30886897	"Down-regulation of METTL3 inhibits the proliferation and mobility of human gastric cancer cells and leads to inactivation of the AKT signaling pathway, suggesting that METTL3 is a potential target for the treatment of human gastric cancer. METTL3 knockdown decreased Bcl2 and increased Bax and active Caspase-3 in gastric cancer cells, which suggested the apoptotic pathway was activated. METTL3 led to inactivation of the AKT signaling pathway in human gastric cancer cells, including decreased phosphorylation levels of AKT and expression of down-stream effectors Ribosomal protein S6 kinase beta-1 (RPS6KB1/p70S6K) and Cyclin D1."
item167	REG00007	M6ATAR00206	Up	M6ADIS0057	.	30886897	"Down-regulation of METTL3 inhibits the proliferation and mobility of human gastric cancer cells and leads to inactivation of the AKT signaling pathway, suggesting that METTL3 is a potential target for the treatment of human gastric cancer. METTL3 knockdown decreased Bcl2 and increased Bax and active Caspase-3 in gastric cancer cells, which suggested the apoptotic pathway was activated. METTL3 led to inactivation of the AKT signaling pathway in human gastric cancer cells, including decreased phosphorylation levels of AKT and expression of down-stream effectors p70S6K and G1/S-specific cyclin-D1 (CCND1)."
item168	REG00001	M6ATAR00441	Up	M6ADIS0007	M6ADRUG0040	30905413	"The m6A demethylase FTO promotes the growth of Non-small cell lung cancer cells by increasing the expression of USP7.Genetic knockdown or pharmacological inhibition (P5091 or P22027) of Ubiquitin carboxyl-terminal hydrolase 7 (USP7) reduced the proliferation rate of lung cancer cells and decreased the capacity of colony formation of lung cancer cells in vitro, whereas lung cancer cells growth inhibition by FTO knockdown is restored by overexertion of USP7."
item169	REG00001	M6ATAR00441	Up	M6ADIS0007	M6ADRUG0077	30905413	"The m6A demethylase FTO promotes the growth of Non-small cell lung cancer cells by increasing the expression of USP7.Genetic knockdown or pharmacological inhibition (P5091 or P22027) of Ubiquitin carboxyl-terminal hydrolase 7 (USP7) reduced the proliferation rate of lung cancer cells and decreased the capacity of colony formation of lung cancer cells in vitro, whereas lung cancer cells growth inhibition by FTO knockdown is restored by overexertion of USP7."
item170	.	M6ATAR00114	.	M6ADIS0057	.	30914234	Reveal the compelling role of m6A in GC and highlight the regulatory function of the microRNA 660 (MIR660)/E2F3 pathway in Gastric cancer progression.
item171	.	M6ATAR00235	.	M6ADIS0057	.	30914234	Reveal the compelling role of m6A in GC and highlight the regulatory function of the miR-660/Transcription factor E2F3 (E2F3) pathway in Gastric cancer progression.
item172	.	.	.	M6ADIS0002	.	30914411	"The pseudogene Olfr29-ps1 regulates the differentiation and function of MDSCs through a m6A-modified Olfr29-ps1/miR-214-3p/MyD88 regulatory network, revealing a mechanism for the regulation of myeloid cells and also providing potential targets for antitumor immunotherapy."
item173	REG00001	M6ATAR00201	Up	M6ADIS0065	.	30922314	FTO mediated m6A demethylation in the 3'UTR of BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3) mRNA and induced its degradation via an YTHDF2 independent mechanism. FTO serves as a novel potential therapeutic target for breast cancer.
item174	REG00004	M6ATAR00107	Up	M6ADIS0061	.	30949406	Urothelial cancer associated 1 (UCA1) increases KRAS phosphorylation by interacting with hnRNPA2B1 and that UCA1 functions as a molecular sponge for miR-590-3p to promote KRAS expression. the UCA1-KRAS axis plays a crucial role in pancreatic ductal adenocarcinoma progression and that UCA1 serves as a target for new PDAC therapies.
item175	REG00004	M6ATAR00379	Up	M6ADIS0061	.	30949406	UCA1 increases GTPase KRas (KRAS) phosphorylation by interacting with hnRNPA2B1 and that UCA1 functions as a molecular sponge for miR-590-3p to promote KRAS expression. the UCA1-KRAS axis plays a crucial role in pancreatic ductal adenocarcinoma progression and that UCA1 serves as a target for new PDAC therapies.
item176	REG00004	M6ATAR00251	Down	M6ADIS0059	.	30979372	"The RP11/hnRNPA2B1/mRNA complex accelerated the mRNA degradation of two E3 ligases, Siah1 and F-box/SPRY domain-containing protein 1 (FBXO45), and subsequently prevented the proteasomal degradation of Zeb1. m6A can regulate the expression of RP11, further, RP11 regulated Siah1-Fbxo45/Zeb1 was involved in the development of Colorectal cancer."
item177	REG00004	M6ATAR00149	Up	M6ADIS0059	.	30979372	"The U4/U6 small nuclear ribonucleoprotein Prp31 (PRPF31/RP11)/hnRNPA2B1/mRNA complex accelerated the mRNA degradation of two E3 ligases, Siah1 and Fbxo45, and subsequently prevented the proteasomal degradation of Zeb1. m6A can regulate the expression of RP11, further, RP11 regulated Siah1-Fbxo45/Zeb1 was involved in the development of Colorectal cancer."
item178	REG00004	M6ATAR00453	Up	M6ADIS0059	.	30979372	"The RP11/hnRNPA2B1/mRNA complex accelerated the mRNA degradation of two E3 ligases, Siah1 and Fbxo45, and subsequently prevented the proteasomal degradation of Zinc finger E-box-binding homeobox 1 (ZEB1). m6A can regulate the expression of RP11, further, RP11 regulated Siah1-Fbxo45/Zeb1 was involved in the development of Colorectal cancer."
item179	REG00004	M6ATAR00392	Down	M6ADIS0059	.	30979372	"The RP11/hnRNPA2B1/mRNA complex accelerated the mRNA degradation of two E3 ligases, E3 ubiquitin-protein ligase SIAH1 (SIAH1) and Fbxo45, and subsequently prevented the proteasomal degradation of Zeb1. m6A can regulate the expression of RP11, further, RP11 regulated Siah1-Fbxo45/Zeb1 was involved in the development of Colorectal cancer."
item180	REG00005	M6ATAR00196	Up	M6ADIS0066	.	30987661	"ALKBH5 is a tumor-promoting gene in epithelial ovarian cancer, which is involved in the mTOR pathway and Apoptosis regulator Bcl-2 (BCL2)-Beclin1 complex. ALKBH5 activated EGFR-PIK3CA-AKT-mTOR signaling pathway. ALKBH5 inhibited autophagy of epithelial ovarian cancer through miR-7 and BCL-2."
item181	REG00005	M6ATAR00237	Up	M6ADIS0066	.	30987661	"ALKBH5 is a tumor-promoting gene in epithelial ovarian cancer, which is involved in the mTOR pathway and BCL-2-Beclin1 complex. ALKBH5 activated Epidermal growth factor receptor (EGFR)-PIK3CA-AKT-mTOR signaling pathway. ALKBH5 inhibited autophagy of epithelial ovarian cancer through miR-7 and BCL-2."
item182	REG00005	M6ATAR00368	Up	M6ADIS0066	.	30987661	"ALKBH5 is a tumor-promoting gene in epithelial ovarian cancer, which is involved in the mTOR pathway and BCL-2-Beclin1 complex. ALKBH5 activated EGFR-PI3-kinase subunit alpha (PI3k/PIK3CA)-AKT-mTOR signaling pathway. ALKBH5 inhibited autophagy of epithelial ovarian cancer through miR-7 and BCL-2."
item183	REG00005	M6ATAR00125	Down	M6ADIS0066	.	30987661	"ALKBH5 is a tumor-promoting gene in epithelial ovarian cancer, which is involved in the mTOR pathway and microRNA 7-1 (MIR7-1)-Beclin1 complex. ALKBH5 activated EGFR-PIK3CA-AKT-mTOR signaling pathway. ALKBH5 inhibited autophagy of epithelial ovarian cancer through microRNA 7-1 (MIR7-1) and BCL-2."
item184	REG00005	M6ATAR00197	Up	M6ADIS0066	.	30987661	"ALKBH5 is a tumor-promoting gene in epithelial ovarian cancer, which is involved in the mTOR pathway and BCL-2-Beclin-1 (BECN1) complex. ALKBH5 activated EGFR-PIK3CA-AKT-mTOR signaling pathway. ALKBH5 inhibited autophagy of epithelial ovarian cancer through miR-7 and BCL-2."
item185	REG00001	.	.	M6ADIS0046	.	30991023	"A prevalent eukaryotic N6-methyladensosine (m6A) post-transcriptional mark can be ""erased"" by the m6A demethylase FTO, which is commonly deregulated in acute myeloid leukemia (AML)."
item186	REG00007	M6ATAR00127	Up	M6ADIS0061	.	31015415	Cigarette smoke-induced microRNA 25 (MIR25) excessive maturation via m6A modification promotes the development and progression of pancreatic cancer. This modification is catalyzed by overexpressed methyltransferase-like 3 (METTL3) due to hypomethylation of the METTL3 promoter also caused by CSC.
item187	REG00008	M6ATAR00007	Down	M6ADIS0046	.	31031138	"Acute myeloid leukemia (AML) is an aggressive clonal disorder of hematopoietic stem cells (HSCs) and primitive progenitors that blocks their myeloid differentiation, generating self-renewing leukemic stem cells (LSCs). YTHDF2 decreases the half-life of diverse m6A transcripts that contribute to the overall integrity of LSC function, including the tumor necrosis factor receptor Tnfrsf2, whose upregulation in Ythdf2-deficient LSCs primes cells for apoptosis."
item188	REG00007	M6ATAR00399	Up	M6ADIS0006	.	31061416	"The upregulation of METTL3 and YTHDF1 act as adverse prognosis factors for overall survival (OS) rate of liver cancer patients. m6A-sequencing and functional studies confirm that Zinc finger protein SNAI1 (SNAI1), a key transcription factor of EMT, is involved in m6A-regulated EMT."
item189	REG00024	M6ATAR00399	Up	M6ADIS0006	.	31061416	"The upregulation of METTL3 and YTHDF1 act as adverse prognosis factors for overall survival (OS) rate of liver cancer patients. m6A-sequencing and functional studies confirm that Zinc finger protein SNAI1 (SNAI1), a key transcription factor of EMT, is involved in m6A-regulated EMT."
item190	REG00007	M6ATAR00795	Up	M6ADIS0057	M6ADRUG0034	31097692	"ARHGAP5-AS1 also stabilized ARHGAP5 mRNA in the cytoplasm by recruiting METTL3 to stimulate m6A modification of Rho GTPase activating protein 5 (ARHGAP5) mRNA. As a result, ARHGAP5 was upregulated to promote chemoresistance and its upregulation was also associated with poor prognosis in gastric cancer. downregulation of ARHGAP5-AS1 in resistant cells evidently reversed the resistance to chemotherapeutic drugs including cisplatin (DDP), ADM, and 5-FU."
item191	REG00007	M6ATAR00795	Up	M6ADIS0057	M6ADRUG0047	31097692	"ARHGAP5-AS1 also stabilized ARHGAP5 mRNA in the cytoplasm by recruiting METTL3 to stimulate m6A modification of Rho GTPase activating protein 5 (ARHGAP5) mRNA. As a result, ARHGAP5 was upregulated to promote chemoresistance and its upregulation was also associated with poor prognosis in gastric cancer. downregulation of ARHGAP5-AS1 in resistant cells evidently reversed the resistance to chemotherapeutic drugs including cisplatin (DDP), ADM, and 5-FU."
item192	REG00007	M6ATAR00795	Up	M6ADIS0057	M6ADRUG0005	31097692	"ARHGAP5-AS1 also stabilized ARHGAP5 mRNA in the cytoplasm by recruiting METTL3 to stimulate m6A modification of Rho GTPase activating protein 5 (ARHGAP5) mRNA. As a result, ARHGAP5 was upregulated to promote chemoresistance and its upregulation was also associated with poor prognosis in gastric cancer. downregulation of ARHGAP5-AS1 in resistant cells evidently reversed the resistance to chemotherapeutic drugs including cisplatin (DDP), ADM, and 5-FU."
item193	.	.	.	.	.	31106001	"In this review, we provide an updated summary of RNA m6A modulation, focusing on the regulatory role of m6A RNA methylation in stem cell fate and cellular processes affecting death and survival."
item194	REG00015	M6ATAR00285	Up	M6ADIS0006	.	31118692	KIAA1429 facilitated migration and invasion of Hepatocellular carcinoma cells by inhibiting DNA-binding protein inhibitor ID-2 (ID2) via upregulating m6A modification of ID2 mRNA.
item195	.	M6ATAR00008	.	M6ADIS0044	.	31127091	"Oncogenic human papillomaviruses (HPVs) generate circRNAs, some of which encompass the E7 oncogene (circE7). Circ_E7 is N6-methyladenosine (m6A) modified, preferentially localized to the cytoplasm, associated with polysomes, and translated to produce E7 oncoprotein."
item196	REG00024	M6ATAR00222	Up	M6ADIS0059	.	31131257	Silencing YTHDF1 significantly inhibited Wnt/Catenin beta-1 (CTNNB1/Beta-catenin) pathway activity in Colorectal cancer cells.
item197	REG00001	M6ATAR00424	Down	M6ADIS0006	.	31143705	"RNA decay assay showed that oncogene Transcriptional enhancer factor TEF-4 (TEAD2) mRNA stability was impaired by FTO. The overexpression of FTO suppressed tumor growth in vivo. In conclusion, our study demonstrated the critical roles of FTO in Intrahepatic cholangiocarcinoma."
item198	REG00007	M6ATAR00357	Up	M6ADIS0035	.	31153635	METTL3 knock down and methylation inhibitor cycloleucine could decrease the m6A levels and the expression of DeltaNp63 in Cutaneous squamous cell carcinoma.
item199	REG00007	M6ATAR00009	Up	M6ADIS0119	.	31156435	METTL3 interacts with the microprocessor protein DGCR8 and positively modulates hsa-miR-873-5p mature process in an m6A-dependent manner.METTL3/m6A in colistin-induced nephrotoxicity and provide a new insight on m6A modification in drug induced toxicity.
item200	REG00007	M6ATAR00333	Up	M6ADIS0110	.	31186141	"METTL3 has a functional role in mediates osteoarthritis progression by regulating NF-Kappa-B signaling and ECM synthesis in chondrocytes that shed insight on developing preventive and curative strategies for OA by focusing on METTL3 and mRNA methylation. Silencing of METTL3 promotes degradation of extracellular matrix (ECM) by reducing the expression of Collagenase 3 (MMP13) and Coll X, elevating the expression of Aggrecan and Coll II."
item201	REG00007	M6ATAR00365	Up	M6ADIS0110	.	31186141	"METTL3 has a functional role in mediates osteoarthritis progression by regulating NF-Kappa-B signaling and ECM synthesis in chondrocytes that shed insight on developing preventive and curative strategies for OA by focusing on METTL3 and mRNA methylation. Silencing of METTL3 promotes degradation of extracellular matrix (ECM) by reducing the expression of MMP-13 and Prostaglandin G/H synthase 2 (Coll X/PTGS2), elevating the expression of Aggrecan and Coll II."
item202	REG00007	M6ATAR00130	Up	M6ADIS0070	.	31228940	METTL3 has an oncogenic role in bladder cancer through interacting with the microprocessor protein DGCR8 and positively modulating the microRNA 221 (MIR221) process in an m6A-dependent manner.
item203	REG00007	M6ATAR00129	Up	M6ADIS0070	.	31228940	METTL3 has an oncogenic role in bladder cancer through interacting with the microprocessor protein DGCR8 and positively modulating the microRNA 222 (MIR222) process in an m6A-dependent manner.
item204	REG00007	M6ATAR00404	Up	M6ADIS0059	.	31230592	"METTL3, acting as an oncogene, maintained Transcription factor SOX-2 (SOX2) expression through an m6A-IGF2BP2-dependent mechanism in CRC cells, and indicated a potential biomarker panel for prognostic prediction in Colorectal carcinoma."
item205	REG00013	M6ATAR00404	Up	M6ADIS0059	.	31230592	"METTL3, acting as an oncogene, maintained Transcription factor SOX-2 (SOX2) expression through an m6A-IGF2BP2-dependent mechanism in CRC cells, and indicated a potential biomarker panel for prognostic prediction in Colorectal carcinoma."
item206	REG00007	M6ATAR00170	Up	M6ADIS0057	.	31232471	"METTL3 knockdown decreased Actin, aortic smooth muscle (ACTA2) muscle actin. Taken together, our finding revealed that m6A methylation writer METTL3 serve as an oncogene in tumorigenesis of Gastric cancer."
item207	REG00001	M6ATAR00223	Up	M6ADIS0029	M6ADRUG0058	31239444	"These findings demonstrate a crucial role of FTO as an m6A demethylase in promoting melanoma tumorigenesis and anti-PD-1 resistance, and suggest that the combination of FTO inhibition with anti-PD-1 blockade reduces the resistance to immunotherapy in melanoma. Knockdown of FTO increases m6A methylation in the critical protumorigenic melanoma cell-intrinsic genes including PD-1 (PDCD1), C-X-C chemokine receptor type 4 (CXCR4), and SOX10, leading to increased RNA decay through the m6A reader YTHDF2."
item208	REG00008	M6ATAR00223	Down	M6ADIS0029	M6ADRUG0058	31239444	"These findings demonstrate a crucial role of FTO as an m6A demethylase in promoting melanoma tumorigenesis and anti-PD-1 resistance, and suggest that the combination of FTO inhibition with anti-PD-1 blockade reduces the resistance to immunotherapy in melanoma. Knockdown of FTO increases m6A methylation in the critical protumorigenic melanoma cell-intrinsic genes including PD-1 (PDCD1), C-X-C chemokine receptor type 4 (CXCR4), and SOX10, leading to increased RNA decay through the m6A reader YTHDF2."
item209	REG00001	M6ATAR00796	Up	M6ADIS0029	M6ADRUG0058	31239444	"These findings demonstrate a crucial role of FTO as an m6A demethylase in promoting melanoma tumorigenesis and anti-PD-1 resistance, and suggest that the combination of FTO inhibition with anti-PD-1 blockade reduces the resistance to immunotherapy in melanoma. Knockdown of FTO increases m6A methylation in the critical protumorigenic melanoma cell-intrinsic genes including Programmed cell death 1 (PD-1) (PDCD1), CXCR4, and SOX10, leading to increased RNA decay through the m6A reader YTHDF2."
item210	REG00008	M6ATAR00796	Down	M6ADIS0029	M6ADRUG0058	31239444	"These findings demonstrate a crucial role of FTO as an m6A demethylase in promoting melanoma tumorigenesis and anti-PD-1 resistance, and suggest that the combination of FTO inhibition with anti-PD-1 blockade reduces the resistance to immunotherapy in melanoma. Knockdown of FTO increases m6A methylation in the critical protumorigenic melanoma cell-intrinsic genes including Programmed cell death 1 (PD-1) (PDCD1), CXCR4, and SOX10, leading to increased RNA decay through the m6A reader YTHDF2."
item211	REG00008	M6ATAR00403	Down	M6ADIS0029	M6ADRUG0058	31239444	"These findings demonstrate a crucial role of FTO as an m6A demethylase in promoting melanoma tumorigenesis and anti-PD-1 resistance, and suggest that the combination of FTO inhibition with anti-PD-1 blockade reduces the resistance to immunotherapy in melanoma. Knockdown of FTO increases m6A methylation in the critical protumorigenic melanoma cell-intrinsic genes including PD-1 (PDCD1), CXCR4, and Transcription factor SOX-10 (SOX10), leading to increased RNA decay through the m6A reader YTHDF2."
item212	REG00001	M6ATAR00403	Up	M6ADIS0029	M6ADRUG0058	31239444	"These findings demonstrate a crucial role of FTO as an m6A demethylase in promoting melanoma tumorigenesis and anti-PD-1 resistance, and suggest that the combination of FTO inhibition with anti-PD-1 blockade reduces the resistance to immunotherapy in melanoma. Knockdown of FTO increases m6A methylation in the critical protumorigenic melanoma cell-intrinsic genes including PD-1 (PDCD1), CXCR4, and Transcription factor SOX-10 (SOX10), leading to increased RNA decay through the m6A reader YTHDF2."
item213	REG00007	M6ATAR00330	Down	M6ADIS0059	.	31239708	"METTL3 played a tumor-suppressive role in Colorectal cancer cell proliferation, migration and invasion through Mitogen-activated protein kinase 14 (p38/MAPK14)/ERK pathways, which indicated that METTL3 was a novel marker for CRC carcinogenesis, progression and survival."
item214	REG00007	M6ATAR00244	Down	M6ADIS0059	.	31239708	"METTL3 played a tumor-suppressive role in Colorectal cancer cell proliferation, migration and invasion through p38/Ephrin type-B receptor 2 (ERK/EPHB2) pathways, which indicated that METTL3 was a novel marker for CRC carcinogenesis, progression and survival."
item215	REG00007	M6ATAR00315	Up	M6ADIS0051	.	31253399	"METTL3 silence decreased the m6A methylation and total mRNA level of Lymphoid enhancer-binding factor 1 (LEF1),the m6A methyltransferase METTL3 promotes osteosarcoma cell progression by regulating the m6A level of LEF1 and activating Wnt/beta-catenin signaling pathway."
item216	REG00004	M6ATAR00010	Down	M6ADIS0065	M6ADRUG0039	31263129	"HNRNPA2B1 is a reader of the N(6)-methyladenosine mark in primary-miRNAs and promotes DROSHA processing to precursor-miRNAs. HNRNPA2B1 downregulated hsa-miR-29a-3p, miR-29b-3p, and miR-222 and upregulated miR-1266-5p, miR-1268a, miR-671-3p. Transient overexpression of HNRNPA2/B1 reduced breast cancer cellMCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for HNRNPA2/B1 in endocrine-resistance."
item217	REG00004	M6ATAR00011	Down	M6ADIS0065	M6ADRUG0039	31263129	"HNRNPA2B1 is a reader of the N(6)-methyladenosine mark in primary-miRNAs and promotes DROSHA processing to precursor-miRNAs. HNRNPA2B1 downregulated miR-29a-3p, hsa-miR-29b-3p, and miR-222 and upregulated miR-1266-5p, miR-1268a, miR-671-3p. Transient overexpression of HNRNPA2/B1 reduced breast cancer cellMCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for HNRNPA2/B1 in endocrine-resistance."
item218	REG00004	M6ATAR00129	Down	M6ADIS0065	M6ADRUG0039	31263129	"HNRNPA2B1 is a reader of the N(6)-methyladenosine mark in primary-miRNAs and promotes DROSHA processing to precursor-miRNAs. HNRNPA2B1 downregulated miR-29a-3p, miR-29b-3p, and microRNA 222 (MIR222) and upregulated miR-1266-5p, miR-1268a, miR-671-3p. Transient overexpression of HNRNPA2/B1 reduced breast cancer cellMCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for HNRNPA2/B1 in endocrine-resistance."
item219	REG00004	M6ATAR00012	Up	M6ADIS0065	M6ADRUG0039	31263129	"HNRNPA2B1 is a reader of the N(6)-methyladenosine mark in primary-miRNAs and promotes DROSHA processing to precursor-miRNAs. HNRNPA2B1 downregulated miR-29a-3p, miR-29b-3p, and miR-222 and upregulated hsa-miR-1266-5p, miR-1268a, miR-671-3p. Transient overexpression of HNRNPA2/B1 reduced breast cancer cellMCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for HNRNPA2/B1 in endocrine-resistance."
item220	REG00004	M6ATAR00013	Up	M6ADIS0065	M6ADRUG0039	31263129	"HNRNPA2B1 is a reader of the N(6)-methyladenosine mark in primary-miRNAs and promotes DROSHA processing to precursor-miRNAs. HNRNPA2B1 downregulated miR-29a-3p, miR-29b-3p, and miR-222 and upregulated miR-1266-5p, hsa-miR-1268a, miR-671-3p. Transient overexpression of HNRNPA2/B1 reduced breast cancer cellMCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for HNRNPA2/B1 in endocrine-resistance."
item221	REG00004	M6ATAR00014	Up	M6ADIS0065	M6ADRUG0039	31263129	"HNRNPA2B1 is a reader of the N(6)-methyladenosine mark in primary-miRNAs and promotes DROSHA processing to precursor-miRNAs. HNRNPA2B1 downregulated miR-29a-3p, miR-29b-3p, and miR-222 and upregulated miR-1266-5p, miR-1268a, hsa-miR-671-3p. Transient overexpression of HNRNPA2/B1 reduced breast cancer cellMCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for HNRNPA2/B1 in endocrine-resistance."
item222	REG00004	M6ATAR00385	Up	M6ADIS0065	M6ADRUG0039	31263129	"HNRNPA2B1 is a reader of the N(6)-methyladenosine mark in primary-miRNAs and promotes Ribonuclease 3 (DROSHA) processing to precursor-miRNAs. HNRNPA2B1 downregulated miR-29a-3p, miR-29b-3p, and miR-222 and upregulated miR-1266-5p, miR-1268a, miR-671-3p. Transient overexpression of HNRNPA2/B1 reduced breast cancer cellMCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for HNRNPA2/B1 in endocrine-resistance."
item223	REG00004	M6ATAR00010	Down	M6ADIS0065	M6ADRUG0028	31263129	"HNRNPA2B1 is a reader of the N(6)-methyladenosine mark in primary-miRNAs and promotes DROSHA processing to precursor-miRNAs. HNRNPA2B1 downregulated hsa-miR-29a-3p, miR-29b-3p, and miR-222 and upregulated miR-1266-5p, miR-1268a, miR-671-3p. Transient overexpression of HNRNPA2/B1 reduced breast cancer cellMCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for HNRNPA2/B1 in endocrine-resistance."
item224	REG00004	M6ATAR00011	Down	M6ADIS0065	M6ADRUG0028	31263129	"HNRNPA2B1 is a reader of the N(6)-methyladenosine mark in primary-miRNAs and promotes DROSHA processing to precursor-miRNAs. HNRNPA2B1 downregulated miR-29a-3p, hsa-miR-29b-3p, and miR-222 and upregulated miR-1266-5p, miR-1268a, miR-671-3p. Transient overexpression of HNRNPA2/B1 reduced breast cancer cellMCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for HNRNPA2/B1 in endocrine-resistance."
item225	REG00004	M6ATAR00129	Down	M6ADIS0065	M6ADRUG0028	31263129	"HNRNPA2B1 is a reader of the N(6)-methyladenosine mark in primary-miRNAs and promotes DROSHA processing to precursor-miRNAs. HNRNPA2B1 downregulated miR-29a-3p, miR-29b-3p, and microRNA 222 (MIR222) and upregulated miR-1266-5p, miR-1268a, miR-671-3p. Transient overexpression of HNRNPA2/B1 reduced breast cancer cellMCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for HNRNPA2/B1 in endocrine-resistance."
item226	REG00004	M6ATAR00012	Up	M6ADIS0065	M6ADRUG0028	31263129	"HNRNPA2B1 is a reader of the N(6)-methyladenosine mark in primary-miRNAs and promotes DROSHA processing to precursor-miRNAs. HNRNPA2B1 downregulated miR-29a-3p, miR-29b-3p, and miR-222 and upregulated hsa-miR-1266-5p, miR-1268a, miR-671-3p. Transient overexpression of HNRNPA2/B1 reduced breast cancer cellMCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for HNRNPA2/B1 in endocrine-resistance."
item227	REG00004	M6ATAR00013	Up	M6ADIS0065	M6ADRUG0028	31263129	"HNRNPA2B1 is a reader of the N(6)-methyladenosine mark in primary-miRNAs and promotes DROSHA processing to precursor-miRNAs. HNRNPA2B1 downregulated miR-29a-3p, miR-29b-3p, and miR-222 and upregulated miR-1266-5p, hsa-miR-1268a, miR-671-3p. Transient overexpression of HNRNPA2/B1 reduced breast cancer cellMCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for HNRNPA2/B1 in endocrine-resistance."
item228	REG00004	M6ATAR00014	Up	M6ADIS0065	M6ADRUG0028	31263129	"HNRNPA2B1 is a reader of the N(6)-methyladenosine mark in primary-miRNAs and promotes DROSHA processing to precursor-miRNAs. HNRNPA2B1 downregulated miR-29a-3p, miR-29b-3p, and miR-222 and upregulated miR-1266-5p, miR-1268a, hsa-miR-671-3p. Transient overexpression of HNRNPA2/B1 reduced breast cancer cellMCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for HNRNPA2/B1 in endocrine-resistance."
item229	REG00004	M6ATAR00385	Up	M6ADIS0065	M6ADRUG0028	31263129	"HNRNPA2B1 is a reader of the N(6)-methyladenosine mark in primary-miRNAs and promotes Ribonuclease 3 (DROSHA) processing to precursor-miRNAs. HNRNPA2B1 downregulated miR-29a-3p, miR-29b-3p, and miR-222 and upregulated miR-1266-5p, miR-1268a, miR-671-3p. Transient overexpression of HNRNPA2/B1 reduced breast cancer cellMCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for HNRNPA2/B1 in endocrine-resistance."
item230	.	M6ATAR00243	.	M6ADIS0010	.	31289360	"MTHFD2 plays a critical role in controlling global N6-methyladenosine (m6A) methylation levels, including the m6A methylation of Endothelial PAS domain-containing protein 1 (HIF-2Alpha/EPAS1) mRNA, which results in enhanced translation of HIF-2-alpha. MTHFD2 links RNA methylation status to the metabolic state of tumor cells in Renal cell carcinoma."
item231	REG00005	M6ATAR00140	Up	M6ADIS0057	.	31290116	ALKBH5 promotes Gastric cancer invasion and metastasis by demethylating the lncRNA Nuclear paraspeckle assembly transcript 1 (NEAT1).
item232	REG00006	M6ATAR00451	Down	M6ADIS0025	.	31318098	METTL14 promotes renal ischemic reperfusion injury via suppressing Transcriptional coactivator YAP1 (YAP1).
item233	REG00007	M6ATAR00143	Up	M6ADIS0054	.	31331909	"Family with sequence similarity 225 member A (FAM225A) functioned as a competing endogenous RNA (ceRNA) for sponging miR-590-3p and miR-1275, leading to the upregulation of their target integrin beta-3 (ITGB3), and the activation of FAK/PI3K/Akt signaling to promote Nasopharyngeal carcinoma cell proliferation and invasion. FAM225A showed lower RNA stability after silencing of METTL3."
item234	REG00007	M6ATAR00155	Up	M6ADIS0054	.	31331909	"FAM225A functioned as a competing endogenous RNA (ceRNA) for sponging miR-590-3p and miR-1275, leading to the upregulation of their target Integrin subunit beta 3 (ITGB3), and the activation of FAK/PI3K/Akt signaling to promote Nasopharyngeal carcinoma cell proliferation and invasion. FAM225A showed lower RNA stability after silencing of METTL3."
item235	REG00007	.	.	M6ADIS0020	M6ADRUG0076	31333841	"METTL3, METTL14, ALKBH5 and YTHDC2 are involved in the regulation of spermatogenesis and oogenesis. MA2 affected CDKs expression through the m6A-dependent mRNA degradation pathway, and thus repressed spermatogonial proliferation. Additionally, mutation of the predicted m6A sites in the Cdk2-3'UTR could mitigated the degradation of CDK2 mRNA after MA2 treatment."
item236	REG00006	.	.	M6ADIS0020	M6ADRUG0076	31333841	"METTL3, METTL14, ALKBH5 and YTHDC2 are involved in the regulation of spermatogenesis and oogenesis. MA2 affected CDKs expression through the m6A-dependent mRNA degradation pathway, and thus repressed spermatogonial proliferation. Additionally, mutation of the predicted m6A sites in the Cdk2-3'UTR could mitigated the degradation of CDK2 mRNA after MA2 treatment."
item237	REG00005	.	.	M6ADIS0020	M6ADRUG0076	31333841	"METTL3, METTL14, ALKBH5 and YTHDC2 are involved in the regulation of spermatogenesis and oogenesis. MA2 affected CDKs expression through the m6A-dependent mRNA degradation pathway, and thus repressed spermatogonial proliferation. Additionally, mutation of the predicted m6A sites in the Cdk2-3'UTR could mitigated the degradation of CDK2 mRNA after MA2 treatment."
item238	REG00023	.	.	M6ADIS0020	M6ADRUG0076	31333841	"METTL3, METTL14, ALKBH5 and YTHDC2 are involved in the regulation of spermatogenesis and oogenesis. MA2 affected CDKs expression through the m6A-dependent mRNA degradation pathway, and thus repressed spermatogonial proliferation. Additionally, mutation of the predicted m6A sites in the Cdk2-3'UTR could mitigated the degradation of CDK2 mRNA after MA2 treatment."
item239	REG00007	.	.	M6ADIS0077	.	31338816	"This reviewed summarize and discuss recent findings regarding the biological functions and underlying mechanisms of m6A modification(i.e., the METTL3/METTL14/WTAP complex and other cofactor proteins) and the associated machinery in normal hematopoiesis and the initiation, progression, and drug response of acute myeloid leukemia (AML), a major subtype of leukemia usually associated with unfavorable prognosis."
item240	REG00006	.	.	M6ADIS0077	.	31338816	"This reviewed summarize and discuss recent findings regarding the biological functions and underlying mechanisms of m6A modification(i.e., the METTL3/METTL14/WTAP complex and other cofactor proteins) and the associated machinery in normal hematopoiesis and the initiation, progression, and drug response of acute myeloid leukemia (AML), a major subtype of leukemia usually associated with unfavorable prognosis."
item241	REG00009	.	.	M6ADIS0077	.	31338816	"This reviewed summarize and discuss recent findings regarding the biological functions and underlying mechanisms of m6A modification(i.e., the METTL3/METTL14/WTAP complex and other cofactor proteins) and the associated machinery in normal hematopoiesis and the initiation, progression, and drug response of acute myeloid leukemia (AML), a major subtype of leukemia usually associated with unfavorable prognosis."
item242	REG00007	M6ATAR00291	Up	M6ADIS0094	.	31357177	"The long-lived endocrine mutants - Snell dwarf, growth hormone receptor deletion and pregnancy-associated plasma protein-A knockout - all show increases in the N6-adenosine-methyltransferases (METTL3/14) that catalyze 6-methylation of adenosine (m6A) in the 5' UTR region of select mRNAs. In addition, these mice have elevated levels of YTHDF1, which recognizes m6A and promotes translation by a cap-independent mechanism. Augmented translation by cap-independent pathways facilitated by m6A modifications contribute to the stress resistance and increased healthy longevity of mice with diminished GH and Insulin-like growth factor I (IGF1) signals."
item243	REG00006	M6ATAR00291	Up	M6ADIS0094	.	31357177	"The long-lived endocrine mutants - Snell dwarf, growth hormone receptor deletion and pregnancy-associated plasma protein-A knockout - all show increases in the N6-adenosine-methyltransferases (METTL3/14) that catalyze 6-methylation of adenosine (m6A) in the 5' UTR region of select mRNAs. In addition, these mice have elevated levels of YTHDF1, which recognizes m6A and promotes translation by a cap-independent mechanism. Augmented translation by cap-independent pathways facilitated by m6A modifications contribute to the stress resistance and increased healthy longevity of mice with diminished GH and Insulin-like growth factor I (IGF1) signals."
item244	REG00024	M6ATAR00291	Up	M6ADIS0094	.	31357177	"The long-lived endocrine mutants - Snell dwarf, growth hormone receptor deletion and pregnancy-associated plasma protein-A knockout - all show increases in the N6-adenosine-methyltransferases (METTL3/14) that catalyze 6-methylation of adenosine (m6A) in the 5' UTR region of select mRNAs. In addition, these mice have elevated levels of YTHDF1, which recognizes m6A and promotes translation by a cap-independent mechanism. Augmented translation by cap-independent pathways facilitated by m6A modifications contribute to the stress resistance and increased healthy longevity of mice with diminished GH and Insulin-like growth factor I (IGF1) signals."
item245	REG00007	M6ATAR00389	Up	M6ADIS0057	.	31395342	"MiR-4429 prevented gastric cancer progression through targeting METTL3 to inhibit m6A-caused stabilization of Translocation protein SEC62 (SEC62), indicating miR-4429 as a promising target for treatment improvement for Gastric cancer. METTL3 interacted with SEC62 to induce the m6A on SEC62 mRNA, therefore facilitated the stabilizing effect of IGF2BP1 on SEC62 mRNA."
item246	REG00012	M6ATAR00389	Up	M6ADIS0057	.	31395342	"MiR-4429 prevented gastric cancer progression through targeting METTL3 to inhibit m6A-caused stabilization of Translocation protein SEC62 (SEC62), indicating miR-4429 as a promising target for treatment improvement for Gastric cancer. METTL3 interacted with SEC62 to induce the m6A on SEC62 mRNA, therefore facilitated the stabilizing effect of IGF2BP1 on SEC62 mRNA."
item247	REG00007	M6ATAR00250	Up	M6ADIS0081	.	31405565	"Type 2 diabetes (T2D) is characterized by lack of insulin, insulin resistance and high blood sugar. METTL3 silence decreased the m6A methylated and total mRNA level of Fatty acid synthase (FASN), subsequently inhibited fatty acid metabolism. The expression of Acc1, Acly, Dgat2, Ehhadh, Fasn, Foxo, Pgc1a and Sirt1, which are critical to the regulation of fatty acid synthesis and oxidation were dramatically decreased in livers of hepatocyte-specific METTL3 knockout mice."
item248	REG00007	M6ATAR00169	Up	M6ADIS0081	.	31405565	"Type 2 diabetes (T2D) is characterized by lack of insulin, insulin resistance and high blood sugar. METTL3 silence decreased the m6A methylated and total mRNA level of Fatty acid synthase (Fasn), subsequently inhibited fatty acid metabolism. The expression of Acc1, ATP-citrate synthase (ACLY), Dgat2, Ehhadh, Fasn, Foxo, Pgc1a and Sirt1, which are critical to the regulation of fatty acid synthesis and oxidation were dramatically decreased in livers of hepatocyte-specific METTL3 knockout mice."
item249	REG00007	M6ATAR00236	Up	M6ADIS0081	.	31405565	"Type 2 diabetes (T2D) is characterized by lack of insulin, insulin resistance and high blood sugar. METTL3 silence decreased the m6A methylated and total mRNA level of Fatty acid synthase (Fasn), subsequently inhibited fatty acid metabolism. The expression of Acc1, Acly, Dgat2, Peroxisomal bifunctional enzyme (EHHADH), Fasn, Foxo, Pgc1a and Sirt1, which are critical to the regulation of fatty acid synthesis and oxidation were dramatically decreased in livers of hepatocyte-specific METTL3 knockout mice."
item250	REG00007	M6ATAR00393	Up	M6ADIS0081	.	31405565	"Type 2 diabetes (T2D) is characterized by lack of insulin, insulin resistance and high blood sugar. METTL3 silence decreased the m6A methylated and total mRNA level of Fatty acid synthase (Fasn), subsequently inhibited fatty acid metabolism. The expression of Acc1, Acly, Dgat2, Ehhadh, Fasn, Foxo, Pgc1a and NAD-dependent protein deacetylase sirtuin-1 (SIRT1), which are critical to the regulation of fatty acid synthesis and oxidation were dramatically decreased in livers of hepatocyte-specific METTL3 knockout mice."
item251	REG00007	M6ATAR00227	Up	M6ADIS0081	.	31405565	"Type 2 diabetes (T2D) is characterized by lack of insulin, insulin resistance and high blood sugar. METTL3 silence decreased the m6A methylated and total mRNA level of Fatty acid synthase (Fasn), subsequently inhibited fatty acid metabolism. The expression of Acc1, Acly, Diacylglycerol O-acyltransferase 2 (DGAT2), Ehhadh, Fasn, Foxo, Pgc1a and Sirt1, which are critical to the regulation of fatty acid synthesis and oxidation were dramatically decreased in livers of hepatocyte-specific METTL3 knockout mice."
item252	REG00007	M6ATAR00168	Up	M6ADIS0081	.	31405565	"Type 2 diabetes (T2D) is characterized by lack of insulin, insulin resistance and high blood sugar. METTL3 silence decreased the m6A methylated and total mRNA level of Fatty acid synthase (Fasn), subsequently inhibited fatty acid metabolism. The expression of Acetyl-CoA carboxylase 1 (ACC1/ACACA), Acly, Dgat2, Ehhadh, Fasn, Foxo, Pgc1a and Sirt1, which are critical to the regulation of fatty acid synthesis and oxidation were dramatically decreased in livers of hepatocyte-specific METTL3 knockout mice."
item253	REG00007	M6ATAR00259	Up	M6ADIS0081	.	31405565	"Type 2 diabetes (T2D) is characterized by lack of insulin, insulin resistance and high blood sugar. METTL3 silence decreased the m6A methylated and total mRNA level of Fatty acid synthase (Fasn), subsequently inhibited fatty acid metabolism. The expression of Acc1, Acly, Dgat2, Ehhadh, Fasn, Forkhead box protein O1 (FOXO1), Pgc1a and Sirt1, which are critical to the regulation of fatty acid synthesis and oxidation were dramatically decreased in livers of hepatocyte-specific METTL3 knockout mice."
item254	REG00007	M6ATAR00373	Up	M6ADIS0081	.	31405565	"Type 2 diabetes (T2D) is characterized by lack of insulin, insulin resistance and high blood sugar. METTL3 silence decreased the m6A methylated and total mRNA level of Fatty acid synthase (Fasn), subsequently inhibited fatty acid metabolism. The expression of Acc1, Acly, Dgat2, Ehhadh, Fasn, Foxo, PPAR-gamma coactivator 1-alpha (PGC-1a/PPARGC1A) and Sirt1, which are critical to the regulation of fatty acid synthesis and oxidation were dramatically decreased in livers of hepatocyte-specific METTL3 knockout mice."
item255	REG00007	M6ATAR00297	Up	M6ADIS0070	.	31409574	"m6A writer METTL3 and eraser ALKBH5 altered cell adhesion by regulating Integrin alpha-6 (ITGA6) expression in bladder cancer cells. m6A is highly enriched within the ITGA6 transcripts, and increased m6A methylations of the ITGA6 mRNA 3'UTR promotes the translation of ITGA6 mRNA via binding of the m6A readers YTHDF1 and YTHDF3. Inhibition of ITGA6 results in decreased growth and progression of bladder cancer cells in vitro and in vivo."
item256	REG00005	M6ATAR00297	.	M6ADIS0070	.	31409574	"m6A writer METTL3 and eraser ALKBH5 altered cell adhesion by regulating Integrin alpha-6 (ITGA6) expression in bladder cancer cells. m6A is highly enriched within the ITGA6 transcripts, and increased m6A methylations of the ITGA6 mRNA 3'UTR promotes the translation of ITGA6 mRNA via binding of the m6A readers YTHDF1 and YTHDF3. Inhibition of ITGA6 results in decreased growth and progression of bladder cancer cells in vitro and in vivo."
item257	REG00024	M6ATAR00297	.	M6ADIS0070	.	31409574	"m6A writer METTL3 and eraser ALKBH5 altered cell adhesion by regulating Integrin alpha-6 (ITGA6) expression in bladder cancer cells. m6A is highly enriched within the ITGA6 transcripts, and increased m6A methylations of the ITGA6 mRNA 3'UTR promotes the translation of ITGA6 mRNA via binding of the m6A readers YTHDF1 and YTHDF3. Inhibition of ITGA6 results in decreased growth and progression of bladder cancer cells in vitro and in vivo."
item258	REG00025	M6ATAR00297	.	M6ADIS0070	.	31409574	"m6A writer METTL3 and eraser ALKBH5 altered cell adhesion by regulating Integrin alpha-6 (ITGA6) expression in bladder cancer cells. m6A is highly enriched within the ITGA6 transcripts, and increased m6A methylations of the ITGA6 mRNA 3'UTR promotes the translation of ITGA6 mRNA via binding of the m6A readers YTHDF1 and YTHDF3. Inhibition of ITGA6 results in decreased growth and progression of bladder cancer cells in vitro and in vivo."
item259	REG00008	M6ATAR00206	Down	M6ADIS0083	.	31434544	"Obesity is becoming a global problem. ZFP217 knockdown-induced adipogenesis inhibition was caused by G1/S-specific cyclin-D1 (CCND1), which was mediated by METTL3 and YTHDF2 in an m6A-dependent manner."
item260	REG00007	M6ATAR00206	Up	M6ADIS0083	.	31434544	"Obesity is becoming a global problem. ZFP217 knockdown-induced adipogenesis inhibition was caused by G1/S-specific cyclin-D1 (CCND1), which was mediated by METTL3 and YTHDF2 in an m6A-dependent manner."
item261	REG00001	M6ATAR00279	Up	M6ADIS0115	.	31434789	Loss of Fto also increased susceptibility of osteoblasts to genotoxic damage from metabolic stress induced by exposure to HF is also consistent with this model for FTO action. FTO functions intrinsically in osteoblasts through Heat shock 70 kDa protein 1A (HSPA1A)-NF-Kappa-B signaling to enhance the stability of mRNA of proteins that function to protect cells from genotoxic damage.
item262	REG00009	M6ATAR00248	Down	M6ADIS0006	.	31438961	WTAP-guided m6A modification contributes to the progression of Hepatocellular carcinoma cells via the HuR-Protein C-ets-1 (ETS1)-p21/p27 axis.
item263	REG00001	M6ATAR00189	Up	M6ADIS0083	.	31451060	"Autophagy protein 5 (ATG5) and Atg7 were the targets of YTHDF2 (YTH N6-methyladenosine RNA binding protein 2). Upon FTO silencing, Atg5 and Atg7 transcripts with higher m6A levels were captured by YTHDF2, which resulted in mRNA degradation and reduction of protein expression, thus alleviating autophagy and adipogenesis."
item264	REG00001	M6ATAR00190	Up	M6ADIS0083	.	31451060	"Atg5 and Ubiquitin-like modifier-activating enzyme ATG7 (ATG7) were the targets of YTHDF2 (YTH N6-methyladenosine RNA binding protein 2). Upon FTO silencing, Atg5 and Atg7 transcripts with higher m6A levels were captured by YTHDF2, which resulted in mRNA degradation and reduction of protein expression, thus alleviating autophagy and adipogenesis."
item265	REG00008	M6ATAR00189	Down	M6ADIS0083	.	31451060	"Autophagy protein 5 (ATG5) and Atg7 were the targets of YTHDF2 (YTH N6-methyladenosine RNA binding protein 2). Upon FTO silencing, Atg5 and Atg7 transcripts with higher m6A levels were captured by YTHDF2, which resulted in mRNA degradation and reduction of protein expression, thus alleviating autophagy and adipogenesis."
item266	REG00008	M6ATAR00190	Down	M6ADIS0083	.	31451060	"Atg5 and Ubiquitin-like modifier-activating enzyme ATG7 (ATG7) were the targets of YTHDF2 (YTH N6-methyladenosine RNA binding protein 2). Upon FTO silencing, Atg5 and Atg7 transcripts with higher m6A levels were captured by YTHDF2, which resulted in mRNA degradation and reduction of protein expression, thus alleviating autophagy and adipogenesis."
item267	REG00007	M6ATAR00196	Up	M6ADIS0065	.	31454538	"Apoptosis regulator Bcl-2 (BCL2) acted as the target of METTL3, thereby regulating the proliferation and apoptosis of breast cancer."
item268	REG00008	M6ATAR00320	Down	.	.	31474572	"m6A reader YTHDF2 sequesters m6A-circRNA and is essential for suppression of innate immunity. Unmodified circRNA, but not m6A-modified circRNA, directly activates RNA pattern recognition receptor RIG-I in the presence of lysine-63-linked polyubiquitin chain to cause filamentation of the adaptor protein Mitochondrial antiviral-signaling protein (MAVS) and activation of the downstream transcription factor IRF3."
item269	REG00008	M6ATAR00296	Down	.	.	31474572	"m6A reader YTHDF2 sequesters m6A-circRNA and is essential for suppression of innate immunity. Unmodified circRNA, but not m6A-modified circRNA, directly activates RNA pattern recognition receptor RIG-I in the presence of lysine-63-linked polyubiquitin chain to cause filamentation of the adaptor protein MAVS and activation of the downstream transcription factor Interferon regulatory factor 3 (IRF3)."
item270	REG00007	M6ATAR00464	Up	M6ADIS0059	.	31492150	"METTL3/miR-1246/Sprouty-related, EVH1 domain-containing protein 2 (SPRED2) axis plays an important role in tumor metastasis and provides a new m6A modification pattern in Colorectal cancer development."
item271	REG00007	M6ATAR00109	Up	M6ADIS0059	.	31492150	METTL3/microRNA 1246 (MIR1246)/SPRED2 axis plays an important role in tumor metastasis and provides a new m6A modification pattern in Colorectal cancer development.
item272	REG00008	M6ATAR00148	Up	M6ADIS0008	.	31497208	"The GAS5-AS1 expression in cervical cancer tissues was markedly decreased when compared with that in the adjacent normal tissues. GAS5-AS1 interacted with the tumor suppressor Growth arrest specific 5 (GAS5), and increased its stability by interacting with RNA demethylase ALKBH5 and decreasing GAS5 N6-methyladenosine (m6A) modification. m6A-mediated GAS5 RNA degradation relied on the m6A reader protein YTHDF2-dependent pathway."
item273	REG00005	M6ATAR00148	Up	M6ADIS0008	.	31497208	"The GAS5-AS1 expression in cervical cancer tissues was markedly decreased when compared with that in the adjacent normal tissues. GAS5-AS1 interacted with the tumor suppressor Growth arrest specific 5 (GAS5), and increased its stability by interacting with RNA demethylase ALKBH5 and decreasing GAS5 N6-methyladenosine (m6A) modification. m6A-mediated GAS5 RNA degradation relied on the m6A reader protein YTHDF2-dependent pathway."
item274	.	M6ATAR00137	.	M6ADIS0016	.	31502903	"m6A modification of pri-miRNA-126 and its binding with DGCR8 decreases blocked microRNA 126 (MIR126) maturation, and then activated the PI3K/AKT/mTOR pathway, which drove the fibro genesis in the lung after CB exposure."
item275	REG00008	M6ATAR00160	Up	M6ADIS0007	.	31504235	"YTHDF2 directly binds to the m6A modification site of 6-phosphogluconate dehydrogenase, decarboxylating (6PGD/PGD) three prime untranslated region (3'-UTR) to promote 6PGD mRNA translation in lung cancer cells."
item276	REG00005	.	.	M6ADIS0058	.	31506804	"The tumor repressive role of ALKBH5 in colon cancer. ALKBH5 was downregulated in human colon cancer tissues, where its decreased expression significantly correlated with distant metastasis and American Joint Committee on Cancer (AJCC) stage."
item277	REG00007	M6ATAR00416	Up	M6ADIS0001	.	31530567	"Silencing METTL3 or overexpressing dominant-negative mutant METTL3 suppressed the growth and self-renewal of Glioblastoma cells. Integrated transcriptome and MeRIP-seq analyses revealed that downregulating the expression of METTL3 decreased m6A modification levels of Serine/arginine-rich splicing factor 3 (SRSF3), which led to YTHDC1-dependent NMD of SRSF transcripts and decreased SRSF protein expression."
item278	REG00007	M6ATAR00417	Up	M6ADIS0001	.	31530567	"Silencing METTL3 or overexpressing dominant-negative mutant METTL3 suppressed the growth and self-renewal of Glioblastoma cells. Integrated transcriptome and MeRIP-seq analyses revealed that downregulating the expression of METTL3 decreased m6A modification levels of Serine/arginine-rich splicing factor 6 (SRSF6), which led to YTHDC1-dependent NMD of SRSF transcripts and decreased SRSF protein expression."
item279	REG00007	M6ATAR00415	Up	M6ADIS0001	.	31530567	"Silencing METTL3 or overexpressing dominant-negative mutant METTL3 suppressed the growth and self-renewal of Glioblastoma cells. Integrated transcriptome and MeRIP-seq analyses revealed that downregulating the expression of METTL3 decreased m6A modification levels of Serine/arginine-rich splicing factor 11 (SRSF11), which led to YTHDC1-dependent NMD of SRSF transcripts and decreased SRSF protein expression."
item280	REG00022	M6ATAR00416	Up	M6ADIS0001	.	31530567	"Silencing METTL3 or overexpressing dominant-negative mutant METTL3 suppressed the growth and self-renewal of Glioblastoma cells. Integrated transcriptome and MeRIP-seq analyses revealed that downregulating the expression of METTL3 decreased m6A modification levels of Serine/arginine-rich splicing factor 3 (SRSF3), which led to YTHDC1-dependent NMD of SRSF transcripts and decreased SRSF protein expression."
item281	REG00022	M6ATAR00417	Up	M6ADIS0001	.	31530567	"Silencing METTL3 or overexpressing dominant-negative mutant METTL3 suppressed the growth and self-renewal of Glioblastoma cells. Integrated transcriptome and MeRIP-seq analyses revealed that downregulating the expression of METTL3 decreased m6A modification levels of Serine/arginine-rich splicing factor 6 (SRSF6), which led to YTHDC1-dependent NMD of SRSF transcripts and decreased SRSF protein expression."
item282	REG00022	M6ATAR00415	Up	M6ADIS0001	.	31530567	"Silencing METTL3 or overexpressing dominant-negative mutant METTL3 suppressed the growth and self-renewal of Glioblastoma cells. Integrated transcriptome and MeRIP-seq analyses revealed that downregulating the expression of METTL3 decreased m6A modification levels of Serine/arginine-rich splicing factor 11 (SRSF11), which led to YTHDC1-dependent NMD of SRSF transcripts and decreased SRSF protein expression."
item283	REG00001	M6ATAR00356	Down	M6ADIS0038	M6ADRUG0006	31578283	"Meclofenamic acid increased Cellular tumor antigen p53 (TP53/p53) mRNA and protein levels in AKI both in vitro and in vivo, and FTO overexpression reduced p53 expression and reversed the MA-induced p53 increase in cisplatin-induced Acute kidney injury."
item284	REG00001	M6ATAR00356	Down	M6ADIS0038	M6ADRUG0047	31578283	"Meclofenamic acid increased Cellular tumor antigen p53 (TP53/p53) mRNA and protein levels in AKI both in vitro and in vivo, and FTO overexpression reduced p53 expression and reversed the MA-induced p53 increase in cisplatin-induced acute kidney injury Acute kidney injury."
item285	.	M6ATAR00400	.	M6ADIS0059	.	31579913	The colorimetric m6A quantification strategy revealed that Staphylococcal nuclease domain-containing protein 1 (SND1) could alter m6A levels in colorectal cancer cell lines.
item286	REG00007	M6ATAR00271	Up	M6ADIS0057	.	31582403	"Elevated METTL3 expression promotes tumour angiogenesis and glycolysis in Gastric cancer. P300-mediated H3K27 acetylation activation in the promoter of METTL3 induced METTL3 transcription, which stimulated m6A modification of Hepatoma-derived growth factor (HDGF) mRNA, and the m6A reader IGF2BP3 then directly recognised and bound to the m6A site on HDGF mRNA and enhanced HDGF mRNA stability."
item287	REG00014	M6ATAR00271	Up	M6ADIS0057	.	31582403	"Elevated METTL3 expression promotes tumour angiogenesis and glycolysis in Gastric cancer. P300-mediated H3K27 acetylation activation in the promoter of METTL3 induced METTL3 transcription, which stimulated m6A modification of Hepatoma-derived growth factor (HDGF) mRNA, and the m6A reader IGF2BP3 then directly recognised and bound to the m6A site on HDGF mRNA and enhanced HDGF mRNA stability."
item288	REG00007	.	Up	M6ADIS0061	.	31606241	"METTL3 knockdown in MIA PaCa-2 and BxPC-3 cells decreased RNA m6A modifications. Cell proliferation, invasion, and migration were decreased by METTL3 knockdown in cancerous cell lines.In conclusion, METTL3 is probably involved in pancreatic carcinogenesis."
item289	REG00007	M6ATAR00454	Up	M6ADIS0057	.	31607270	"The m6A modification of Zinc finger MYM-type protein 1 (ZMYM1) mRNA by METTL3 enhanced its stability relying on the ""reader"" protein HuR (also known as ELAVL1) dependent pathway.The study uncover METTL3/ZMYM1/E-cadherin signaling as a potential therapeutic target in anti-metastatic strategy against Gastric cancer."
item290	REG00025	M6ATAR00148	Down	M6ADIS0059	.	31619268	A new mechanism for m6A-induced decay of Growth arrest specific 5 (GAS5) on YAP signaling in progression of Colorectal cancer which offers a promising approach for CRC treatment. LncRNA GAS5 expressions is negatively correlated with YAP and YTHDF3 protein levels in tumors from CRC patients.
item291	REG00013	M6ATAR00353	Up	M6ADIS0059	.	31619685	"N6-methyladenosine modification of RNA cytosine C(5)-methyltransferase NSUN2 (NSUN2) modulates cytoplasmic export and stabilizes HMGA2 to promote Colorectal carcinoma LM. By forming a circNSUN2/IGF2BP2/HMGA2 RNA-protein ternary complex in the cytoplasm, circNSUN2 enhances the stability of HMGA2 mRNA to promote CRC metastasis progression."
item292	REG00001	M6ATAR00312	Down	M6ADIS0006	.	31632576	The overexpression of demethylase FTO in the HCC tissue and cells. FTO could regulate the demethylation of Pyruvate kinase PKM (PKM2/PKM) in the hepatocellular carcinoma.
item293	REG00007	M6ATAR00280	Down	M6ADIS0001	.	31639789	"m6A regulated cell proliferation by influencing apoptosis of U251 cells through regulating Heat shock protein HSP 90-alpha (HSP90/HSP90AA1) expression. m6A level was decreased in glioma tissue, which was caused by decreased METTL3 and increased FTO levels."
item294	REG00001	M6ATAR00280	Down	M6ADIS0001	.	31639789	"m6A regulated cell proliferation by influencing apoptosis of U251 cells through regulating Heat shock protein HSP 90-alpha (HSP90/HSP90AA1) expression.m6A level was decreased in glioma tissue, which was caused by decreased METTL3 and increased FTO levels."
item295	REG00007	M6ATAR00342	Up	M6ADIS0022	.	31643040	"METTL3 positively regulates expression of Myeloid differentiation primary response protein MyD88 (MYD88), a critical upstream regulator of NF-Kappa-B signaling, by facilitating m6A methylation modification to MYD88-RNA, subsequently inducing the activation of NF-Kappa-B which is widely regarded as a repressor of osteogenesis and therefore suppressing osteogenic progression. The METTL3-mediated m6A methylation is found to be dynamically reversed by the demethylase ALKBH5."
item296	REG00005	M6ATAR00342	Down	M6ADIS0022	.	31643040	"METTL3 positively regulates expression of Myeloid differentiation primary response protein MyD88 (MYD88), a critical upstream regulator of NF-Kappa-B signaling, by facilitating m6A methylation modification to MYD88-RNA, subsequently inducing the activation of NF-Kappa-B which is widely regarded as a repressor of osteogenesis and therefore suppressing osteogenic progression. The METTL3-mediated m6A methylation is found to be dynamically reversed by the demethylase ALKBH5."
item297	REG00006	.	.	M6ADIS0051	.	31650864	"The transcriptome-wide m6A methylome of osteosarcoma cells enriched by chemotherapy, revealing a tight relationship between m6A methylation and the emergence and maintaining of OSCs."
item298	REG00001	.	.	M6ADIS0051	.	31650864	"The transcriptome-wide m6A methylome of osteosarcoma cells enriched by chemotherapy, revealing a tight relationship between m6A methylation and the emergence and maintaining of OSCs."
item299	REG00024	M6ATAR00210	Up	M6ADIS0007	M6ADRUG0047	31653849	"YTHDF1 deficiency inhibits Non-small cell lung cancer cell proliferation and xenograft tumor formation through regulating the translational efficiency of Cyclin-dependent kinase 2 (CDK2), CDK4, p27, and cyclin D1, and that YTHDF1 depletion restrains de novo lung adenocarcinomas (ADC) progression. Mechanistic studies identified the Keap1-Nrf2-AKR1C1 axis as the downstream mediator of YTHDF1. YTHDF1 high expression correlates with better clinical outcome, with its depletion rendering cancerous cells resistant to cisplatin (DDP) treatment."
item300	REG00024	M6ATAR00211	Up	M6ADIS0007	M6ADRUG0047	31653849	"YTHDF1 deficiency inhibits Non-small cell lung cancer cell proliferation and xenograft tumor formation through regulating the translational efficiency of CDK2, Cyclin-dependent kinase 4 (CDK4), p27, and cyclin D1, and that YTHDF1 depletion restrains de novo lung adenocarcinomas (ADC) progression. Mechanistic studies identified the Keap1-Nrf2-AKR1C1 axis as the downstream mediator of YTHDF1. YTHDF1 high expression correlates with better clinical outcome, with its depletion rendering cancerous cells resistant to cisplatin (DDP) treatment."
item301	REG00024	M6ATAR00206	Up	M6ADIS0007	M6ADRUG0047	31653849	"YTHDF1 deficiency inhibits Non-small cell lung cancer cell proliferation and xenograft tumor formation through regulating the translational efficiency of CDK2, CDK4, p27, and G1/S-specific cyclin-D1 (CCND1), and that YTHDF1 depletion restrains de novo lung adenocarcinomas (ADC) progression. Mechanistic studies identified the Keap1-Nrf2-AKR1C1 axis as the downstream mediator of YTHDF1. YTHDF1 high expression correlates with better clinical outcome, with its depletion rendering cancerous cells resistant to cisplatin (DDP) treatment."
item302	REG00024	M6ATAR00306	Up	M6ADIS0007	M6ADRUG0047	31653849	"YTHDF1 deficiency inhibits Non-small cell lung cancer cell proliferation and xenograft tumor formation through regulating the translational efficiency of CDK2, CDK4, p27, and cyclin D1, and that YTHDF1 depletion restrains de novo lung adenocarcinomas (ADC) progression. Mechanistic studies identified the Kelch-like ECH-associated protein 1 (KEAP1)-Nrf2-AKR1C1 axis as the downstream mediator of YTHDF1. YTHDF1 high expression correlates with better clinical outcome, with its depletion rendering cancerous cells resistant to cisplatin (DDP) treatment."
item303	REG00024	M6ATAR00214	Down	M6ADIS0007	M6ADRUG0047	31653849	"YTHDF1 deficiency inhibits Non-small cell lung cancer cell proliferation and xenograft tumor formation through regulating the translational efficiency of CDK2, CDK4, Cyclin-dependent kinase inhibitor 1B (CDKN1B/p27), and cyclin D1, and that YTHDF1 depletion restrains de novo lung adenocarcinomas (ADC) progression. Mechanistic studies identified the Keap1-Nrf2-AKR1C1 axis as the downstream mediator of YTHDF1. YTHDF1 high expression correlates with better clinical outcome, with its depletion rendering cancerous cells resistant to cisplatin (DDP) treatment."
item304	REG00024	M6ATAR00348	Down	M6ADIS0007	M6ADRUG0047	31653849	"YTHDF1 deficiency inhibits Non-small cell lung cancer cell proliferation and xenograft tumor formation through regulating the translational efficiency of CDK2, CDK4, p27, and cyclin D1, and that YTHDF1 depletion restrains de novo lung adenocarcinomas (ADC) progression. Mechanistic studies identified the Keap1-Nuclear factor erythroid 2-related factor 2 (NFE2L2)-AKR1C1 axis as the downstream mediator of YTHDF1. YTHDF1 high expression correlates with better clinical outcome, with its depletion rendering cancerous cells resistant to cisplatin (DDP) treatment."
item305	REG00024	M6ATAR00174	Down	M6ADIS0007	M6ADRUG0047	31653849	"YTHDF1 deficiency inhibits Non-small cell lung cancer cell proliferation and xenograft tumor formation through regulating the translational efficiency of CDK2, CDK4, p27, and cyclin D1, and that YTHDF1 depletion restrains de novo lung adenocarcinomas (ADC) progression. Mechanistic studies identified the Keap1-Nrf2-Aldo-keto reductase family 1 member C1 (AKR1C1) axis as the downstream mediator of YTHDF1. YTHDF1 high expression correlates with better clinical outcome, with its depletion rendering cancerous cells resistant to cisplatin (DDP) treatment."
item306	REG00005	M6ATAR00258	Up	M6ADIS0007	.	31677788	m6A demethylase ALKBH5 affects the proliferation and invasion of lung adenocarcinoma cells under IH by downregulating m6A modification on Forkhead box protein M1 (FOXM1) mRNA and by promoting FOXM1 expression.high FOXM1 expression was associated with cisplatin-based chemotherapy resistance and poor prognosis.
item307	REG00006	.	.	M6ADIS0103	.	31697949	"METTL14 expression increases in calcific arteries and in HASMCs induced by indoxyl sulfate, thereby increasing the m6A level in RNA and decreasing the vascular repair function.METTL14 m6A regulates vascular calcification induced by indoxyl sulfate."
item308	REG00023	M6ATAR00218	Down	M6ADIS0006	.	31706844	"In the Hepatocellular carcinoma cells YTHDC2 promotes CYP2C8 mRNA degradation via recognizing the m6A in CYP2C8 mRNA, which is installed by METTL3/14 and removed by FTO."
item309	REG00007	M6ATAR00218	Up	M6ADIS0006	.	31706844	"In the Hepatocellular carcinoma cells YTHDC2 promotes CYP2C8 mRNA degradation via recognizing the m6A in CYP2C8 mRNA, which is installed by METTL3/14 and removed by FTO."
item310	REG00006	M6ATAR00218	Up	M6ADIS0006	.	31706844	"In the Hepatocellular carcinoma cells YTHDC2 promotes CYP2C8 mRNA degradation via recognizing the m6A in CYP2C8 mRNA, which is installed by METTL3/14 and removed by FTO."
item311	REG00001	M6ATAR00218	Down	M6ADIS0006	.	31706844	"In the Hepatocellular carcinoma cells YTHDC2 promotes CYP2C8 mRNA degradation via recognizing the m6A in CYP2C8 mRNA, which is installed by METTL3/14 and removed by FTO."
item312	REG00008	M6ATAR00157	Up	M6ADIS0057	.	31711642	Long intergenic non-protein coding RNA 470 (LINC00470)-METTL3-mediated PTEN mRNA degradation relied on the m6A reader protein YTHDF2-dependent pathway. LINC00470 served as a therapeutic target for Gastric cancer patients.
item313	REG00007	M6ATAR00157	Up	M6ADIS0057	.	31711642	Long intergenic non-protein coding RNA 470 (LINC00470)-METTL3-mediated PTEN mRNA degradation relied on the m6A reader protein YTHDF2-dependent pathway.LINC00470 served as a therapeutic target for Gastric cancer patients.
item314	REG00024	M6ATAR00275	Up	M6ADIS0029	.	31722709	"YTHDF1 promoted the translation of methylated Adenosine 5'-monophosphoramidase HINT2 (HINT2) mRNA, a tumor suppressor in ocular melanoma."
item315	.	M6ATAR00016	.	M6ADIS0056	.	31726270	"The biological characteristics of Circ_SLC7A5 including location, miRNAs binding, m6A modification were analyzed. Our study reveals a novel prognosis biomarker of circ-SLC7A5, providing a preliminary landscape of circRNA expression for detection of esophageal squamous cell carcinoma."
item316	REG00006	M6ATAR00351	Down	M6ADIS0070	.	31760940	Mettl14 and m6A modification participate in the RNA stability of Neurogenic locus notch homolog protein 1 (NOTCH1) mRNA. Notch1 plays an essential role in bladder tumorigenesis and bladder TIC self-renewal.
item317	REG00012	M6ATAR00282	Up	M6ADIS0046	.	31768017	"IGF2BP1 decreases leukemia cells' tumorigenicity, promotes myeloid differentiation, increases leukemia cell death, and sensitizes acute myeloid leukemia cells to chemotherapeutic drugs. IGF2BP1 affects proliferation and tumorigenic potential of leukemia cells through critical regulators of self-renewal Homeobox protein Hox-B4 (HOXB4) and MYB and through regulation of expression of the aldehyde dehydrogenase, ALDH1A1."
item318	REG00012	M6ATAR00340	Up	M6ADIS0046	.	31768017	"IGF2BP1 decreases leukemia cells' tumorigenicity, promotes myeloid differentiation, increases leukemia cell death, and sensitizes acute myeloid leukemia cells to chemotherapeutic drugs. IGF2BP1 affects proliferation and tumorigenic potential of leukemia cells through critical regulators of self-renewal HOXB4 and Transcriptional activator Myb (MYB) and through regulation of expression of the aldehyde dehydrogenase, ALDH1A1."
item319	REG00012	M6ATAR00177	Up	M6ADIS0046	.	31768017	"IGF2BP1 decreases leukemia cells' tumorigenicity, promotes myeloid differentiation, increases leukemia cell death, and sensitizes acute myeloid leukemia cells to chemotherapeutic drugs. IGF2BP1 affects proliferation and tumorigenic potential of leukemia cells through critical regulators of self-renewal HOXB4 and MYB and through regulation of expression of the aldehyde dehydrogenase, Aldehyde dehydrogenase 1A1 (ALDH1A1)."
item320	REG00007	.	Up	M6ADIS0112	.	31772500	"LPS could enhance the expression and biological activity of METTL3 in macrophages, while overexpression of METTL3 significantly attenuated the inflammatory response induced by LPS in macrophages.This study firstly demonstrates the critical role of METTL3 in RA, which provides novel insights into recognizing the pathogenesis of Rheumatoid Arthritis(RA) and a promising biomarker for RA."
item321	REG00013	M6ATAR00341	Up	M6ADIS0059	.	31791342	"LINRIS blocked K139 ubiquitination of IGF2BP2, maintaining its stability. This process prevented the degradation of IGF2BP2 through the autophagy-lysosome pathway (ALP). The LINRIS-IGF2BP2-Myc proto-oncogene protein (MYC) axis promotes the progression of Colorectal cancer and is a promising therapeutic target. MYC-mediated glycolysis was influenced by the interaction between LINRIS and IGF2BP2."
item322	REG00013	M6ATAR00224	Up	M6ADIS0061	.	31804607	"IGF2BP2 functions in partnerships with Putative uncharacterized protein DANCR (DANCR) to regulate its stability. In tumor cells, IGF2BP2 is upregulated, which increases the chance of IGF2PB2 to interact with and stabilize DANCR.DANCR is a novel target for IGF2BP2 through m6A modification, and IGF2BP2 and DANCR work together to promote cancer stemness-like properties and pancreatic cancer pathogenesis."
item323	REG00007	M6ATAR00267	Up	M6ADIS0068	.	31806999	"METTL3 silence decreased the m6A modification and expression of Zinc finger protein GLI1 (GLI1), an important component of hedgehog pathway, which led to cell apoptosis.the m6A methyltransferase METTL3 promotes the growth and motility of prostate cancer cells by regulating hedgehog pathway."
item324	REG00025	M6ATAR00141	Up	M6ADIS0007	M6ADRUG0047	31818312	"METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.m6A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the Metastasis associated lung adenocarcinoma transcript 1 (MALAT1)-miR-1914-3p-YAP axis to induce Non-small cell lung cancer drug resistance and metastasis."
item325	REG00007	M6ATAR00141	Up	M6ADIS0007	M6ADRUG0047	31818312	"METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.m6A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the Metastasis associated lung adenocarcinoma transcript 1 (MALAT1)-miR-1914-3p-YAP axis to induce Non-small cell lung cancer drug resistance and metastasis."
item326	REG00024	M6ATAR00141	Up	M6ADIS0007	M6ADRUG0047	31818312	"METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.m6A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the Metastasis associated lung adenocarcinoma transcript 1 (MALAT1)-miR-1914-3p-YAP axis to induce Non-small cell lung cancer drug resistance and metastasis."
item327	REG00007	M6ATAR00451	Up	M6ADIS0007	M6ADRUG0047	31818312	"METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.m6A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the MALAT1-miR-1914-3p-Transcriptional coactivator YAP1 (YAP1) axis to induce Non-small cell lung cancer drug resistance and metastasis."
item328	REG00025	M6ATAR00451	Up	M6ADIS0007	M6ADRUG0047	31818312	"METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.m6A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the MALAT1-miR-1914-3p-Transcriptional coactivator YAP1 (YAP1) axis to induce Non-small cell lung cancer drug resistance and metastasis."
item329	REG00024	M6ATAR00451	Up	M6ADIS0007	M6ADRUG0047	31818312	"METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.m6A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the MALAT1-miR-1914-3p-Transcriptional coactivator YAP1 (YAP1) axis to induce Non-small cell lung cancer drug resistance and metastasis."
item330	REG00007	M6ATAR00465	Up	M6ADIS0007	M6ADRUG0047	31818312	"METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.m6A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the MALAT1-hsa-miR-1914-3p-YAP axis to induce Non-small cell lung cancer drug resistance and metastasis."
item331	REG00025	M6ATAR00465	Up	M6ADIS0007	M6ADRUG0047	31818312	"METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.m6A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the MALAT1-hsa-miR-1914-3p-YAP axis to induce Non-small cell lung cancer drug resistance and metastasis."
item332	REG00024	M6ATAR00465	Up	M6ADIS0007	M6ADRUG0047	31818312	"METTL3, YTHDF3, YTHDF1, and eIF3b directly promoted YAP translation through an interaction with the translation initiation machinery. METTL3 knockdown inhibits tumor growth and enhances sensitivity to DDP in vivo.m6A mRNA methylation initiated by METTL3 directly promotes YAP translation and increases YAP activity by regulating the MALAT1-hsa-miR-1914-3p-YAP axis to induce Non-small cell lung cancer drug resistance and metastasis."
item333	REG00007	M6ATAR00017	Down	M6ADIS0007	.	31823788	m6A methyltransferase Mettl3 can increase the splicing of precursor hsa-miR-143-3p to facilitate its biogenesis. The miR-143-3p/VASH1 axis in BM of lung cancers and suggests their critical roles in lung cancer pathogenesis.
item334	REG00001	M6ATAR00341	Up	M6ADIS0008	.	31827395	"FTO interacts with transcripts of E2F1 and Myc proto-oncogene protein (MYC), inhibition of FTO significantly impairs the translation efficiency of E2F1 and Myc.FTO plays important oncogenic role in regulating cervical cancer cells' proliferation."
item335	REG00001	M6ATAR00234	Up	M6ADIS0008	.	31827395	"FTO interacts with transcripts of Transcription factor E2F1 (E2F1) and Myc, inhibition of FTO significantly impairs the translation efficiency of E2F1 and Myc.FTO plays important oncogenic role in regulating cervical cancer cells' proliferation."
item336	REG00006	M6ATAR00118	Up	M6ADIS0059	.	31839484	"METTL14 suppressed Colorectal cancer cell growth, migration, and invasion via the microRNA 375 (MIR375)/YAP1 and miR-375/SP1 pathways."
item337	REG00015	M6ATAR00265	Down	M6ADIS0006	.	31856849	"KIAA1429 induced m6A methylation on the 3' UTR of Trans-acting T-cell-specific transcription factor GATA-3 (GATA3) pre-mRNA, leading to the separation of the RNA-binding protein HuR and the degradation of GATA3 pre-mRNA. KIAA1429 was considerably upregulated in Hepatocellular carcinoma tissues."
item338	REG00007	M6ATAR00222	Up	M6ADIS0006	.	31870368	METTL3 is significantly up-regulated in Hepatoblastoma(HB) and promotes HB development.m6A mRNA methylation contributes significantly to regulate the Wnt/beta-catenin pathway. Reduced m6A methylation can lead to a decrease in expression and stability of the Catenin beta-1 (CTNNB1/Beta-catenin).
item339	REG00007	M6ATAR00397	Down	M6ADIS0125	.	31892163	METTL3 knockdown inhibits osteoblast differentiation and Smad-dependent signaling by stabilizing Mothers against decapentaplegic homolog 7 (SMAD7) and Smurf1 mRNA transcripts via YTHDF2 involvement and activates the inflammatory response by regulating MAPK signaling in LPS-induced inflammation.
item340	REG00007	M6ATAR00398	Down	M6ADIS0125	.	31892163	METTL3 knockdown inhibits osteoblast differentiation and Smad-dependent signaling by stabilizing Smad7 and E3 ubiquitin-protein ligase SMURF1 (SMURF1) mRNA transcripts via YTHDF2 involvement and activates the inflammatory response by regulating MAPK signaling in LPS-induced inflammation.
item341	REG00008	M6ATAR00397	Down	M6ADIS0125	.	31892163	METTL3 knockdown inhibits osteoblast differentiation and Smad-dependent signaling by stabilizing Mothers against decapentaplegic homolog 7 (SMAD7) and Smurf1 mRNA transcripts via YTHDF2 involvement and activates the inflammatory response by regulating MAPK signaling in LPS-induced inflammation.
item342	REG00008	M6ATAR00398	Down	M6ADIS0125	.	31892163	METTL3 knockdown inhibits osteoblast differentiation and Smad-dependent signaling by stabilizing Smad7 and E3 ubiquitin-protein ligase SMURF1 (SMURF1) mRNA transcripts via YTHDF2 involvement and activates the inflammatory response by regulating MAPK signaling in LPS-induced inflammation.
item343	REG00005	M6ATAR00175	Up	M6ADIS0113	M6ADRUG0078	31897529	"The overexpression of ALKBH5 led to the activation of RAC-alpha serine/threonine-protein kinase (AKT1), and BMP2 was regulated by ALKBH5 through the AKT signaling pathway. ALKBH5 promoted the osteogenesis of the ligamentum flavum cells through BMP2 demethylation and AKT activation. MK22606 is an AKT inhibitor. Moreover, when ALKBH5 was knocked down in the ligamentum flavum cells, p-AKT was inhibited when compared with that in the overexpressed ALKBH5 and control groups."
item344	REG00005	M6ATAR00200	Up	M6ADIS0113	M6ADRUG0078	31897529	"The overexpression of ALKBH5 led to the activation of p-AKT, and Bone morphogenetic protein 2 (BMP2) was regulated by ALKBH5 through the AKT signaling pathway. ALKBH5 promoted the osteogenesis of the ligamentum flavum cells through BMP2 demethylation and AKT activation. MK22606 is an AKT inhibitor. Moreover, when ALKBH5 was knocked down in the ligamentum flavum cells, p-AKT was inhibited when compared with that in the overexpressed ALKBH5 and control groups."
item345	REG00005	M6ATAR00450	Up	M6ADIS0061	M6ADRUG0024	31906946	"ALKBH5 overexpression sensitizes Pancreatic cancer cells to gemcitabine treatment, and it represses PDAC tumorigenesis by reducing m6A levels of Wnt inhibitory factor 1 (WIF1) and hindering activation of Wnt signaling."
item346	REG00007	M6ATAR00018	Up	M6ADIS0024	.	31914601	METTL3 positively modulated the mmu-miR-365-3p processing in a microprocessor protein DiGeorge critical region 8-dependent manner.METTL3-mediated m6A modification in nociceptive sensitization and provide a novel perspective on m6A modification in the development of Inflammatory pain.
item347	REG00007	M6ATAR00088	Up	M6ADIS0006	.	31915027	"Long intergenic non-protein coding RNA 958 (LINC00958) sponged miR-3619-5p to upregulate hepatoma-derived growth factor (HDGF) expression, thereby facilitating Hepatocellular carcinoma lipogenesis and progression. METTL3-mediated N6-methyladenosine modification led to LINC00958 upregulation through stabilizing its RNA transcript."
item348	REG00005	M6ATAR00431	Down	M6ADIS0007	.	31927006	"ALKBH5 repress Metalloproteinase inhibitor 3 (TIMP3) transcript stability, thereby inhibiting TIMP3 translational production.the present research confirmed the ALKBH5/TIMP3 pathway in the non-small cell lung cancer(NSCLC) oncogenesis progress, providing a novel insight for the epitranscriptome and potential therapeutic target for NSCLC."
item349	REG00014	M6ATAR00086	Up	M6ADIS0029	M6ADRUG0069	31935372	"CDR1 antisense RNA (CDR1-AS) a regulator of miR-7, as a hallmark of melanoma progression. CDR1as depletion results from epigenetic silencing of LINC00632, its originating long non-coding RNA (lncRNA) and promotes invasion in vitro and metastasis in vivo through a miR-7-independent, IGF2BP3-mediated mechanism. IGF2BP3 interacts with CDR1as and mediates invasion induced by CDR1as depletion. CDR1asHigh melanoma cell lines were strikingly more sensitive to three different GPX4 inhibitors, which are known to elicit ferroptotic cell death."
item350	REG00014	M6ATAR00086	Up	M6ADIS0029	M6ADRUG0072	31935372	"CDR1 antisense RNA (CDR1-AS) a regulator of miR-7, as a hallmark of melanoma progression. CDR1as depletion results from epigenetic silencing of LINC00632, its originating long non-coding RNA (lncRNA) and promotes invasion in vitro and metastasis in vivo through a miR-7-independent, IGF2BP3-mediated mechanism. IGF2BP3 interacts with CDR1as and mediates invasion induced by CDR1as depletion. CDR1asHigh melanoma cell lines were strikingly more sensitive to three different GPX4 inhibitors, which are known to elicit ferroptotic cell death."
item351	REG00014	M6ATAR00086	Up	M6ADIS0029	M6ADRUG0068	31935372	"CDR1 antisense RNA (CDR1-AS) a regulator of miR-7, as a hallmark of melanoma progression. CDR1as depletion results from epigenetic silencing of LINC00632, its originating long non-coding RNA (lncRNA) and promotes invasion in vitro and metastasis in vivo through a miR-7-independent, IGF2BP3-mediated mechanism. IGF2BP3 interacts with CDR1as and mediates invasion induced by CDR1as depletion. CDR1asHigh melanoma cell lines were strikingly more sensitive to three different GPX4 inhibitors, which are known to elicit ferroptotic cell death."
item352	REG00024	M6ATAR00239	Up	M6ADIS0064	.	31947544	Knockdown of YTHDF1 in Merkel cell carcinoma (MCC) cell lines negatively affected the translation initiation factor Eukaryotic translation initiation factor 3 subunit A (EIF3A/EIF3) and reduced proliferation and clonogenic capacity in vitro.
item353	REG00007	M6ATAR00134	Down	M6ADIS0006	.	31967701	microRNA 186 (MIR186)/METTL3 axis contributed to the progression of Hepatoblastoma via the Wnt/beta-catenin signalling pathway.
item354	REG00007	M6ATAR00302	Up	M6ADIS0007	.	31982139	m6A methyltransferase METTL3 is indispensable for TGF-beta-induced EMT of lung cancer cells through the regulation of Transcription factor JunB (JUNB).
item355	REG00024	M6ATAR00372	Up	M6ADIS0020	.	31983283	"m6A modification promoted translation of Protein phosphatase 1A (PPM1A) (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone. Rapamycin could effectively inhibit phosphorylation of RPS6KB1."
item356	REG00024	M6ATAR00372	Up	M6ADIS0020	.	31983283	"m6A modification promoted translation of Protein phosphatase 1A (PPM1A) (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone."
item357	REG00005	M6ATAR00372	Up	M6ADIS0020	.	31983283	"m6A modification promoted translation of Protein phosphatase 1A (PPM1A) (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone."
item358	REG00005	M6ATAR00372	Up	M6ADIS0020	.	31983283	"m6A modification promoted translation of Protein phosphatase 1A (PPM1A) (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone."
item359	REG00008	M6ATAR00309	Down	M6ADIS0020	.	31983283	"m6A modification promoted translation of PPM1A (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of Calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone. knock down of YTHDF2 increased expression of Camkk2 at both mRNA and protein levels to a similar extent as knock down of METTL14 in both TM3 cells and primary LCs."
item360	REG00008	M6ATAR00309	Down	M6ADIS0020	.	31983283	"m6A modification promoted translation of PPM1A (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of Calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone. knock down of YTHDF2 increased expression of Camkk2 at both mRNA and protein levels to a similar extent as knock down of METTL14 in both TM3 cells and primary LCs."
item361	REG00006	M6ATAR00372	Up	M6ADIS0020	.	31983283	"m6A modification promoted translation of Protein phosphatase 1A (PPM1A) (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone."
item362	REG00006	M6ATAR00372	Up	M6ADIS0020	.	31983283	"m6A modification promoted translation of Protein phosphatase 1A (PPM1A) (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone."
item363	REG00006	M6ATAR00309	Down	M6ADIS0020	.	31983283	"m6A modification promoted translation of PPM1A (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of Calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone."
item364	REG00006	M6ATAR00309	Down	M6ADIS0020	.	31983283	"m6A modification promoted translation of PPM1A (protein phosphatase 1A, magnesium dependent, alpha isoform), a negative AMP-activated protein kinase (AMPK) regulator, but decreased expression of Calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) (calcium/calmodulin-dependent protein kinase kinase 2, beta), a positive AMPK regulator, by reducing its RNA stability. Similar regulation of METTL14, ALKBH5, and m6A was also observed in LCs upon treatment with human chorionic gonadotropin (HsCG). Knock down of YTHDF1 failed to change the expression of CAMKK2 Providing insight into novel therapeutic strategies by exploiting m6A RNA methylation as targets for treating azoospermatism and oligospermatism patients with reduction in serum testosterone."
item365	REG00001	.	.	M6ADIS0010	.	31985880	"The m6A-demethylases ALKBH5 and FTO are dysregulated in clear cell renal cell carcinoma and could be used as prognostic biomarkers. ALKBH5 mRNA, as well as ALKBH5 and FTO protein expressions, was significantly downregulated in ccRCC compared to normal tissue and most of the other studied tumour entities."
item366	REG00005	.	.	M6ADIS0010	.	31985880	"The m6A-demethylases ALKBH5 and FTO are dysregulated in clear cell renal cell carcinoma and could be used as prognostic biomarkers. ALKBH5 mRNA, as well as ALKBH5 and FTO protein expressions, was significantly downregulated in ccRCC compared to normal tissue and most of the other studied tumour entities."
item367	REG00024	M6ATAR00240	Up	M6ADIS0066	.	31996915	"YTHDF1 augments the translation of Eukaryotic translation initiation factor 3 subunit C (EIF3C) in an m6A-dependent manner by binding to m6A-modified EIF3C mRNA and concomitantly promotes the overall translational output, thereby facilitating tumorigenesis and metastasis of ovarian cancer."
item368	REG00005	M6ATAR00153	Up	M6ADIS0051	.	32021563	"ALKBH5 decreased the m6A modification of Pvt1 oncogene (PVT1), thus inhibiting the binding of reader protein YTHDF2 in PVT1. ALKBH5-mediated PVT1 upregulation promoted the osteosarcoma cell proliferation in vitro and tumor growth in vivo."
item369	REG00008	M6ATAR00153	Up	M6ADIS0051	.	32021563	"ALKBH5 decreased the m6A modification of Pvt1 oncogene (PVT1), thus inhibiting the binding of reader protein YTHDF2 in PVT1. ALKBH5-mediated PVT1 upregulation promoted the osteosarcoma cell proliferation in vitro and tumor growth in vivo."
item370	REG00005	M6ATAR00381	Down	.	.	32029706	"Apoptosis of NPCs under compression could be inhibited by coculturing with BMSCs, which regulates the process of autophagy in NPCs by upregulating ALKBH5, which protects RB1-inducible coiled-coil protein 1 (RB1CC1/FIP200) mRNA from YTHDF2-mediated degradation."
item371	REG00008	M6ATAR00381	Down	.	.	32029706	"Apoptosis of NPCs under compression could be inhibited by coculturing with BMSCs, which regulates the process of autophagy in NPCs by upregulating ALKBH5, which protects RB1-inducible coiled-coil protein 1 (RB1CC1/FIP200) mRNA from YTHDF2-mediated degradation."
item372	REG00017	.	Down	.	.	32033081	"In a subset of irradiated cells, only the METTL16 enzyme, responsible for m6A in non-coding RNAs as well as for splicing regulation, was recruited to microirradiated sites. Importantly, the levels of the studied splicing factors were not changed by UVA light."
item373	REG00001	M6ATAR00333	Up	M6ADIS0056	.	32035950	"Up-regulation of FTO is frequently observed in esophageal squamous cell carcinoma tissues, and FTO facilitates cell proliferation and migration in ESCC by up-regulating Collagenase 3 (MMP13)."
item374	REG00007	M6ATAR00208	Up	M6ADIS0059	.	32039568	"METTL3 promotes colorectal cancer proliferation by stabilizing G1/S-specific cyclin-E1 (CCNE1) mRNA in an m6A-dependent manner, representing a promising therapeutic strategy for the treatment of CRC."
item375	REG00007	M6ATAR00183	Up	M6ADIS0051	.	32044716	"METTL3 functions as an oncogene in the growth and invasion of osteosarcoma by regulating ATPase family AAA domain-containing protein 2 (ATAD2), suggesting a potential therapeutic target for osteosarcoma treatment."
item376	REG00023	M6ATAR00207	Up	M6ADIS0056	.	32047883	Knockdown of YTHDC2 substantially promoted the proliferation rate of esophageal squamous cell carcinoma cells by affecting several cancer-related signaling pathways.
item377	REG00023	M6ATAR00213	Up	M6ADIS0056	.	32047883	Knockdown of YTHDC2 substantially promoted the proliferation rate of esophageal squamous cell carcinoma cells by affecting several cancer-related signaling pathways.
item378	REG00023	M6ATAR00428	Up	M6ADIS0056	.	32047883	Knockdown of YTHDC2 substantially promoted the proliferation rate of esophageal squamous cell carcinoma cells by affecting several cancer-related signaling pathways.
item379	REG00015	M6ATAR00301	Up	M6ADIS0057	.	32052427	KIAA1429 played a key role in promoting gastric cancer by regulating Transcription factor Jun (c-Jun/JUN) expression in an m6A independent manner.
item380	REG00009	M6ATAR00302	Up	.	.	32070750	"MeRIP-Seq of mRNAs of MCF7 with or without treated by TGF-beta showed that mRNA with upregulated m6A modification level after TGF-beta treatment were enriched in TGF-beta signaling pathway. Phosphorylated level of SMAD2 or SMAD3 induced by TGF-beta was impaired when WTAP was silenced. The m6A modification and mRNA level of Transcription factor JunB (JUNB), which is known as a cell cycle inhibitor, both were increased after induction of TGF-beta and decreased after knockdown of WTAP. Phosphorylated level of SMAD2 or SMAD3 induced by TGF-beta was impaired when WTAP was silenced."
item381	.	M6ATAR00287	.	M6ADIS0031	.	32106582	"Zika virus (ZIKV) is a mosquito-borne virus associated with neurological disorders such as Guillain-Barre syndrome and microcephaly. This review summarizes relevant aspects of the complex crosstalk between RNA metabolism and cellular stress responses against ZIKV and discusses their possible impact on viral pathogenesis. ZIKV replication is known to induce cellular stress, which triggers both the expression of innate immune genes and the phosphorylation of eukaryotic translation initiation factor 2 (eIF2-alpha), shutting-off host protein synthesis."
item382	.	M6ATAR00287	.	M6ADIS0121	.	32106582	"Zika virus (ZIKV) is a mosquito-borne virus associated with neurological disorders such as Guillain-Barre syndrome and microcephaly. This review summarizes relevant aspects of the complex crosstalk between RNA metabolism and cellular stress responses against ZIKV and discusses their possible impact on viral pathogenesis. ZIKV replication is known to induce cellular stress, which triggers both the expression of innate immune genes and the phosphorylation of eukaryotic translation initiation factor 2 (eIF2-alpha), shutting-off host protein synthesis."
item383	REG00005	M6ATAR00451	.	M6ADIS0007	.	32106857	m6A demethylase ALKBH5 inhibits tumor growth and metastasis by reducing YTHDFs-mediated Transcriptional coactivator YAP1 (YAP1) expression and inhibiting miR-107/LATS2-mediated YAP activity in non-small cell lung cancer.
item384	REG00005	M6ATAR00138	.	M6ADIS0007	.	32106857	m6A demethylase ALKBH5 inhibits tumor growth and metastasis by reducing YTHDFs-mediated YAP expression and inhibiting microRNA 107 (MIR107)/LATS2-mediated YAP activity in non-small cell lung cancer.
item385	REG00005	M6ATAR00314	.	M6ADIS0007	.	32106857	m6A demethylase ALKBH5 inhibits tumor growth and metastasis by reducing YTHDFs-mediated YAP expression and inhibiting miR-107/Serine/threonine-protein kinase LATS2 (LATS2)-mediated YAP activity in non-small cell lung cancer.
item386	REG00001	.	.	M6ADIS0007	.	32110044	FTO facilitates lung adenocarcinoma cell progression by activating cell migration through m6A demethylation.
item387	REG00008	M6ATAR00152	Down	M6ADIS0059	.	32111213	"In colorectal cancer, knockdown of METTL14 substantially abolished m6A level of X inactive specific transcript (XIST) and augmented XIST expression. m6A-methylated XIST was recognized by YTHDF2, a m6A reader protein, to mediate the degradation of XIST."
item388	REG00006	M6ATAR00152	Up	M6ADIS0059	.	32111213	"In colorectal cancer, knockdown of METTL14 substantially abolished m6A level of X inactive specific transcript (XIST) and augmented XIST expression. m6A-methylated XIST was recognized by YTHDF2, a m6A reader protein, to mediate the degradation of XIST."
item389	REG00008	M6ATAR00390	Down	M6ADIS0070	.	32126149	METTL3/YTHDF2/Histone-lysine N-methyltransferase SETD7 (SETD7)/KLF4 m6 A axis provide the insight into the underlying mechanism of carcinogenesis and highlight potential therapeutic targets for bladder cancer.
item390	REG00007	M6ATAR00390	Down	M6ADIS0070	.	32126149	METTL3/YTHDF2/Histone-lysine N-methyltransferase SETD7 (SETD7)/KLF4 m6 A axis provide the insight into the underlying mechanism of carcinogenesis and highlight potential therapeutic targets for bladder cancer.
item391	REG00008	M6ATAR00310	Down	M6ADIS0070	.	32126149	METTL3/YTHDF2/SETD7/Krueppel-like factor 4 (KLF4) m6 A axis provide the insight into the underlying mechanism of carcinogenesis and highlight potential therapeutic targets for bladder cancer.
item392	REG00007	M6ATAR00310	Down	M6ADIS0070	.	32126149	METTL3/YTHDF2/SETD7/Krueppel-like factor 4 (KLF4) m6 A axis provide the insight into the underlying mechanism of carcinogenesis and highlight potential therapeutic targets for bladder cancer.
item393	REG00024	M6ATAR00341	Up	M6ADIS0055	.	32145676	"In oral squamous cell carcinoma, YTH N6-methyladenosine RNA binding protein 1 (YTH domain family, member 1 [YTHDF1]) mediated the m6A-increased stability of Myc proto-oncogene protein (MYC) mRNA catalyzed by METTL3."
item394	REG00007	M6ATAR00341	Up	M6ADIS0055	.	32145676	"In oral squamous cell carcinoma, YTH N6-methyladenosine RNA binding protein 1 (YTH domain family, member 1 [YTHDF1]) mediated the m6A-increased stability of Myc proto-oncogene protein (MYC) mRNA catalyzed by METTL3."
item395	REG00023	M6ATAR00411	Down	M6ADIS0107	.	32150756	"In nonalcoholic fatty liver disease, Ythdc2 could bind to mRNA of lipogenic genes, including Sterol regulatory element-binding protein 1 (SREBF1), fatty acid synthase, stearoyl-CoA desaturase 1, and acetyl-CoA carboxylase 1, to decrease their mRNA stability and inhibit gene expression."
item396	REG00023	M6ATAR00433	Down	M6ADIS0107	.	32150756	"In nonalcoholic fatty liver disease, Ythdc2 could bind to mRNA of lipogenic genes, including sterol regulatory element-binding protein 1c, Tumor necrosis factor receptor superfamily member 6 (FAS), stearoyl-CoA desaturase 1, and acetyl-CoA carboxylase 1, to decrease their mRNA stability and inhibit gene expression."
item397	REG00023	M6ATAR00388	Down	M6ADIS0107	.	32150756	"In nonalcoholic fatty liver disease, Ythdc2 could bind to mRNA of lipogenic genes, including sterol regulatory element-binding protein 1c, fatty acid synthase, Stearoyl-CoA desaturase (SCD), and acetyl-CoA carboxylase 1, to decrease their mRNA stability and inhibit gene expression."
item398	REG00023	M6ATAR00168	Down	M6ADIS0107	.	32150756	"In nonalcoholic fatty liver disease, Ythdc2 could bind to mRNA of lipogenic genes, including sterol regulatory element-binding protein 1c, fatty acid synthase, stearoyl-CoA desaturase 1, and Acetyl-CoA carboxylase 1 (ACC1/ACACA), to decrease their mRNA stability and inhibit gene expression."
item399	REG00001	.	.	M6ADIS0006	.	32154934	"SIRT1 destabilizes FTO, steering the m6A of downstream molecules and subsequent mRNA expression in hepatocellular carcinoma tumorigenesis. A crucial component of small ubiquitin-related modifiers (SUMOs) E3 ligase, RANBP2, is activated by SIRT1, and it is indispensable for FTO SUMOylation at Lysine (K)-216 site that promotes FTO degradation."
item400	REG00007	M6ATAR00278	Up	M6ADIS0073	.	32158230	Silence of METTL3 inhibited migratory ability and Wnt activity in TPC-1 cells. METTL3 positively regulated the enrichment abundance of Hepatocyte nuclear factor 1-alpha (HNF1A/TCF1) in anti-IGF2BP2. TCF1 was responsible for METTL3-regulated thyroid carcinoma progression via the m6A methylation.
item401	REG00013	M6ATAR00278	Up	M6ADIS0073	.	32158230	Silence of METTL3 inhibited migratory ability and Wnt activity in TPC-1 cells. METTL3 positively regulated the enrichment abundance of Hepatocyte nuclear factor 1-alpha (HNF1A/TCF1) in anti-IGF2BP2. TCF1 was responsible for METTL3-regulated thyroid carcinoma progression via the m6A methylation.
item402	.	M6ATAR00142	.	M6ADIS0053	.	32163372	RHPN1 antisense RNA 1 (head to head) (RHPN1-AS1)-miR-596-LETM1 axis plays a crucial role in epithelial ovarian cancer progression.
item403	REG00007	M6ATAR00284	Up	M6ADIS0014	.	32163892	METTL3 modulates the proliferation and apoptosis of lens epithelial cells in diabetic cataract. METTL3 targets the 3' UTR of Intercellular adhesion molecule 1 (ICAM1) to stabilize mRNA stability.
item404	REG00022	M6ATAR00019	Down	M6ADIS0052	.	32165496	"Knockdown of METTL3 prolonged the half-life of PncRNA-D, and among the known m6A recognition proteins, YTHDC1 was responsible for binding m6A of pncRNA-D Knockdown of METTL3 or YTHDC1 also enhanced the interaction of pncRNA-D with TLS, and results from RNA pulldown assays implicated YTHDC1 in the inhibitory effect on the TLS-pncRNA-D interaction."
item405	REG00007	M6ATAR00019	Down	M6ADIS0052	.	32165496	"Knockdown of METTL3 prolonged the half-life of PncRNA-D, and among the known m6A recognition proteins, YTHDC1 was responsible for binding m6A of pncRNA-D Knockdown of METTL3 or YTHDC1 also enhanced the interaction of pncRNA-D with TLS, and results from RNA pulldown assays implicated YTHDC1 in the inhibitory effect on the TLS-pncRNA-D interaction."
item406	.	M6ATAR00105	.	M6ADIS0056	.	32169859	"Downregulation of YY1BM significantly upregulated eEF2K expression and inhibited apoptosis, thus conferring esophageal squamous cell carcinoma cells more adaptive to nutrient deprivation. Cigarette smoking decreased m6A modification of Long intergenic non-protein coding RNA 278 (LINC00278) and YY1BM translation."
item407	REG00007	M6ATAR00341	Up	M6ADIS0057	.	32175271	"In gastric cancer, several component molecules (e.g., MCM5, MCM6, etc.) of Myc proto-oncogene protein (MYC) target genes were mediated by METTL3 via altered m6A modification."
item408	REG00007	M6ATAR00321	Up	M6ADIS0057	.	32175271	"In gastric cancer, several component molecules (e.g., DNA replication licensing factor MCM5 (MCM5), MCM6, etc.) of MYC target genes were mediated by METTL3 via altered m6A modification."
item409	REG00007	M6ATAR00322	Up	M6ADIS0057	.	32175271	"In gastric cancer, several component molecules (e.g., MCM5, DNA replication licensing factor MCM6 (MCM6), etc.) of MYC target genes were mediated by METTL3 via altered m6A modification."
item410	REG00009	.	.	M6ADIS0057	.	32176425	"Wilms' tumour 1-associated protein was highly expressed in gastric cancer, which indicated a poor prognosis, and WTAP expression served as an independent predictor of GC survival. High WTAP expression correlated with RNA methylation and that low expression correlated with a high T cell-related immune response."
item411	REG00007	.	.	M6ADIS0089	.	32184705	The alterations of m6A RNA methylation in alzheimer's disease and in C57BL/6 mice were investigated using high-throughput sequencing. The expression of the m6A methyltransferase METTL3 was elevated and that of the m6A demethylase FTO was decreased in AD mice.
item412	REG00001	.	.	M6ADIS0089	.	32184705	The alterations of m6A RNA methylation in alzheimer's disease and in C57BL/6 mice were investigated using high-throughput sequencing. The expression of the m6A methyltransferase METTL3 was elevated and that of the m6A demethylase FTO was decreased in AD mice.
item413	REG00007	M6ATAR00141	.	M6ADIS0117	M6ADRUG0041	32203053	Renal fibrosis is a key factor in chronic kidney disease (CKD). Metastasis associated lung adenocarcinoma transcript 1 (MALAT1)/miR-145/FAK pathway was involved in the effect of dihydroartemisinin (DHA) on TGF-beta1-induced renal fibrosis in vitro and in vivo.
item414	.	M6ATAR00247	.	.	.	32206097	m6A induced Estrogen-related receptor gamma (ERRgamma/ESRRG) confers chemoresistance of cancer cells through upregulation of ABCB1 and CPT1B.
item415	.	M6ATAR00220	.	M6ADIS0002	.	32206097	"m6A induced ERR-Gamma confers chemoresistance of cancer cells through upregulation of ABCB1 and Carnitine O-palmitoyltransferase 1, muscle isoform (CPT1B)."
item416	.	M6ATAR00323	.	M6ADIS0002	.	32206097	m6A induced ERR-Gamma confers chemoresistance of cancer cells through upregulation of ATP-dependent translocase ABCB1 (ABCB1) and CPT1B.
item417	REG00007	M6ATAR00080	Up	M6ADIS0055	.	32216017	The N6-methyladenosine (m6A) modification mediated by METTL3 and METTL14 enhanced the stability of LncRNA activating regulator of DKK1 (LNCAROD) in head and neck squamous cell carcinoma cells. LNCAROD is stabilized by m6A methylation and promotes cancer progression via forming a ternary complex with HSPA1A and YBX1 in head and neck squamous cell carcinoma.
item418	REG00006	M6ATAR00080	Up	M6ADIS0055	.	32216017	The N6-methyladenosine (m6A) modification mediated by METTL3 and METTL14 enhanced the stability of LncRNA activating regulator of DKK1 (LNCAROD) in head and neck squamous cell carcinoma cells. LNCAROD is stabilized by m6A methylation and promotes cancer progression via forming a ternary complex with HSPA1A and YBX1 in head and neck squamous cell carcinoma.
item419	REG00015	M6ATAR00092	Up	M6ADIS0068	.	32218194	VIRMA downregulation attenuates the aggressive phenotype of prostate cancer by overall reduction of m6A-levels decreasing stability and abundance of oncogenic lncRNAs. VIRMA depletion and m6A reduction decreased the stability and abundance of Colon cancer associated transcript 1 (CCAT1) transcripts.
item420	REG00015	M6ATAR00091	Up	M6ADIS0068	.	32218194	VIRMA downregulation attenuates the aggressive phenotype of prostate cancer by overall reduction of m6A-levels decreasing stability and abundance of oncogenic lncRNAs. VIRMA depletion and m6A reduction decreased the stability and abundance of Colon cancer associated transcript 2 (CCAT2) transcripts.
item421	REG00007	M6ATAR00283	Up	M6ADIS0059	.	32245489	METTL3 stabilizes Hexokinase-2 (HK2) and SLC2A1 (GLUT1) expression in colorectal cancer through an m6A-IGF2BP2/3- dependent mechanism.
item422	REG00007	M6ATAR00269	Up	M6ADIS0059	.	32245489	METTL3 stabilizes HK2 and Glucose transporter type 1 (SLC2A1) (GLUT1) expression in colorectal cancer through an m6A-IGF2BP2/3- dependent mechanism.
item423	REG00013	M6ATAR00283	Up	M6ADIS0059	.	32245489	METTL3 stabilizes Hexokinase-2 (HK2) and SLC2A1 (GLUT1) expression in colorectal cancer through an m6A-IGF2BP2/3- dependent mechanism.
item424	REG00013	M6ATAR00269	Up	M6ADIS0059	.	32245489	METTL3 stabilizes HK2 and Glucose transporter type 1 (SLC2A1) (GLUT1) expression in colorectal cancer through an m6A-IGF2BP2/3- dependent mechanism.
item425	REG00014	M6ATAR00283	Up	M6ADIS0059	.	32245489	METTL3 stabilizes Hexokinase-2 (HK2) and SLC2A1 (GLUT1) expression in colorectal cancer through an m6A-IGF2BP2/3- dependent mechanism.
item426	REG00014	M6ATAR00269	Up	M6ADIS0059	.	32245489	METTL3 stabilizes HK2 and Glucose transporter type 1 (SLC2A1) (GLUT1) expression in colorectal cancer through an m6A-IGF2BP2/3- dependent mechanism.
item427	REG00012	M6ATAR00076	Up	.	.	32245947	"The oncopeptide RBRP encoded by Septin 14 pseudogene 20 (SEPTIN14P20/LINC00266-1) is a regulatory subunit of m6A readers and strengthens m6A recognition on the target RNAs by the m6A reader to exert its oncogenic functions. RBRP binds to IGF2BP1 and strengthens m6A recognition by IGF2BP1 on RNAs, such as c-Myc mRNA, to increase the mRNA stability and expression of c-Myc, thereby promoting tumorigenesis."
item428	REG00007	M6ATAR00175	Up	M6ADIS0066	.	32256816	METTL3 knockdown downregulated the phosphorylation levels of RAC-alpha serine/threonine-protein kinase (AKT1) and the expression of the downstream effector Cyclin D1 in ovarian cancer.
item429	REG00007	M6ATAR00206	Up	M6ADIS0066	.	32256816	METTL3 knockdown downregulated the phosphorylation levels of AKT and the expression of the downstream effector G1/S-specific cyclin-D1 (CCND1) in ovarian cancer.
item430	REG00007	M6ATAR00298	Up	M6ADIS0068	.	32266107	"METTL3 regulates the expression of Integrin beta-1 (ITGB1) through m6A-HuR-dependent mechanism, which affects the binding of ITGB1 to Collagen I and tumor cell motility, so as to promote the bone metastasis of prostate cancer."
item431	REG00007	M6ATAR00230	Up	M6ADIS0051	.	32266933	"ELAVL1 knockdown impaired the stability of DRG1 mRNA, thereby reducing both the mRNA and protein levels of Developmentally-regulated GTP-binding protein 1 (DRG1). In all, DRG1 exerted tumorigenic effects in osteosarcoma, and the up-regulation of DRG1 in OS was induced by METTL3 and ELAVL1 in an m6A-dependent manner."
item432	REG00002	M6ATAR00230	Up	M6ADIS0051	.	32266933	"ELAVL1 knockdown impaired the stability of DRG1 mRNA, thereby reducing both the mRNA and protein levels of Developmentally-regulated GTP-binding protein 1 (DRG1). In all, DRG1 exerted tumorigenic effects in osteosarcoma, and the up-regulation of DRG1 in OS was induced by METTL3 and ELAVL1 in an m6A-dependent manner."
item433	REG00007	M6ATAR00341	Up	M6ADIS0068	.	32284755	"METTL3 enhanced Myc proto-oncogene protein (MYC) expression by increasing m6A levels of MYC mRNA transcript, leading to oncogenic functions in prostate cancer."
item434	REG00007	M6ATAR00020	Up	M6ADIS0026	.	32307908	"Down-regulation of METTL3 promotes osteogenic processes both in vitro and in vivo, and this effect is recapitulated by the suppression of mmu-miR-7212-5p maturation. miR-7212-5p inhibits osteoblast differentiation in MC3T3-E1 cells by targeting FGFR3."
item435	REG00016	M6ATAR00369	Up	M6ADIS0061	M6ADRUG0055	32312789	"N6-methyladenosine mRNA methylation of PIK3CB regulates AKT signalling to promote PTEN-deficient pancreatic cancer progression. Rs142933486 is significantly associated with the overall survival of PDAC by reducing the PIK3CB m6A level, which facilitated its mRNA and protein expression levels mediated by the m6A 'writer' complex (METTL13/METTL14/WTAP) and the m6A 'reader' YTHDF2. KIN-193, a PI3-kinase subunit beta (PIK3CB)-selective inhibitor, is shown to serve as an effective anticancer agent for blocking PTEN-deficient PDAC."
item436	REG00006	M6ATAR00369	Up	M6ADIS0061	M6ADRUG0055	32312789	"N6-methyladenosine mRNA methylation of PIK3CB regulates AKT signalling to promote PTEN-deficient pancreatic cancer progression. Rs142933486 is significantly associated with the overall survival of PDAC by reducing the PIK3CB m6A level, which facilitated its mRNA and protein expression levels mediated by the m6A 'writer' complex (METTL13/METTL14/WTAP) and the m6A 'reader' YTHDF2. KIN-193, a PI3-kinase subunit beta (PIK3CB)-selective inhibitor, is shown to serve as an effective anticancer agent for blocking PTEN-deficient PDAC."
item437	REG00009	M6ATAR00369	Up	M6ADIS0061	M6ADRUG0055	32312789	"N6-methyladenosine mRNA methylation of PIK3CB regulates AKT signalling to promote PTEN-deficient pancreatic cancer progression. Rs142933486 is significantly associated with the overall survival of PDAC by reducing the PIK3CB m6A level, which facilitated its mRNA and protein expression levels mediated by the m6A 'writer' complex (METTL13/METTL14/WTAP) and the m6A 'reader' YTHDF2. KIN-193, a PI3-kinase subunit beta (PIK3CB)-selective inhibitor, is shown to serve as an effective anticancer agent for blocking PTEN-deficient PDAC."
item438	REG00008	M6ATAR00369	Down	M6ADIS0061	M6ADRUG0055	32312789	"N6-methyladenosine mRNA methylation of PIK3CB regulates AKT signalling to promote PTEN-deficient pancreatic cancer progression. Rs142933486 is significantly associated with the overall survival of PDAC by reducing the PIK3CB m6A level, which facilitated its mRNA and protein expression levels mediated by the m6A 'writer' complex (METTL13/METTL14/WTAP) and the m6A 'reader' YTHDF2. KIN-193, a PI3-kinase subunit beta (PIK3CB)-selective inhibitor, is shown to serve as an effective anticancer agent for blocking PTEN-deficient PDAC."
item439	.	M6ATAR00111	.	.	.	32323721	m6A modification can regulate the expression of H19 and microRNA 675 (MIR675) which induce cell apoptosis.
item440	REG00006	M6ATAR00063	Up	M6ADIS0065	.	32323801	"In breast cancer, hsa-miR-146a-5p modulated by METTL14 promoted cell migration and invasion."
item441	REG00005	M6ATAR00344	Up	M6ADIS0066	.	32329191	Homeobox protein NANOG (NANOG) served as a target in ALKBH5-mediated m6A modification in ovarian cancer.
item442	REG00007	M6ATAR00315	Up	M6ADIS0068	.	32329830	"METTL3 influences the activity of the Wnt pathway through m6A methylation on Lymphoid enhancer-binding factor 1 (LEF1) mRNA, thereafter, promoting the progression of prostate cancer."
item443	REG00007	M6ATAR00021	Up	M6ADIS0015	.	32365051	"METTL3 involves in the pathogenesis of diabetic retinopathy (DR). Both METTL3 mRNA and hsa-miR-25-3p were low-expressed in the peripheral venous blood samples of diabetes mellitus (DM) patients compared to normal volunteers, and high-glucose inhibited METTL3 and miR-25-3p expressions in RPE cells. Overexpression of METTL3 attenuates high-glucose induced RPE cell pyroptosis by regulating miR-25-3p/PTEN/Akt signaling cascade through DGCR8."
item444	REG00007	M6ATAR00021	Up	M6ADIS0080	.	32365051	"METTL3 involves in the pathogenesis of diabetic retinopathy (DR). Both METTL3 mRNA and hsa-miR-25-3p were low-expressed in the peripheral venous blood samples of diabetes mellitus (DM) patients compared to normal volunteers, and high-glucose inhibited METTL3 and miR-25-3p expressions in RPE cells. Overexpression of METTL3 attenuates high-glucose induced RPE cell pyroptosis by regulating miR-25-3p/PTEN/Akt signaling cascade through DGCR8."
item445	REG00008	M6ATAR00022	Up	M6ADIS0006	.	32366907	"YTHDF2 promotes the CSC liver phenotype and cancer metastasis by modulating the m6A methylation of POU domain, class 5, transcription factor 1 (POU5F1) mRNA. YTHDF2 expression is positively correlated with OCT4 expression and m6A levels in the 5'-UTR of OCT4 mRNA in clinical hepatocellular carcinoma specimens."
item446	REG00007	M6ATAR00260	Down	M6ADIS0006	M6ADRUG0032	32368828	"METTL3 and Forkhead box protein O3 (FOXO3) levels are tightly correlated in hepatocellular carcinoma patients. In mouse xenograft models, METTL3 depletion significantly enhances sorafenib resistance of HCC by abolishing the identified METTL3-mediated FOXO3 mRNA stabilization, and overexpression of FOXO3 restores m6 A-dependent sorafenib sensitivity."
item447	REG00007	M6ATAR00249	Down	M6ADIS0054	.	32373970	"METTL3 was highly expressed in nasopharyngeal carcinoma tissues, which inhibited Histone-lysine N-methyltransferase EZH2 (EZH2) expression by mediating m6A modification of EZH2 mRNA."
item448	REG00007	M6ATAR00165	Down	M6ADIS0054	M6ADRUG0047	32382014	TRIM11 regulates nasopharyngeal carcinoma drug resistance by positively modulating the Daple/beta-catenin/ATP-binding cassette sub-family C member 9 (ABCC9) signaling pathway. TRIM11 enhanced the multidrug resistance in NPC by inhibiting apoptosis in vitro and promoting cisplatin (DDP) resistance in vivo. METTL3-mediated m6A modification caused the upregulation of TRIM11 via IGF2BP2 in NPC drug-resistant cells.
item449	REG00007	M6ATAR00466	Down	M6ADIS0054	M6ADRUG0047	32382014	TRIM11 regulates nasopharyngeal carcinoma drug resistance by positively modulating the Daple/beta-catenin/E3 ubiquitin-protein ligase TRIM11 (TRIM11) signaling pathway. TRIM11 enhanced the multidrug resistance in NPC by inhibiting apoptosis in vitro and promoting cisplatin (DDP) resistance in vivo. METTL3-mediated m6A modification caused the upregulation of TRIM11 via IGF2BP2 in NPC drug-resistant cells.
item450	.	M6ATAR00341	.	M6ADIS0006	.	32391046	"m6A-related genes have a prognostic value in liver cancer, and the constructed riskscore can identify patients who are high risk and can enable individualized therapy. Gene set enrichment analysis showed that tumorigenic markers, including DNA repair, E2F targets, G2M checkpoint, and Myc proto-oncogene protein (MYC) targets V1, were enriched in Cluster2."
item451	REG00005	M6ATAR00422	Up	M6ADIS0046	.	32402250	"ALKBH5 exerts tumor-promoting effects in acute myeloid leukemia by post-transcriptional regulation of its critical targets such as Transforming acidic coiled-coil-containing protein 3 (TACC3), a prognosis-associated oncogene in various cancers."
item452	REG00005	M6ATAR00443	Down	M6ADIS0046	.	32402251	"Expression of m6A demethylase ALKBH5 is regulated by chromatin state alteration during leukemogenesis of human acute myeloid leukemia (AML), and ALKBH5 is required for maintaining leukemia stem cell (LSC) function but is dispensable for normal hematopoiesis. ALKBH5 affects mRNA stability of receptor tyrosine kinase Tyrosine-protein kinase receptor UFO (AXL) in an m6A-dependent way."
item453	REG00022	M6ATAR00455	Up	.	.	32402287	"Specific m6As control its accumulation and that METTL3 and YTHDC1 are required to direct the back-splicing reaction. Because Zinc finger protein 609 (ZNF609) displays the ability to be translated, we show that m6A modifications, through recognition by YTHDF3 and eIF4G2, modulate its translation."
item454	REG00007	M6ATAR00455	Up	.	.	32402287	"Specific m6As control its accumulation and that METTL3 and YTHDC1 are required to direct the back-splicing reaction. Because Zinc finger protein 609 (ZNF609) displays the ability to be translated, we show that m6A modifications, through recognition by YTHDF3 and eIF4G2, modulate its translation."
item455	REG00025	M6ATAR00455	Up	.	.	32402287	"Specific m6As control its accumulation and that METTL3 and YTHDC1 are required to direct the back-splicing reaction. Because Zinc finger protein 609 (ZNF609) displays the ability to be translated, we show that m6A modifications, through recognition by YTHDF3 and eIF4G2, modulate its translation."
item456	REG00005	M6ATAR00364	Up	M6ADIS0061	.	32429928	"ALKBH5 serves as a pancreatic cancer suppressor by regulating the posttranscriptional activation of Period circadian protein homolog 1 (PER1) through m6A abolishment, which highlights a demethylation-based approach for PC diagnosis and therapy. ALKBH5 loss downregulated PER1 mRNA levels in an m6A-YTHDF2-dependent manner."
item457	REG00008	M6ATAR00364	Down	M6ADIS0061	.	32429928	"ALKBH5 serves as a pancreatic cancer suppressor by regulating the posttranscriptional activation of Period circadian protein homolog 1 (PER1) through m6A abolishment, which highlights a demethylation-based approach for PC diagnosis and therapy. ALKBH5 loss downregulated PER1 mRNA levels in an m6A-YTHDF2-dependent manner."
item458	REG00001	.	.	M6ADIS0117	.	32439179	Targeting RNA m6A modification is a novel strategy for the treatment of chronic kidney diseases and autophagy. Knockdown of FTO or inhibit the m6A by 3-deazaadenosine blocks the effects of indoxyl sulfate on autophagy activation in cells.
item459	REG00001	.	.	M6ADIS0117	.	32439179	Targeting RNA m6A modification is a novel strategy for the treatment of chronic kidney diseases and autophagy. Knockdown of FTO or inhibit the m6A by 3-deazaadenosine blocks the effects of indoxyl sulfate on autophagy activation in cells.
item460	REG00024	.	.	M6ADIS0001	.	32449290	"m6A RNA methylation regulators play a potential role in the progression of gliomas. Predicted one microRNA, microRNA 346 that regulated and binded to 3'UTR of YTHDF1, which was confirmed by our fluorescent enzyme reporter gene experiment."
item461	REG00005	M6ATAR00213	Down	M6ADIS0056	.	32449584	"Expression of CDKN1A (p21) was significantly up-regulated in ALKBH5-depleted cells, and m6 A modification and stability of Cyclin-dependent kinase inhibitor 1 (CDKN1A) mRNA were increased by ALKBH5 knockdown. Identify ALKBH5 as the first m6 A demethylase that accelerates cell cycle progression and promotes cell proliferation of ESCC cells, which is associated with poor prognosis of esophageal squamous cell carcinoma patients."
item462	REG00007	M6ATAR00399	Up	M6ADIS0006	.	32483411	SUMOylation of Mettl3 was found to regulate hepatocellular carcinoma progression via controlling Zinc finger protein SNAI1 (SNAI1) mRNA homeostasis in an m6A methyltransferase activity-dependent manner.
item463	REG00007	M6ATAR00341	Up	M6ADIS0059	.	32509177	"METTL3 exerted its function through enhancing Myc proto-oncogene protein (MYC) expression, at least partially in an m6A-IGF2BP1-dependent manner. Knockdown of METTL3 suppressed colorectal cancer cell proliferation in vitro and in vivo."
item464	REG00007	M6ATAR00399	Up	M6ADIS0054	.	32512975	Overexpression of Zinc finger protein SNAI1 (SNAI1) partially reversed the regulatory effects of METTL3 on EMT-related gene expressions and metastatic abilities in nasopharyngeal carcinoma. Knockdown of METTL3 decreased the enrichment abundance of Snail in anti-IGF2BP2.
item465	REG00013	M6ATAR00399	Up	M6ADIS0054	.	32512975	Overexpression of Zinc finger protein SNAI1 (SNAI1) partially reversed the regulatory effects of METTL3 on EMT-related gene expressions and metastatic abilities in nasopharyngeal carcinoma. Knockdown of METTL3 decreased the enrichment abundance of Snail in anti-IGF2BP2.
item466	REG00005	.	.	M6ADIS0055	.	32547941	"In head and neck squamous cell carcinoma patients, a majority of highly expressed m6A regulatory genes is associated with poor OS, in particular ALKBH5<regulator/>, whereas YTHDC2 was associated with better prognosis."
item467	REG00023	.	.	M6ADIS0055	.	32547941	"In head and neck squamous cell carcinoma patients, a majority of highly expressed m6A regulatory genes is associated with poor OS, in particular ALKBH5, whereas YTHDC2<regulator/> was associated with better prognosis."
item468	REG00006	M6ATAR00405	Down	M6ADIS0059	.	32552762	METTL14 inhibited colorectal cancer malignant process partly through Transcription factor SOX-4 (SOX4)-mediated EMT process and PI3K/Akt signals.
item469	REG00005	M6ATAR00193	Up	M6ADIS0010	.	32566583	ALKBH5 plays a carcinogenic role in renal cell carcinoma by stabilizing Aurora kinase B (AURKB) mRNA in a m6A-dependent manner.
item470	REG00006	M6ATAR00223	Up	M6ADIS0065	.	32576970	"LNC942-METTL14-C-X-C chemokine receptor type 4 (CXCR4)/CYP1B1 signaling axis, which provides new targets and crosstalk m6A epigenetic modification mechanism for breast cancer prevention and treatment."
item471	REG00006	M6ATAR00217	Up	M6ADIS0065	.	32576970	"LNC942-METTL14-CXCR4/Cytochrome P450 1B1 (CYP1B1) signaling axis, which provides new targets and crosstalk m6A epigenetic modification mechanism for breast cancer prevention and treatment."
item472	REG00007	M6ATAR00121	Up	M6ADIS0091	.	32581712	"METTL3-mediated m6A methylation increases the maturation of microRNA 335 (MIR335), which promotes SG formation and reduces the apoptosis level of injury neurons and cells, and provides a potential therapeutic strategy for acute ischemic stroke."
item473	REG00001	.	Up	M6ADIS0066	.	32606006	"FTO-Dependent N 6-Methyladenosine Modifications Inhibit Ovarian Cancer Stem Cell Self-Renewal by Blocking cAMP Signaling. cAMP pathway as a new FTO target in CSCs, associated with tumor inhibiting functions, and provide key new information on the role of m6A modifications regulated by FTO in the fine tuning of cellular fate in HGSOC."
item474	REG00007	.	.	.	.	32615088	"METTL3-m6A-YTHDC1 axis modulates accumulation of DNA-RNA hybrids at double-strand breaks sites, which then recruit RAD51 and BRCA1 for homologous recombination (HR)-mediated repair."
item475	REG00022	.	.	.	.	32615088	"METTL3-m6A-YTHDC1 axis modulates accumulation of DNA-RNA hybrids at double-strand breaks sites, which then recruit RAD51 and BRCA1 for homologous recombination (HR)-mediated repair."
item476	REG00006	M6ATAR00024	Up	M6ADIS0099	.	32633395	"METTL14 increased the m6A modification of pri-miR-19a and promoted the processing of mature hsa-miR-19a-3p, thus promoting the proliferation and invasion of atherosclerotic vascular endothelial cells."
item477	REG00025	M6ATAR00453	Up	M6ADIS0006	.	32653519	"Circ_KIAA1429 could accelerate HCC advancement, maintained the expression of Zeb1 through the mechanism of m6A-YTHDF3-Zinc finger E-box-binding homeobox 1 (ZEB1) in hepatocellular carcinoma."
item478	.	M6ATAR00061	.	M6ADIS0057	.	32657141	.
item479	REG00007	M6ATAR00068	Down	M6ADIS0098	.	32674051	"The relative RNA expression level of hsa_circ_0029589 in macrophages was decreased, whereas the N6-methyladenosine (m6A) level of hsa_circ_0029589 and the expression of m6A methyltransferase METTL3 were validated to be significantly elevated in macrophages in patients with acute coronary syndrome."
item480	REG00007	M6ATAR00172	Up	M6ADIS0070	.	32676121	"METTL3 regulates the m6A modification and thereby the expression of AF4/FMR2 family member 4 (AFF4), knockdown of which phenocopies the METTL3 ablation and diminishes the tumor-initiating capability of bladder cancer stem cells in vivo."
item481	REG00001	M6ATAR00128	.	M6ADIS0001	M6ADRUG0010	32680921	FTO Inhibition Enhances the Antitumor Effect of Temozolomide by Targeting MYC-miR-155/microRNA 23a (MIR23A) Cluster-MXI1 Feedback Circuit in Glioma.
item482	REG00001	M6ATAR00135	.	M6ADIS0001	M6ADRUG0010	32680921	FTO Inhibition Enhances the Antitumor Effect of Temozolomide by Targeting MYC-microRNA 155 (MIR155)/miR-23a Cluster-MXI1 Feedback Circuit in Glioma.
item483	.	M6ATAR00023	.	M6ADIS0072	.	32682400	"m6A RNA methylation regulators take a crucial role in the potential malignant progression and prognostic value of uveal melanoma and were regarded as a new promising biomarker for UM prognosis and treatment strategy development. The malignant hallmarks of Mammalian target of rapamycin complex 1 (mTORC1) signaling, oxidative phosphorylation, interferon-a response and apoptosis signaling are also significantly enriched in the C1 subtype."
item484	REG00022	M6ATAR00141	Up	M6ADIS0004	.	32703936	MALAT1 hijacks both chimeric mRNAs and fusion protein in nuclear speckles during chromosomal translocation and mediates colocalization with METTL14 in an oncogenic fusion protein such as PML-RARalpha. Reducing MALAT1 or m6A methyltransferases and the 'reader' YTHDC1 result in the universal retention of distinct oncogenic gene (PML-RARalpha) mRNAs in nucleus. Targeting the lncRNA-triggered autoregulatory loop to disrupt chimeric mRNA transport represents a new common paradigm for treating blood malignancies.
item485	REG00006	M6ATAR00141	Up	M6ADIS0004	.	32703936	MALAT1 hijacks both chimeric mRNAs and fusion protein in nuclear speckles during chromosomal translocation and mediates colocalization with METTL14 in an oncogenic fusion protein such as PML-RARalpha. Reducing MALAT1 or m6A methyltransferases and the 'reader' YTHDC1 result in the universal retention of distinct oncogenic gene (PML-RARalpha) mRNAs in nucleus. Targeting the lncRNA-triggered autoregulatory loop to disrupt chimeric mRNA transport represents a new common paradigm for treating blood malignancies.
item486	REG00001	.	.	M6ADIS0006	.	32724383	FTO contributes to liver cancer oncogenesis via the downregulation of m6A RNA methylation levels.
item487	REG00015	.	.	M6ADIS0061	M6ADRUG0024	32754191	"Lasso regression identified a six-m6A-regulator-signature prognostic model (KIAA1429, HNRNPC, METTL3, YTHDF1, IGF2BP2, and IGF2BP3). Gene set enrichment analysis revealed m6A regulators (KIAA1429, HNRNPC, and IGF2BP2) were related to multiple biological behaviors in pancreatic cancer, including adipocytokine signaling, the well vs. poorly differentiated tumor pathway, tumor metastasis pathway, epithelial mesenchymal transition pathway, gemcitabine resistance pathway, and stemness pathway."
item488	REG00003	.	.	M6ADIS0061	M6ADRUG0024	32754191	"Lasso regression identified a six-m6A-regulator-signature prognostic model (KIAA1429, HNRNPC, METTL3, YTHDF1, IGF2BP2, and IGF2BP3). Gene set enrichment analysis revealed m6A regulators (KIAA1429, HNRNPC, and IGF2BP2) were related to multiple biological behaviors in pancreatic cancer, including adipocytokine signaling, the well vs. poorly differentiated tumor pathway, tumor metastasis pathway, epithelial mesenchymal transition pathway, gemcitabine resistance pathway, and stemness pathway."
item489	REG00007	.	.	M6ADIS0061	M6ADRUG0024	32754191	"Lasso regression identified a six-m6A-regulator-signature prognostic model (KIAA1429, HNRNPC, METTL3, YTHDF1, IGF2BP2, and IGF2BP3). Gene set enrichment analysis revealed m6A regulators (KIAA1429, HNRNPC, and IGF2BP2) were related to multiple biological behaviors in pancreatic cancer, including adipocytokine signaling, the well vs. poorly differentiated tumor pathway, tumor metastasis pathway, epithelial mesenchymal transition pathway, gemcitabine resistance pathway, and stemness pathway."
item490	REG00024	.	.	M6ADIS0061	M6ADRUG0024	32754191	"Lasso regression identified a six-m6A-regulator-signature prognostic model (KIAA1429, HNRNPC, METTL3, YTHDF1, IGF2BP2, and IGF2BP3). Gene set enrichment analysis revealed m6A regulators (KIAA1429, HNRNPC, and IGF2BP2) were related to multiple biological behaviors in pancreatic cancer, including adipocytokine signaling, the well vs. poorly differentiated tumor pathway, tumor metastasis pathway, epithelial mesenchymal transition pathway, gemcitabine resistance pathway, and stemness pathway."
item491	REG00013	.	.	M6ADIS0061	M6ADRUG0024	32754191	"Lasso regression identified a six-m6A-regulator-signature prognostic model (KIAA1429, HNRNPC, METTL3, YTHDF1, IGF2BP2, and IGF2BP3). Gene set enrichment analysis revealed m6A regulators (KIAA1429, HNRNPC, and IGF2BP2) were related to multiple biological behaviors in pancreatic cancer, including adipocytokine signaling, the well vs. poorly differentiated tumor pathway, tumor metastasis pathway, epithelial mesenchymal transition pathway, gemcitabine resistance pathway, and stemness pathway."
item492	REG00014	.	.	M6ADIS0061	M6ADRUG0024	32754191	"Lasso regression identified a six-m6A-regulator-signature prognostic model (KIAA1429, HNRNPC, METTL3, YTHDF1, IGF2BP2, and IGF2BP3). Gene set enrichment analysis revealed m6A regulators (KIAA1429, HNRNPC, and IGF2BP2) were related to multiple biological behaviors in pancreatic cancer, including adipocytokine signaling, the well vs. poorly differentiated tumor pathway, tumor metastasis pathway, epithelial mesenchymal transition pathway, gemcitabine resistance pathway, and stemness pathway."
item493	REG00007	M6ATAR00075	Up	.	.	32792482	The significantly reduced gene expression of the lncRNA THOR and the decreased m6A level on the lncRNA THOR in the METTL3stop/stop cells were determined by qRT-PCR and methylated RNA immunoprecipitation (MeRIP) assay. RIP-qRT-PCR and RNA pull-down assay results revealed that the specific m6A readers YTHDF1 and YTHDF2 can read the m6A motifs and regulate the stability of the lncRNA THOR (stabilization and decay).
item494	REG00008	M6ATAR00075	Down	.	.	32792482	The significantly reduced gene expression of the lncRNA THOR and the decreased m6A level on the lncRNA THOR in the METTL3stop/stop cells were determined by qRT-PCR and methylated RNA immunoprecipitation (MeRIP) assay. RIP-qRT-PCR and RNA pull-down assay results revealed that the specific m6A readers YTHDF1 and YTHDF2 can read the m6A motifs and regulate the stability of the lncRNA THOR (stabilization and decay).
item495	REG00024	M6ATAR00075	Up	.	.	32792482	The significantly reduced gene expression of the lncRNA THOR and the decreased m6A level on the lncRNA THOR in the METTL3stop/stop cells were determined by qRT-PCR and methylated RNA immunoprecipitation (MeRIP) assay. RIP-qRT-PCR and RNA pull-down assay results revealed that the specific m6A readers YTHDF1 and YTHDF2 can read the m6A motifs and regulate the stability of the lncRNA THOR (stabilization and decay).
item496	REG00001	M6ATAR00162	Up	M6ADIS0010	M6ADRUG0082	32817424	Genetic inactivation of FTO using multiple orthogonal approaches revealed that FTO inhibition selectively reduces the growth and survival of VHL-deficient cells in vitro and in vivo. Integrated analysis of transcriptome-wide m6A-seq and mRNA-seq analysis identified the glutamine transporter Neutral amino acid transporter B(0) (SLC1A5) as an FTO target that promotes metabolic reprogramming and survival of VHL-deficient ccRCC cells. GLS1 inhibitors that target mitochondrial glutaminase and the conversion of glutamine to glutamate are currently being evaluated in early-phase clinical trials in ccRCC. These findings identify FTO as a potential HIF-independent therapeutic target for the treatment of VHL-deficient renal cell carcinoma.
item497	REG00012	M6ATAR00235	.	M6ADIS0007	.	32849929	"GSEA revealed that KIAA1429, METTL3, and IGF2BP1 were significantly related to multiple biological behaviors, including proliferation, apoptosis, metastasis, energy metabolism, drug resistance, and recurrence, and that KIAA1429 and IGF2BP1 had potential target genes, including Transcription factor E2F3 (E2F3), WTAP, CCND1, CDK4, EGR2, YBX1, and TLX, which were associated with lung cancers."
item498	REG00012	M6ATAR00253	.	M6ADIS0007	.	32849929	"GSEA revealed that KIAA1429, METTL3, and IGF2BP1 were significantly related to multiple biological behaviors, including proliferation, apoptosis, metastasis, energy metabolism, drug resistance, and recurrence, and that KIAA1429 and IGF2BP1 had potential target genes, including E2F3, Pre-mRNA-splicing regulator WTAP (WTAP), CCND1, CDK4, EGR2, YBX1, and TLX, which were associated with lung cancers."
item499	REG00012	M6ATAR00206	.	M6ADIS0007	.	32849929	"GSEA revealed that KIAA1429, METTL3, and IGF2BP1 were significantly related to multiple biological behaviors, including proliferation, apoptosis, metastasis, energy metabolism, drug resistance, and recurrence, and that KIAA1429 and IGF2BP1 had potential target genes, including E2F3, WTAP, G1/S-specific cyclin-D1 (CCND1), CDK4, EGR2, YBX1, and TLX, which were associated with lung cancers."
item500	REG00012	M6ATAR00211	.	M6ADIS0007	.	32849929	"GSEA revealed that KIAA1429, METTL3, and IGF2BP1 were significantly related to multiple biological behaviors, including proliferation, apoptosis, metastasis, energy metabolism, drug resistance, and recurrence, and that KIAA1429 and IGF2BP1 had potential target genes, including E2F3, WTAP, CCND1, Cyclin-dependent kinase 4 (CDK4), EGR2, YBX1, and TLX, which were associated with lung cancers."
item501	REG00012	M6ATAR00238	.	M6ADIS0007	.	32849929	"GSEA revealed that KIAA1429, METTL3, and IGF2BP1 were significantly related to multiple biological behaviors, including proliferation, apoptosis, metastasis, energy metabolism, drug resistance, and recurrence, and that KIAA1429 and IGF2BP1 had potential target genes, including E2F3, WTAP, CCND1, CDK4, E3 SUMO-protein ligase EGR2 (EGR2), YBX1, and TLX, which were associated with lung cancers."
item502	REG00012	M6ATAR00452	.	M6ADIS0007	.	32849929	"GSEA revealed that KIAA1429, METTL3, and IGF2BP1 were significantly related to multiple biological behaviors, including proliferation, apoptosis, metastasis, energy metabolism, drug resistance, and recurrence, and that KIAA1429 and IGF2BP1 had potential target genes, including E2F3, WTAP, CCND1, CDK4, EGR2, Y-box-binding protein 1 (YBX1), and TLX, which were associated with lung cancers."
item503	REG00012	M6ATAR00352	.	M6ADIS0007	.	32849929	"GSEA revealed that KIAA1429, METTL3, and IGF2BP1 were significantly related to multiple biological behaviors, including proliferation, apoptosis, metastasis, energy metabolism, drug resistance, and recurrence, and that KIAA1429 and IGF2BP1 had potential target genes, including E2F3, WTAP, CCND1, CDK4, EGR2, YBX1, and Nuclear receptor subfamily 2 group E member 1 (TLX/NR2E1), which were associated with lung cancers."
item504	REG00015	M6ATAR00235	.	M6ADIS0007	.	32849929	"GSEA revealed that KIAA1429, METTL3, and IGF2BP1 were significantly related to multiple biological behaviors, including proliferation, apoptosis, metastasis, energy metabolism, drug resistance, and recurrence, and that KIAA1429 and IGF2BP1 had potential target genes, including Transcription factor E2F3 (E2F3), WTAP, CCND1, CDK4, EGR2, YBX1, and TLX, which were associated with lung cancers."
item505	REG00015	M6ATAR00253	.	M6ADIS0007	.	32849929	"GSEA revealed that KIAA1429, METTL3, and IGF2BP1 were significantly related to multiple biological behaviors, including proliferation, apoptosis, metastasis, energy metabolism, drug resistance, and recurrence, and that KIAA1429 and IGF2BP1 had potential target genes, including E2F3, Pre-mRNA-splicing regulator WTAP (WTAP), CCND1, CDK4, EGR2, YBX1, and TLX, which were associated with lung cancers."
item506	REG00015	M6ATAR00206	.	M6ADIS0007	.	32849929	"GSEA revealed that KIAA1429, METTL3, and IGF2BP1 were significantly related to multiple biological behaviors, including proliferation, apoptosis, metastasis, energy metabolism, drug resistance, and recurrence, and that KIAA1429 and IGF2BP1 had potential target genes, including E2F3, WTAP, G1/S-specific cyclin-D1 (CCND1), CDK4, EGR2, YBX1, and TLX, which were associated with lung cancers."
item507	REG00015	M6ATAR00211	.	M6ADIS0007	.	32849929	"GSEA revealed that KIAA1429, METTL3, and IGF2BP1 were significantly related to multiple biological behaviors, including proliferation, apoptosis, metastasis, energy metabolism, drug resistance, and recurrence, and that KIAA1429 and IGF2BP1 had potential target genes, including E2F3, WTAP, CCND1, Cyclin-dependent kinase 4 (CDK4), EGR2, YBX1, and TLX, which were associated with lung cancers."
item508	REG00015	M6ATAR00238	.	M6ADIS0007	.	32849929	"GSEA revealed that KIAA1429, METTL3, and IGF2BP1 were significantly related to multiple biological behaviors, including proliferation, apoptosis, metastasis, energy metabolism, drug resistance, and recurrence, and that KIAA1429 and IGF2BP1 had potential target genes, including E2F3, WTAP, CCND1, CDK4, E3 SUMO-protein ligase EGR2 (EGR2), YBX1, and TLX, which were associated with lung cancers."
item509	REG00015	M6ATAR00452	.	M6ADIS0007	.	32849929	"GSEA revealed that KIAA1429, METTL3, and IGF2BP1 were significantly related to multiple biological behaviors, including proliferation, apoptosis, metastasis, energy metabolism, drug resistance, and recurrence, and that KIAA1429 and IGF2BP1 had potential target genes, including E2F3, WTAP, CCND1, CDK4, EGR2, Y-box-binding protein 1 (YBX1), and TLX, which were associated with lung cancers."
item510	REG00015	M6ATAR00352	.	M6ADIS0007	.	32849929	"GSEA revealed that KIAA1429, METTL3, and IGF2BP1 were significantly related to multiple biological behaviors, including proliferation, apoptosis, metastasis, energy metabolism, drug resistance, and recurrence, and that KIAA1429 and IGF2BP1 had potential target genes, including E2F3, WTAP, CCND1, CDK4, EGR2, YBX1, and Nuclear receptor subfamily 2 group E member 1 (TLX/NR2E1), which were associated with lung cancers."
item511	REG00007	M6ATAR00180	Up	M6ADIS0009	M6ADRUG0047	32857912	METTL3 potentiates resistance to cisplatin through m6A modification of Transcription factor AP-2 gamma (TFAP2C) in seminoma. Enhanced stability of TFAP2C mRNA promoted seminoma cell survival under cisplatin treatment burden probably through up-regulation of DNA repair-related genes. IGF2BP1 binds to TFAP2C and enhances TFAP2C mRNA stability.
item512	REG00012	M6ATAR00180	Up	M6ADIS0009	M6ADRUG0047	32857912	METTL3 potentiates resistance to cisplatin through m6A modification of Transcription factor AP-2 gamma (TFAP2C) in seminoma. Enhanced stability of TFAP2C mRNA promoted seminoma cell survival under cisplatin treatment burden probably through up-regulation of DNA repair-related genes. IGF2BP1 binds to TFAP2C and enhances TFAP2C mRNA stability.
item513	REG00006	.	.	M6ADIS0066	.	32869897	METTL3 can regulate m6A methylation independently of METTL14 and WTAP in endometrioid epithelial ovarian cancer.
item514	REG00007	.	.	M6ADIS0066	.	32869897	METTL3 can regulate m6A methylation independently of METTL14 and WTAP in endometrioid epithelial ovarian cancer.
item515	REG00009	.	.	M6ADIS0066	.	32869897	METTL3 can regulate m6A methylation independently of METTL14 and WTAP in endometrioid epithelial ovarian cancer.
item516	REG00009	M6ATAR00341	Up	M6ADIS0046	M6ADRUG0021	32880751	"WTAP made acute myeloid leukemia cells resistant to daunorubicin. In further investigations, m6A methylation level was downregulated when knocking down WTAP, and Myc proto-oncogene protein (MYC) was upregulated due to the decreased m6A methylation of MYC mRNA."
item517	REG00005	M6ATAR00404	Up	M6ADIS0067	.	32913192	"HIF-dependent ALKBH5 expression increases in hypoxic TMEs, resulting in the demethylation of Transcription factor SOX-2 (SOX2) mRNA and the maintenance of the Endometrial cancer stem cells phenotype; these data indicate that ECSCs maintain their stemness by activating the HIF/ALKBH5/SOX2 axis under hypoxic conditions."
item518	REG00005	M6ATAR00140	Up	M6ADIS0059	.	32913527	"ALKBH5 knockdown suppressed malignant behavior of colon cancer partially through Nuclear paraspeckle assembly transcript 1 (NEAT1) by demethylation in vitro and vivo, suggesting that ALKBH5-NEAT1 axis is a potential therapeutic target for colon cancer treatment."
item519	REG00007	M6ATAR00025	Up	M6ADIS0066	.	32939058	"METTL3 promoted the maturation of hsa-miR-126-5p via the m6A modification of pri-miR-126-5p. Finally, in vitro and in vivo experiments substantiated that silencing of METTL3 impeded the progression and tumorigenesis of ovarian cancer by impairing the miR-126-5p-targeted inhibition of PTEN and thus blocking the PI3K/Akt/mTOR pathway."
item520	REG00008	.	.	M6ADIS0066	.	32948220	"YTHDF2 and microRNA 145, as two crucial m6A regulators, were involved in the progression of epithelial ovarian cancer by indirectly modulating m6A levels."
item521	REG00007	M6ATAR00257	Down	M6ADIS0025	.	32954854	"METTL3 contributes to renal ischemia-reperfusion injury by regulating Forkhead box protein D1 (FOXD1) methylation. When METTL3 was inhibited, m6A levels were accordingly decreased and cell apoptosis was suppressed in the H/R in vitro model. Based on MeRIP sequencing, transcription factor activating enhancer binding protein 2-alpha (tfap2a), cytochrome P-450 1B1 (cyp1b1), and forkhead box D1 (foxd1) were significantly differentially expressed, as was m6A, which is involved in the negative regulation of cell proliferation and kidney development."
item522	REG00007	M6ATAR00179	Up	M6ADIS0025	.	32954854	"METTL3 contributes to renal ischemia-reperfusion injury by regulating Foxd1 methylation. When METTL3 was inhibited, m6A levels were accordingly decreased and cell apoptosis was suppressed in the H/R in vitro model. Based on MeRIP sequencing, Transcription factor AP-2-alpha (TFAP2A), cytochrome P-450 1B1 (cyp1b1), and forkhead box D1 (foxd1) were significantly differentially expressed, as was m6A, which is involved in the negative regulation of cell proliferation and kidney development."
item523	REG00007	M6ATAR00217	Up	M6ADIS0025	.	32954854	"METTL3 contributes to renal ischemia-reperfusion injury by regulating Foxd1 methylation. When METTL3 was inhibited, m6A levels were accordingly decreased and cell apoptosis was suppressed in the H/R in vitro model. Based on MeRIP sequencing, transcription factor activating enhancer binding protein 2-alpha (tfap2a), Cytochrome P450 1B1 (CYP1B1), and forkhead box D1 (foxd1) were significantly differentially expressed, as was m6A, which is involved in the negative regulation of cell proliferation and kidney development."
item524	REG00007	M6ATAR00303	Up	M6ADIS0065	M6ADRUG0039	32956623	"Adenylate kinase 4 modulates the resistance of breast cancer cells to tamoxifen through an m6A-based epitranscriptomic mechanism. Genetic depletion of METTL3 in TamR MCF-7 cells led to a diminished Adenylate kinase 4, mitochondrial (AK4) protein level and attenuated resistance to tamoxifen."
item525	REG00003	M6ATAR00402	Up	M6ADIS0070	.	32964246	"SNP rs5746136 affects m6A modification and regulate Superoxide dismutase [Mn], mitochondrial (SOD2) expression by guiding the binding of hnRNPC to SOD2, which played a critical tumor suppressor role in bladder cancer cells by promoting cell apoptosis and inhibiting proliferation, migration and invasion."
item526	.	.	.	M6ADIS0002	.	32985068	"In this review, we provide the first overview of the current knowledge of m6A modification implicated in CSCs and their impact on CSC properties, tumor progression, and responses to treatment."
item527	REG00007	M6ATAR00001	Down	M6ADIS0026	.	32999283	Oxygen glucose deprivation/re-oxygenation (OGD/R) induces neuronal injury via mechanisms that are believed to mimic the pathways associated with brain ischemia. METTL3 shRNA reversed OGD/R-induced Lnc_D63785 m6A methylation to decrease miR-422a accumulation.
item528	REG00007	M6ATAR00026	Up	M6ADIS0026	.	32999283	Oxygen glucose deprivation/re-oxygenation (OGD/R) induces neuronal injury via mechanisms that are believed to mimic the pathways associated with brain ischemia. METTL3 shRNA reversed OGD/R-induced Lnc-D63785 m6A methylation to decrease hsa-miR-422a accumulation.
item529	REG00024	M6ATAR00436	Up	M6ADIS0066	M6ADRUG0047	33011193	m6A-YTHDF1-mediated Tripartite motif-containing protein 29 (TRIM29) upregulation facilitates the stem cell-like phenotype of cisplatin-resistant ovarian cancer cells. TRIM29 acts as an oncogene to promote the CSC-like features of cisplatin-resistant ovarian cancer in an m6A-YTHDF1-dependent manner.
item530	REG00014	M6ATAR00078	Up	M6ADIS0008	.	33028109	KCNMB2 antisense RNA 1 (KCNMB2-AS1) and IGF2BP3 formed a positive regulatory circuit that enlarged the tumorigenic effect of KCNMB2-AS1 in cervical cancer.
item531	REG00007	M6ATAR00341	Up	M6ADIS0057	.	33048840	"METTL3 enhanced Myc proto-oncogene protein (MYC) m6A methylation and increased MYC translation, which could potentiate the proliferation, migration and invasion of gastric cancer cells."
item532	REG00009	M6ATAR01576	.	M6ADIS0046	.	33061801	"MicroRNA 550a-1 mediated a decrease in m6A levels via targeting WTAP, which led to a further reduction in WWTR1 stability. Using gain- and loss-of-function approaches, we were able to determine that miR-550-1 disrupted the proliferation and tumorigenesis of acute myeloid leukemia cells at least in part via the direct targeting of WWTR1."
item533	.	.	.	M6ADIS0002	.	33062255	"In this review, we summarized the regulatory mechanisms and biological functions of m6A and its role in cancer metabolic reprogramming."
item534	REG00001	M6ATAR00250	Down	M6ADIS0083	.	33079435	FTO regulates hepatic lipogenesis via FTO-dependent m6A demethylation in Fatty acid synthase (FASN) mRNA and indicate the critical role of FTO-mediated lipid metabolism in the survival of HepG2 cells. This study provides novel insights into a unique RNA epigenetic mechanism by which FTO mediates hepatic lipid accumulation through m6 A modification and indicates that FTO could be a potential target for obesity-related diseases and cancer.
item535	REG00001	M6ATAR00250	Down	M6ADIS0002	.	33079435	FTO regulates hepatic lipogenesis via FTO-dependent m6A demethylation in Fatty acid synthase (FASN) mRNA and indicate the critical role of FTO-mediated lipid metabolism in the survival of HepG2 cells. This study provides novel insights into a unique RNA epigenetic mechanism by which FTO mediates hepatic lipid accumulation through m6 A modification and indicates that FTO could be a potential target for obesity-related diseases and cancer.
item536	REG00008	M6ATAR00336	Down	M6ADIS0068	.	33087165	Activation of the KDM5A/miRNA-495/YTHDF2/m6A-MOB3B axis facilitates prostate cancer progression. YTHDF2 could inhibit MOB kinase activator 3B (MOB3B) expression by recognizing m6A modification of MOB3B mRNA and inducing mRNA degradation.
item537	REG00007	M6ATAR00025	Up	M6ADIS0114	.	33098220	"Interleukin 1-beta (IL-1-beta) is an important inducer of cartilage degeneration that can induce an inflammatory cascade reaction in chondrocytes and inhibit the normal biological function of cells. METTL3 could regulate hsa-miR-126-5p maturation, we first confirmed that METTL3 can bind the key protein underlying pri-miRNA processing, DGCR8. Additionally, when METTL3 expression was inhibited, the miR-126-5p maturation process was blocked."
item538	REG00007	M6ATAR00228	Up	M6ADIS0114	.	33098220	"Interleukin 1-beta (IL-1-beta) is an important inducer of cartilage degeneration that can induce an inflammatory cascade reaction in chondrocytes and inhibit the normal biological function of cells. METTL3 could regulate miR-126-5p maturation, we first confirmed that METTL3 can bind the key protein underlying pri-miRNA processing, Microprocessor complex subunit DGCR8 (DGCR8). Additionally, when METTL3 expression was inhibited, the miR-126-5p maturation process was blocked."
item539	.	.	.	M6ADIS0087	.	33112671	The rat models of diabetes mellitus suffered from cognitive disorders and hippocampal neuron damage. The findings suggest that m6A modification is altered in the diabetic hippocampus and provide new insight into diabetic hippocampal injury.
item540	.	M6ATAR00103	.	M6ADIS0007	.	33174014	"FEZF1 antisense RNA 1 (FEZF1-AS1) was upregulated and acted as an oncogene in non-small cell lung cancer by regulating the ITGA11/miR-516b-5p axis, suggesting that FEZF1-AS1 is a potential prognostic biomarker and therapeutic target for NSCLC."
item541	.	.	.	M6ADIS0017	.	33174480	m6A methylation plays an important role in the progression and reversal of hepatic fibrosis.
item542	REG00007	M6ATAR00410	Up	M6ADIS0007	M6ADRUG0074	33177491	"METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, ATG7, LC3B, and Sequestosome-1 (SQSTM1). beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance."
item543	REG00007	M6ATAR00331	Up	M6ADIS0007	M6ADRUG0074	33177491	"METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, ATG7, LC3B, and SQSTM1. beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and Microtubule-associated proteins 1A/1B light chain 3B (MAP1LC3B/LC3B-II). beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance."
item544	REG00007	M6ATAR00189	Up	M6ADIS0007	M6ADRUG0074	33177491	"METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as Autophagy protein 5 (ATG5), ATG7, LC3B, and SQSTM1. beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance."
item545	REG00007	M6ATAR00190	Up	M6ADIS0007	M6ADRUG0074	33177491	"METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, Ubiquitin-like modifier-activating enzyme ATG7 (ATG7), LC3B, and SQSTM1. beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance."
item546	REG00007	M6ATAR00410	Up	M6ADIS0007	M6ADRUG0030	33177491	"METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, ATG7, LC3B, and Sequestosome-1 (SQSTM1). beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance."
item547	REG00007	M6ATAR00331	Up	M6ADIS0007	M6ADRUG0030	33177491	"METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, ATG7, LC3B, and SQSTM1. beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and Microtubule-associated proteins 1A/1B light chain 3B (MAP1LC3B/LC3B-II). beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance."
item548	REG00007	M6ATAR00189	Up	M6ADIS0007	M6ADRUG0030	33177491	"METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as Autophagy protein 5 (ATG5), ATG7, LC3B, and SQSTM1. beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance."
item549	REG00007	M6ATAR00190	Up	M6ADIS0007	M6ADRUG0030	33177491	"METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, Ubiquitin-like modifier-activating enzyme ATG7 (ATG7), LC3B, and SQSTM1. beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance."
item550	REG00007	M6ATAR00410	Up	M6ADIS0007	M6ADRUG0003	33177491	"METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, ATG7, LC3B, and Sequestosome-1 (SQSTM1). beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance."
item551	REG00007	M6ATAR00331	Up	M6ADIS0007	M6ADRUG0003	33177491	"METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, ATG7, LC3B, and SQSTM1. beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and Microtubule-associated proteins 1A/1B light chain 3B (MAP1LC3B/LC3B-II). beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance."
item552	REG00007	M6ATAR00189	Up	M6ADIS0007	M6ADRUG0003	33177491	"METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as Autophagy protein 5 (ATG5), ATG7, LC3B, and SQSTM1. beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance."
item553	REG00007	M6ATAR00190	Up	M6ADIS0007	M6ADRUG0003	33177491	"METTL3 could positively regulate the autophagy by targeting the autophagy-related genes such as ATG5, Ubiquitin-like modifier-activating enzyme ATG7 (ATG7), LC3B, and SQSTM1. beta-elemene inhibited the autophagy flux by preventing autophagic lysosome acidification, resulting in increasing expression of SQSTM1 and LC3B-II. beta-elemene could reverse gefitinib resistance in non-small cell lung cancer cells by inhibiting cell autophagy process in a manner of chloroquine. METTL3-mediated autophagy in reversing gefitinib resistance of NSCLC cells by beta-elemene, which shed light on providing potential molecular-therapy target and clinical-treatment method in NSCLC patients with gefitinib resistance."
item554	REG00001	.	.	M6ADIS0059	.	33183350	MiR-96 antagomir could potentially retard the cancerogenesis in colorectal cancer via AMPK subunit alpha-2 (AMPKAlpha2/PRKAA2)-dependent inhibition of FTO and blocking FTO-mediated m6A modification of MYC.
item555	REG00001	M6ATAR00341	Up	M6ADIS0059	.	33183350	MiR-96 antagomir could potentially retard the cancerogenesis in colorectal cancer via AMPK-alpha-2-dependent inhibition of FTO and blocking FTO-mediated m6A modification of Myc proto-oncogene protein (MYC).
item556	REG00007	M6ATAR00156	Up	M6ADIS0123	.	33197240	"Either knockdown of METTL3 or METTL14 notably reversed the hypoxic preconditioning-induced enhancement of cell viability, anti-apoptosis ability, and H19 imprinted maternally expressed transcript (H19) expression."
item557	REG00006	M6ATAR00156	Up	M6ADIS0123	.	33197240	"Either knockdown of METTL3 or METTL14 notably reversed the hypoxic preconditioning-induced enhancement of cell viability, anti-apoptosis ability, and H19 imprinted maternally expressed transcript (H19) expression."
item558	REG00009	M6ATAR00233	Up	M6ADIS0004	M6ADRUG0047	33205540	"m6A methyltransferase Wilms' tumor 1-associated protein facilitates cell proliferation and cisplatin resistance in NK/T cell lymphoma by regulating dual-specificity phosphatases 6 expression via m6A RNA methylation. WTAP enhanced Dual specificity protein phosphatase 6 (DUSP6) expression by increasing m6A levels of DUSP6 mRNA transcript, leading to oncogenic functions in NKTCL."
item559	.	M6ATAR00071	.	M6ADIS0006	M6ADRUG0032	33222692	"N6-methyladenosine-modified hsa_circ_0087293 (SORE) sequestered miR-103a-2-5p and miR-660-3p by acting as a microRNA sponge, thereby competitively activating the Wnt/beta-catenin pathway and inducing sorafenib resistance in hepatocellular carcinoma."
item560	REG00013	M6ATAR00445	Up	M6ADIS0007	.	33228740	Up-regulation of Vang-like protein 1 (VANGL1) by IGF2BPs and miR-29b-3p attenuates the detrimental effect of irradiation on lung adenocarcinoma. Increased m6A level of VANGL1 and reduced miR-29b-3p took the responsibility of VANGL1 overexpression upon irradiation.
item561	REG00014	M6ATAR00445	Up	M6ADIS0007	.	33228740	Up-regulation of Vang-like protein 1 (VANGL1) by IGF2BPs and miR-29b-3p attenuates the detrimental effect of irradiation on lung adenocarcinoma. Increased m6A level of VANGL1 and reduced miR-29b-3p took the responsibility of VANGL1 overexpression upon irradiation.
item562	REG00007	M6ATAR00112	.	M6ADIS0008	.	33235466	"ZNFX1 antisense RNA 1 (ZFAS1) sequestered miR-647, and this RNA-RNA interaction is regulated by METLL3-mediated m6A modification in cervical cancer."
item563	REG00006	M6ATAR00062	Up	M6ADIS0007	.	33237585	"GPER promotes non-small-cell lung cancer cell growth by regulating YAP1-TEAD/QKI/circNOTCH1/m6A methylated NOTCH1 signalling. Further exploration of the mechanism demonstrated that GPER could up-regulate hsa_circ_0089552 (circNOTCH1), which could compete with NOTCH1 mRNA for METTL14 binding."
item564	REG00024	M6ATAR00222	Up	M6ADIS0007	.	33280517	"ECs transmitted miR-376c into NSCLC cells through Evs, and inhibited the intracellular YTHDF1 expression and the Wnt/Catenin beta-1 (CTNNB1/Beta-catenin) pathway activation. YTHDF1 overexpression reversed the inhibitory role of miR-376c released by EC-Evs in non-small cell lung cancer cells."
item565	REG00014	M6ATAR00027	Up	M6ADIS0010	.	33293428	DMDRMR is a protumorigenic lncRNA that mediates the stabilization of IGF2BP3 targets in an m6A-dependent manner in clear cell renal cell carcinoma. IGF2BP3 and DMDRMR cooperate to play oncogenic roles. IGF2BP3 cooperates with DMDRMR to regulate CDK4 by enhancing mRNA stability.
item566	REG00014	M6ATAR00211	Up	M6ADIS0010	.	33293428	DMDRMR is a protumorigenic lncRNA that mediates the stabilization of IGF2BP3 targets in an m6A-dependent manner in clear cell renal cell carcinoma. IGF2BP3 and DMDRMR cooperate to play oncogenic roles. IGF2BP3 cooperates with DMDRMR to regulate Cyclin-dependent kinase 4 (CDK4) by enhancing mRNA stability.
item567	REG00006	M6ATAR00380	.	M6ADIS0099	.	33301833	.
item568	REG00006	M6ATAR00112	.	M6ADIS0099	.	33301833	.
item569	REG00007	M6ATAR00274	Up	M6ADIS0006	.	33305825	"HBXIP drives metabolic reprogramming in hepatocellular carcinoma cells via METTL3-mediated m6A modification of Hypoxia-inducible factor 1-alpha (HIF-1-Alpha/HIF1A). Highly expressed HBXIP and METTL3 are associated with dismal oncologic outcomes of patients with hepatocellular carcinoma. The positive relation between HBXIP and METTL3 can activate reprogramming of HCC cell metabolism by inducing m6A modification of HIF-1-alpha, which is unraveled to enhance aggressive biological behaviors of HCC cells."
item570	.	M6ATAR00387	.	M6ADIS0038	M6ADRUG0047	33329722	"m6A plays an important role in cisplatin induced acute kidney injury and berberine alleviates this process. Cisplatin induced an increase in Solute carrier family 12 member 1 (SLC12A1) protein levels and a decrease in FGA and Havcr1 protein levels. However, berberine pretreatment reversed these effects."
item571	.	M6ATAR00468	.	M6ADIS0038	M6ADRUG0047	33329722	"m6A plays an important role in cisplatin induced acute kidney injury and berberine alleviates this process. Cisplatin induced an increase in Slc12a1 protein levels and a decrease in Fibrinogen alpha chain (FGA) and Havcr1 protein levels. However, berberine pretreatment reversed these effects."
item572	.	M6ATAR00469	.	M6ADIS0038	M6ADRUG0047	33329722	"m6A plays an important role in cisplatin induced acute kidney injury and berberine alleviates this process. Cisplatin induced an increase in Slc12a1 protein levels and a decrease in FGA and Hepatitis A virus cellular receptor 1 (HAVCR1) protein levels. However, berberine pretreatment reversed these effects."
item573	.	M6ATAR00387	.	M6ADIS0038	M6ADRUG0002	33329722	"m6A plays an important role in cisplatin induced acute kidney injury and berberine alleviates this process. Cisplatin induced an increase in Solute carrier family 12 member 1 (SLC12A1) protein levels and a decrease in FGA and Havcr1 protein levels. However, berberine pretreatment reversed these effects."
item574	.	M6ATAR00468	.	M6ADIS0038	M6ADRUG0002	33329722	"m6A plays an important role in cisplatin induced acute kidney injury and berberine alleviates this process. Cisplatin induced an increase in Slc12a1 protein levels and a decrease in Fibrinogen alpha chain (FGA) and Havcr1 protein levels. However, berberine pretreatment reversed these effects."
item575	.	M6ATAR00469	.	M6ADIS0038	M6ADRUG0002	33329722	"m6A plays an important role in cisplatin induced acute kidney injury and berberine alleviates this process. Cisplatin induced an increase in Slc12a1 protein levels and a decrease in FGA and Hepatitis A virus cellular receptor 1 (HAVCR1) protein levels. However, berberine pretreatment reversed these effects."
item576	REG00001	M6ATAR00268	Up	M6ADIS0102	.	33330653	"FTO expression significantly contributes to the phenotype conversion of VSMCs and the aortic dissecting aneurysm by the demethylation function (m6A), thereby providing a novel therapeutic target. Knockdown of FTO suppresses the Glycogen synthase kinase-3 beta (GSK3Beta/GSK3B) levels and Klf5 expression regardless of AngII treatment."
item577	REG00001	M6ATAR00311	Up	M6ADIS0102	.	33330653	"FTO expression significantly contributes to the phenotype conversion of VSMCs and the aortic dissecting aneurysm by the demethylation function (m6A), thereby providing a novel therapeutic target. Knockdown of FTO suppresses the p-GSK3-beta levels and Krueppel-like factor 5 (KLF5) expression regardless of AngII treatment."
item578	REG00006	M6ATAR00203	Up	M6ADIS0051	.	33335426	"METTL14 can promote osteosarcoma cell apoptosis, inhibit cell viability, and have a tumor suppressor effect on osteosarcoma. METTL14 finally achieves apoptosis by activating Caspase-3 (CASP3)."
item579	REG00022	M6ATAR00152	.	.	.	33335959	"RBM15 and WTAP are required for X inactive specific transcript (XIST)-mediated silencing, are co-localized, and potentially interact with XIST RNA. YTHDC1 is the m6A reader of XIST and is required for XIST function."
item580	REG00009	M6ATAR00152	.	.	.	33335959	"RBM15 and WTAP are required for X inactive specific transcript (XIST)-mediated silencing, are co-localized, and potentially interact with XIST RNA. YTHDC1 is the m6A reader of XIST and is required for XIST function."
item581	REG00020	M6ATAR00152	.	.	.	33335959	"RBM15 and WTAP are required for X inactive specific transcript (XIST)-mediated silencing, are co-localized, and potentially interact with XIST RNA. YTHDC1 is the m6A reader of XIST and is required for XIST function."
item582	REG00027	M6ATAR00141	.	.	.	33335959	HNRNPG can bind the m6A-modified hairpin of Metastasis associated lung adenocarcinoma transcript 1 (MALAT1).
item583	REG00005	M6ATAR00074	Down	M6ADIS0059	.	33335959	Overexpression of METTL3 upregulates Long intergenic non-protein coding RNA 2598 (LINC02598/RP11) expression in colorectal cancer cells. Overexpression of ALKBH5 downregulates RP11 expression.
item584	REG00007	M6ATAR00074	Up	M6ADIS0059	.	33335959	Overexpression of METTL3 upregulates Long intergenic non-protein coding RNA 2598 (LINC02598/RP11) expression in colorectal cancer cells. Overexpression of ALKBH5 downregulates RP11 expression.
item585	REG00006	M6ATAR00255	Down	M6ADIS0006	M6ADRUG0032	33361765	The Hepatocyte nuclear factor 3-gamma (HNF3gamma/FOXA3) reduction in hepatocellular carcinoma could be mediated by METTL14-dependent m6A methylation of HNF3-Gamma mRNA. HNF3-Gamma plays an essential role in HCC differentiation and serves as a therapeutic target and predictor of sorafenib benefit in patients.
item586	REG00024	.	Up	M6ADIS0006	.	33363211	YTHDF1 promotes the aggressive phenotypes by facilitating epithelial-mesenchymal transition (EMT) and activating AKT/glycogen synthase kinase (GSK)-3-beta/beta-catenin signaling in hepatocellular carcinoma.
item587	REG00001	.	.	M6ADIS0002	.	33364780	"FTO was implicated in multiple biological processes, such as cancer cell apoptosis, proliferation, migration, invasion, metastasis, cell-cycle, differentiation, stem cell self-renewal and so on."
item588	REG00022	M6ATAR00072	Up	M6ADIS0006	.	33372396	"hsa_circ_0092493 (circ_ARL3) is a critical regulator in HBV-related HCC, targeting the axis of circ-ARL3/miR-1305 can be a promising treatment for HBV+ HCC patients. HBx protein upregulated N6 -methyladenosine (m6A) methyltransferases METTL3 expression, increasing the m6A modification of circ-ARL3; then, m6A reader YTHDC1 bound to m6A-modified of circ-ARL3 and favored its reverse splicing and biogenesis. Furthermore, circ-ARL3 was able to sponge miR-1305, antagonizing the inhibitory effects of miR-1305 on a cohort of target oncogenes, thereby promoting HBV+ HCC progression."
item589	REG00007	M6ATAR00072	Up	M6ADIS0006	.	33372396	"hsa_circ_0092493 (circ_ARL3) is a critical regulator in HBV-related HCC, targeting the axis of circ-ARL3/miR-1305 can be a promising treatment for HBV+ HCC patients. HBx protein upregulated N6 -methyladenosine (m6A) methyltransferases METTL3 expression, increasing the m6A modification of circ-ARL3; then, m6A reader YTHDC1 bound to m6 A-modified of circ-ARL3 and favored its reverse splicing and biogenesis. Furthermore, circ-ARL3 was able to sponge miR-1305, antagonizing the inhibitory effects of miR-1305 on a cohort of target oncogenes, thereby promoting HBV+ HCC progression."
item590	REG00007	M6ATAR00110	Up	M6ADIS0006	.	33372396	"Circ-ARL3 is a critical regulator in HBV-related HCC, targeting the axis of circ-ARL3/microRNA 1305 (MIR1305) can be a promising treatment for HBV+ HCC patients. HBx protein upregulated N6 -methyladenosine (m6A) methyltransferases METTL3 expression, increasing the m6A modification of circ-ARL3; then, m6A reader YTHDC1 bound to m6 A-modified of circ-ARL3 and favored its reverse splicing and biogenesis. Furthermore, circ-ARL3 was able to sponge miR-1305, antagonizing the inhibitory effects of miR-1305 on a cohort of target oncogenes, thereby promoting HBV+ HCC progression."
item591	REG00001	M6ATAR00023	Down	M6ADIS0057	M6ADRUG0089	33393595	"Omeprazole pretreatment could enhance the inhibitory effect of 5-Fu, DDP and TAX on gastric cancer cells. FTO inhibition induced by omeprazole enhanced the activation of Mammalian target of rapamycin complex 1 (mTORC1) signal pathway that inhibited the prosurvival autophagy so as to improve the antitumor efficiency of chemotherapeutic drugs on GC cells. Meanwhile, transcript level of DDIT3, which is an apoptosis-related tumor suppressor gene downstream of mTORC1, was regulated by omeprazole-induced FTO silence through an m6A-dependent mechanism. m6A modification and its eraser FTO plays a role in the improvement of chemosensitivity mediated by proton pump inhibitor omeprazole."
item592	REG00001	M6ATAR00470	Down	M6ADIS0057	M6ADRUG0089	33393595	"Omeprazole pretreatment could enhance the inhibitory effect of 5-Fu, DDP and TAX on gastric cancer cells. FTO inhibition induced by omeprazole enhanced the activation of mTORC1 signal pathway that inhibited the prosurvival autophagy so as to improve the antitumor efficiency of chemotherapeutic drugs on GC cells. Meanwhile, transcript level of DNA damage-inducible transcript 3 protein (DDIT3), which is an apoptosis-related tumor suppressor gene downstream of mTORC1, was regulated by omeprazole-induced FTO silence through an m6A-dependent mechanism. m6A modification and its eraser FTO plays a role in the improvement of chemosensitivity mediated by proton pump inhibitor omeprazole."
item593	REG00001	M6ATAR00023	Down	M6ADIS0057	M6ADRUG0047	33393595	"Omeprazole pretreatment could enhance the inhibitory effect of 5-Fu, DDP and TAX on gastric cancer cells. FTO inhibition induced by omeprazole enhanced the activation of Mammalian target of rapamycin complex 1 (mTORC1) signal pathway that inhibited the prosurvival autophagy so as to improve the antitumor efficiency of chemotherapeutic drugs on GC cells. Meanwhile, transcript level of DDIT3, which is an apoptosis-related tumor suppressor gene downstream of mTORC1, was regulated by omeprazole-induced FTO silence through an m6A-dependent mechanism. m6A modification and its eraser FTO plays a role in the improvement of chemosensitivity mediated by proton pump inhibitor omeprazole."
item594	REG00001	M6ATAR00470	Down	M6ADIS0057	M6ADRUG0047	33393595	"Omeprazole pretreatment could enhance the inhibitory effect of 5-Fu, DDP and TAX on gastric cancer cells. FTO inhibition induced by omeprazole enhanced the activation of mTORC1 signal pathway that inhibited the prosurvival autophagy so as to improve the antitumor efficiency of chemotherapeutic drugs on GC cells. Meanwhile, transcript level of DNA damage-inducible transcript 3 protein (DDIT3), which is an apoptosis-related tumor suppressor gene downstream of mTORC1, was regulated by omeprazole-induced FTO silence through an m6A-dependent mechanism. m6A modification and its eraser FTO plays a role in the improvement of chemosensitivity mediated by proton pump inhibitor omeprazole."
item595	REG00001	M6ATAR00023	Down	M6ADIS0057	M6ADRUG0005	33393595	"Omeprazole pretreatment could enhance the inhibitory effect of 5-Fu, DDP and TAX on gastric cancer cells. FTO inhibition induced by omeprazole enhanced the activation of Mammalian target of rapamycin complex 1 (mTORC1) signal pathway that inhibited the prosurvival autophagy so as to improve the antitumor efficiency of chemotherapeutic drugs on GC cells. Meanwhile, transcript level of DDIT3, which is an apoptosis-related tumor suppressor gene downstream of mTORC1, was regulated by omeprazole-induced FTO silence through an m6A-dependent mechanism. m6A modification and its eraser FTO plays a role in the improvement of chemosensitivity mediated by proton pump inhibitor omeprazole."
item596	REG00001	M6ATAR00470	Down	M6ADIS0057	M6ADRUG0005	33393595	"Omeprazole pretreatment could enhance the inhibitory effect of 5-Fu, DDP and TAX on gastric cancer cells. FTO inhibition induced by omeprazole enhanced the activation of mTORC1 signal pathway that inhibited the prosurvival autophagy so as to improve the antitumor efficiency of chemotherapeutic drugs on GC cells. Meanwhile, transcript level of DNA damage-inducible transcript 3 protein (DDIT3), which is an apoptosis-related tumor suppressor gene downstream of mTORC1, was regulated by omeprazole-induced FTO silence through an m6A-dependent mechanism. m6A modification and its eraser FTO plays a role in the improvement of chemosensitivity mediated by proton pump inhibitor omeprazole."
item597	REG00007	M6ATAR00028	Up	M6ADIS0065	M6ADRUG0022	33420414	"METTL3 promotes adriamycin resistance in MCF-7 breast cancer cells by accelerating hsa-miR-221-3p maturation in a m6A-dependent manner. METTL3 knockdown was shown to reduce the expression of miR-221-3p by reducing pri-miR-221-3p m6A mRNA methylation, reducing the expression of MDR1 and BCRP, and inducing apoptosis. Identified the METTL3/miR-221-3p/HIPK2/Che-1 axis as a novel signaling event that will be responsible for resistance of BC cells to ADR."
item598	REG00007	M6ATAR00323	Up	M6ADIS0065	M6ADRUG0022	33420414	"METTL3 promotes adriamycin resistance in MCF-7 breast cancer cells by accelerating pri-microRNA-221-3p maturation in a m6A-dependent manner. METTL3 knockdown was shown to reduce the expression of miR-221-3p by reducing pri-miR-221-3p m6A mRNA methylation, reducing the expression of ATP-dependent translocase ABCB1 (ABCB1) and BCRP, and inducing apoptosis. Identified the METTL3/miR-221-3p/HIPK2/Che-1 axis as a novel signaling event that will be responsible for resistance of BC cells to ADR."
item599	REG00007	M6ATAR00472	Up	M6ADIS0065	M6ADRUG0022	33420414	"METTL3 promotes adriamycin resistance in MCF-7 breast cancer cells by accelerating pri-microRNA-221-3p maturation in a m6A-dependent manner. METTL3 knockdown was shown to reduce the expression of miR-221-3p by reducing pri-miR-221-3p m6A mRNA methylation, reducing the expression of MDR1 and Broad substrate specificity ATP-binding cassette transporter ABCG2 (BCRP/ABCG2), and inducing apoptosis. Identified the METTL3/miR-221-3p/HIPK2/Che-1 axis as a novel signaling event that will be responsible for resistance of BC cells to ADR."
item600	REG00007	M6ATAR00473	Up	M6ADIS0065	M6ADRUG0022	33420414	"METTL3 promotes adriamycin resistance in MCF-7 breast cancer cells by accelerating pri-microRNA-221-3p maturation in a m6A-dependent manner. METTL3 knockdown was shown to reduce the expression of miR-221-3p by reducing pri-miR-221-3p m6A mRNA methylation, reducing the expression of MDR1 and BCRP, and inducing apoptosis. Identified the METTL3/miR-221-3p/Homeodomain-interacting protein kinase 2 (HIPK2)/Che-1 axis as a novel signaling event that will be responsible for resistance of BC cells to ADR."
item601	REG00007	M6ATAR00474	Up	M6ADIS0065	M6ADRUG0022	33420414	"METTL3 promotes adriamycin resistance in MCF-7 breast cancer cells by accelerating pri-microRNA-221-3p maturation in a m6A-dependent manner. METTL3 knockdown was shown to reduce the expression of miR-221-3p by reducing pri-miR-221-3p m6A mRNA methylation, reducing the expression of MDR1 and BCRP, and inducing apoptosis. Identified the METTL3/miR-221-3p/HIPK2/Protein AATF (AATF/CHE1) axis as a novel signaling event that will be responsible for resistance of BC cells to ADR."
item602	REG00007	M6ATAR00229	Down	M6ADIS0006	.	33425489	"CircMEG3 inhibits the expression of m6A methyltransferase METTL3 dependent on HULC. Moreover, CircMEG3 inhibits the expression of H/ACA ribonucleoprotein complex subunit DKC1 (DKC1), a component of telomere synthetase H/ACA ribonucleoprotein (RNP; catalyst RNA pseudouracil modification) through METTL3 dependent on HULC. These observations provide important basic information for finding effective liver cancer therapeutic targets."
item603	REG00005	M6ATAR00258	Up	M6ADIS0072	.	33428593	AKLBH5-induced m6A demethylation of Forkhead box protein M1 (FOXM1) mRNA promotes uveal melanoma progression.
item604	REG00005	M6ATAR00030	Down	M6ADIS0051	.	33431791	"ALKBH5 is an anti-tumor factor or a pro-apoptotic factor, acting at least partially by suppressing YAP expression through dual mechanisms with direct m6A methylation of YAP and indirect downregulation of YAP level due to methylation of hsa-mir-181b-1. Further results revealed that m6A methylated pre-miR-181b-1 was subsequently recognized by m6A-binding protein YTHDF2 to mediate RNA degradation. However, methylated YAP transcripts were recognized by YTHDF1 to promote its translation. ALKBH5 overexpression was considered a new approach of replacement therapy for osteosarcoma treatment."
item605	REG00008	M6ATAR00030	Down	M6ADIS0051	.	33431791	"ALKBH5 is an anti-tumor factor or a pro-apoptotic factor, acting at least partially by suppressing YAP expression through dual mechanisms with direct m6A methylation of YAP and indirect downregulation of YAP level due to methylation of hsa-mir-181b-1. Further results revealed that m6A methylated pre-miR-181b-1 was subsequently recognized by m6A-binding protein YTHDF2 to mediate RNA degradation. However, methylated YAP transcripts were recognized by YTHDF1 to promote its translation. ALKBH5 overexpression was considered a new approach of replacement therapy for osteosarcoma treatment."
item606	REG00005	M6ATAR00451	Down	M6ADIS0051	.	33431791	"ALKBH5 is an anti-tumor factor or a pro-apoptotic factor, acting at least partially by suppressing Transcriptional coactivator YAP1 (YAP1) expression through dual mechanisms with direct m6A methylation of YAP and indirect downregulation of YAP level due to methylation of pre-miR-181b-1. Further results revealed that m6A methylated pre-miR-181b-1 was subsequently recognized by m6A-binding protein YTHDF2 to mediate RNA degradation. However, methylated YAP transcripts were recognized by YTHDF1 to promote its translation. ALKBH5 overexpression was considered a new approach of replacement therapy for osteosarcoma treatment."
item607	REG00008	M6ATAR00451	.	M6ADIS0051	.	33431791	"ALKBH5 is an anti-tumor factor or a pro-apoptotic factor, acting at least partially by suppressing Transcriptional coactivator YAP1 (YAP1) expression through dual mechanisms with direct m6A methylation of YAP and indirect downregulation of YAP level due to methylation of pre-miR-181b-1. Further results revealed that m6A methylated pre-miR-181b-1 was subsequently recognized by m6A-binding protein YTHDF2 to mediate RNA degradation. However, methylated YAP transcripts were recognized by YTHDF1 to promote its translation. ALKBH5 overexpression was considered a new approach of replacement therapy for osteosarcoma treatment."
item608	REG00024	M6ATAR00451	Up	M6ADIS0051	.	33431791	"ALKBH5 is an anti-tumor factor or a pro-apoptotic factor, acting at least partially by suppressing Transcriptional coactivator YAP1 (YAP1) expression through dual mechanisms with direct m6A methylation of YAP and indirect downregulation of YAP level due to methylation of pre-miR-181b-1. Further results revealed that m6A methylated pre-miR-181b-1 was subsequently recognized by m6A-binding protein YTHDF2 to mediate RNA degradation. However, methylated YAP transcripts were recognized by YTHDF1 to promote its translation. ALKBH5 overexpression was considered a new approach of replacement therapy for osteosarcoma treatment."
item609	REG00012	M6ATAR00346	Down	M6ADIS0007	.	33436560	"Complex I-AGGG (NDUFB2) interacts with IGF2BP1/2/3 in NSCLC cells. circNDUFB2 participates in the degradation of IGF2BPs and activation of anti-tumor immunity during NSCLC progression via the modulation of both protein ubiquitination and degradation, as well as cellular immune responses."
item610	REG00013	M6ATAR00346	Down	M6ADIS0007	.	33436560	"Complex I-AGGG (NDUFB2) interacts with IGF2BP1/2/3 in NSCLC cells. circNDUFB2 participates in the degradation of IGF2BPs and activation of anti-tumor immunity during NSCLC progression via the modulation of both protein ubiquitination and degradation, as well as cellular immune responses."
item611	REG00014	M6ATAR00346	Down	M6ADIS0007	.	33436560	"Complex I-AGGG (NDUFB2) interacts with IGF2BP1/2/3 in NSCLC cells. circNDUFB2 participates in the degradation of IGF2BPs and activation of anti-tumor immunity during NSCLC progression via the modulation of both protein ubiquitination and degradation, as well as cellular immune responses."
item612	REG00006	M6ATAR00178	Up	.	.	33459381	"Protein arginine N-methyltransferase 1 (PRMT1) interacts with, and methylates the intrinsically disordered C terminus of METTL14, which promotes its interaction with RNA substrates, enhances its RNA methylation activity, and is crucial for its interaction with RNA polymerase II (RNAPII)."
item613	.	M6ATAR00356	.	M6ADIS0121	.	33462115	"Post-transcriptional regulation by the exosome complex is required for cell survival and forebrain development via repression of Cellular tumor antigen p53 (TP53/p53) signaling. N6-methyladenosine (m6A) methylation-mediated degradation of RNA is essential for brain development,m6A methylation impacts not only RNA stability, but also other RNA metabolism processes. Exosc10 in suppressing the P53 pathway, in which the rapid turnover of the apoptosis effectors Aen and Bbc3 mRNAs is essential for cell survival and normal cortical histogenesis."
item614	REG00012	M6ATAR00031	Up	M6ADIS0065	.	33469161	Hypoxia-induced lncRNA KB-1980E6.3 is involved in the self-renewal and stemness maintenance of breast cancer stem cells by recruiting IGF2BP1 to regulate c-Myc mRNA stability.
item615	REG00012	M6ATAR00341	Up	M6ADIS0065	.	33469161	Hypoxia-induced lncRNA KB-1980E6.3 is involved in the self-renewal and stemness maintenance of breast cancer stem cells by recruiting IGF2BP1 to regulate Myc proto-oncogene protein (MYC) mRNA stability.
item616	REG00003	M6ATAR00032	Down	M6ADIS0061	.	33474615	"Rs7495 in 3'UTR of hnRNPC was associated with pancreatic ductal adenocarcinoma susceptibility in a Chinese population. The rs7495, in the hnRNPC 3'UTR, might disrupt a binding site for hsa-miR-183-3p, thus increasing the expression of hnRNPC and promoting the proliferation of PDAC cells."
item617	REG00007	.	.	M6ADIS0109	.	33519432	"The beneficial effect of resveratrol on lipid metabolism disorder under HFD is due to a decrease of m6A RNA methylation and an increase of PPARalpha mRNA, providing mechanistic insights into the function of resveratrol in alleviating the disturbance of lipid metabolism in mice. The resveratrol in HFD increased the transcript levels of methyltransferase like 3 (METTL3), alkB homolog 5 (ALKBH5), fat mass and obesity associated protein (FTO), and YTH domain family 2 (YTHDF2), whereas it decreased the level of YTH domain family 3 (YTHDF3) and m6A abundance in mice liver."
item618	REG00005	.	.	M6ADIS0109	.	33519432	"The beneficial effect of resveratrol on lipid metabolism disorder under HFD is due to a decrease of m6A RNA methylation and an increase of PPARalpha mRNA, providing mechanistic insights into the function of resveratrol in alleviating the disturbance of lipid metabolism in mice. The resveratrol in HFD increased the transcript levels of methyltransferase like 3 (METTL3), alkB homolog 5 (ALKBH5), fat mass and obesity associated protein (FTO), and YTH domain family 2 (YTHDF2), whereas it decreased the level of YTH domain family 3 (YTHDF3) and m6A abundance in mice liver."
item619	REG00001	.	.	M6ADIS0109	.	33519432	"The beneficial effect of resveratrol on lipid metabolism disorder under HFD is due to a decrease of m6A RNA methylation and an increase of PPARalpha mRNA, providing mechanistic insights into the function of resveratrol in alleviating the disturbance of lipid metabolism in mice. The resveratrol in HFD increased the transcript levels of methyltransferase like 3 (METTL3), alkB homolog 5 (ALKBH5), fat mass and obesity associated protein (FTO), and YTH domain family 2 (YTHDF2), whereas it decreased the level of YTH domain family 3 (YTHDF3) and m6A abundance in mice liver."
item620	REG00008	.	.	M6ADIS0109	.	33519432	"The beneficial effect of resveratrol on lipid metabolism disorder under HFD is due to a decrease of m6A RNA methylation and an increase of PPARalpha mRNA, providing mechanistic insights into the function of resveratrol in alleviating the disturbance of lipid metabolism in mice. The resveratrol in HFD increased the transcript levels of methyltransferase like 3 (METTL3), alkB homolog 5 (ALKBH5), fat mass and obesity associated protein (FTO), and YTH domain family 2 (YTHDF2), whereas it decreased the level of YTH domain family 3 (YTHDF3) and m6A abundance in mice liver."
item621	REG00025	.	.	M6ADIS0109	.	33519432	"The beneficial effect of resveratrol on lipid metabolism disorder under HFD is due to a decrease of m6A RNA methylation and an increase of PPARalpha mRNA, providing mechanistic insights into the function of resveratrol in alleviating the disturbance of lipid metabolism in mice. The resveratrol in HFD increased the transcript levels of methyltransferase like 3 (METTL3), alkB homolog 5 (ALKBH5), fat mass and obesity associated protein (FTO), and YTH domain family 2 (YTHDF2), whereas it decreased the level of YTH domain family 3 (YTHDF3) and m6A abundance in mice liver."
item622	REG00007	.	.	M6ADIS0006	.	33519919	METTL3 and YTHDF1 expression were found to be correlated with an increased risk and were included in an m6A-related gene signature for predicting prognosis of hepatocellular carcinoma.
item623	REG00024	.	.	M6ADIS0006	.	33519919	METTL3 and YTHDF1 expression were found to be correlated with an increased risk and were included in an m6A-related gene signature for predicting prognosis of hepatocellular carcinoma.
item624	REG00007	M6ATAR00476	Up	M6ADIS0059	.	33526059	LINC00460 is a novel oncogene of colorectal cancer through interacting with IGF2BP2 and DHX9 and bind to the m6A modified High mobility group protein HMG-I/HMG-Y (HMGA1) mRNA to enhance the HMGA1 mRNA stability. The N6-methyladenosine (m6A) modification of HMGA1 mRNA by METTL3 enhanced HMGA1 expression in CRC.
item625	REG00007	M6ATAR00100	Up	M6ADIS0059	.	33526059	Long intergenic non-protein coding RNA 460 (LINC00460) is a novel oncogene of colorectal cancer through interacting with IGF2BP2 and DHX9 and bind to the m6A modified HMGA1 mRNA to enhance the HMGA1 mRNA stability. The N6-methyladenosine (m6A) modification of HMGA1 mRNA by METTL3 enhanced HMGA1 expression in CRC.
item626	REG00013	M6ATAR00476	Up	M6ADIS0059	.	33526059	LINC00460 is a novel oncogene of colorectal cancer through interacting with IGF2BP2 and DHX9 and bind to the m6A modified High mobility group protein HMG-I/HMG-Y (HMGA1) mRNA to enhance the HMGA1 mRNA stability. The N6-methyladenosine (m6A) modification of HMGA1 mRNA by METTL3 enhanced HMGA1 expression in CRC.
item627	REG00007	M6ATAR00088	Up	M6ADIS0065	.	33531456	m6A methyltransferase-like 3 (METTL3) gave rise to the upregulation of Long intergenic non-protein coding RNA 958 (LINC00958) by promoting its RNA transcript stability in breast cancer.
item628	REG00001	M6ATAR00079	Up	M6ADIS0101	.	33548009	FTO overexpression inhibits H/R-indcued apoptosis in myocardial cells by regulating m6A modification of Myosin heavy chain associated RNA transcript (MHRT). FTO is a target gene for heart failure treatment.
item629	.	M6ATAR00327	.	M6ADIS0059	.	33557837	"WM_Score correlated highly with the regulation of transcription and post-transcriptional events contributing to the development of colorectal cancer. In response to anti-cancer drugs, WM_Score highly negatively correlated (drug sensitive) with drugs which targeted oncogenic related pathways, such as Mitogen-activated protein kinase 1 (MAPK/ERK2/MAPK1), EGFR, and mTOR signaling pathways, positively correlated (drug resistance) with drugs which targeted in apoptosis and cell cycle. Importantly, the WM_Score was associated with the therapeutic efficacy of PD-L1 blockade, suggesting that the development of potential drugs targeting these ""writers"" to aid the clinical benefits of immunotherapy."
item630	.	M6ATAR00360	.	M6ADIS0059	.	33557837	"WM_Score correlated highly with the regulation of transcription and post-transcriptional events contributing to the development of colorectal cancer. In response to anti-cancer drugs, WM_Score highly negatively correlated (drug sensitive) with drugs which targeted oncogenic related pathways, such as MAPK, EGFR, and mTOR signaling pathways, positively correlated (drug resistance) with drugs which targeted in apoptosis and cell cycle. Importantly, the WM_Score was associated with the therapeutic efficacy of Programmed cell death 1 ligand 1 (CD274/PD-L1) blockade, suggesting that the development of potential drugs targeting these ""writers"" to aid the clinical benefits of immunotherapy."
item631	.	M6ATAR00237	.	M6ADIS0059	.	33557837	"WM_Score correlated highly with the regulation of transcription and post-transcriptional events contributing to the development of colorectal cancer. In response to anti-cancer drugs, WM_Score highly negatively correlated (drug sensitive) with drugs which targeted oncogenic related pathways, such as MAPK, Epidermal growth factor receptor (EGFR), and mTOR signaling pathways, positively correlated (drug resistance) with drugs which targeted in apoptosis and cell cycle. Importantly, the WM_Score was associated with the therapeutic efficacy of PD-L1 blockade, suggesting that the development of potential drugs targeting these ""writers"" to aid the clinical benefits of immunotherapy."
item632	.	M6ATAR00339	.	M6ADIS0059	.	33557837	"WM_Score correlated highly with the regulation of transcription and post-transcriptional events contributing to the development of colorectal cancer. In response to anti-cancer drugs, WM_Score highly negatively correlated (drug sensitive) with drugs which targeted oncogenic related pathways, such as MAPK, EGFR, and Serine/threonine-protein kinase mTOR (MTOR) signaling pathways, positively correlated (drug resistance) with drugs which targeted in apoptosis and cell cycle. Importantly, the WM_Score was associated with the therapeutic efficacy of PD-L1 blockade, suggesting that the development of potential drugs targeting these ""writers"" to aid the clinical benefits of immunotherapy."
item633	REG00008	.	.	.	.	33593354	"YTHDF2 takes a great part in multiple biological processes, such as migration, invasion, metastasis, proliferation, apoptosis, cell cycle, cell viability, cell adhesion, differentiation and inflammation, in both human cancers and non-cancers."
item634	REG00007	M6ATAR00033	Up	M6ADIS0056	M6ADRUG0019	33596916	"Platinum can increase the overall m6A level of esophageal cancer. SNHG3/hsa-miR-186-5p, induced by platinum, was involved in regulating m6A level by targeting METTL3. miR-186-5p binds to the 3'UTR of METTL3 to inhibit its expression. Our manuscript has provided clues that regulating m6A level was a novel way to enhance the platinum efficacy."
item635	REG00007	M6ATAR00477	Up	M6ADIS0056	M6ADRUG0019	33596916	"Platinum can increase the overall m6A level of esophageal cancer. Small nucleolar RNA host gene 3 (SNHG3)/miR-186-5p, induced by platinum, was involved in regulating m6A level by targeting METTL3. miR-186-5p binds to the 3'UTR of METTL3 to inhibit its expression. Our manuscript has provided clues that regulating m6A level was a novel way to enhance the platinum efficacy."
item636	REG00024	M6ATAR00187	Up	M6ADIS0006	.	33619246	HIF-1-alpha-induced YTHDF1 expression was associated with hypoxia-induced autophagy and autophagy-related hepatocellular carcinoma progression via promoting translation of autophagy-related genes Autophagy-related protein 2 homolog A (ATG2A) and ATG14 in a m6A-dependent manner.
item637	REG00024	M6ATAR00194	Up	M6ADIS0006	.	33619246	HIF-1-alpha-induced YTHDF1 expression was associated with hypoxia-induced autophagy and autophagy-related hepatocellular carcinoma progression via promoting translation of autophagy-related genes ATG2A and Beclin 1-associated autophagy-related key regulator (ATG14) in a m6A-dependent manner.
item638	REG00020	M6ATAR00219	Up	M6ADIS0027	.	33637103	"RBM15-mediated m6A modification of TMBIM6 mRNA enhanced TMBIM6 stability through IGF2BP3-dependent. Laryngeal squamous cell cancer cells were transfected with shRBM15 lentivirus for 48h, and the qRT-PCR data indicated that the mRNA levels of Copine-5 (CPNE5), TMBIM6, and ATAD3A decreased after RBM15 knockdown."
item639	REG00014	M6ATAR00198	Up	M6ADIS0027	.	33637103	"RBM15-mediated m6A modification of Bax inhibitor 1 (TMBIM6) mRNA enhanced TMBIM6 stability through IGF2BP3-dependent. Laryngeal squamous cell cancer cells were transfected with shRBM15 lentivirus for 48h, and the qRT-PCR data indicated that the mRNA levels of CPNE5, TMBIM6, and ATAD3A decreased after RBM15 knockdown."
item640	REG00020	M6ATAR00198	Up	M6ADIS0027	.	33637103	"RBM15-mediated m6A modification of Bax inhibitor 1 (TMBIM6) mRNA enhanced TMBIM6 stability through IGF2BP3-dependent. Laryngeal squamous cell cancer cells were transfected with shRBM15 lentivirus for 48h, and the qRT-PCR data indicated that the mRNA levels of CPNE5, TMBIM6, and ATAD3A decreased after RBM15 knockdown."
item641	REG00020	M6ATAR00184	Up	M6ADIS0027	.	33637103	"RBM15-mediated m6A modification of TMBIM6 mRNA enhanced TMBIM6 stability through IGF2BP3-dependent. Laryngeal squamous cell cancer cells were transfected with shRBM15 lentivirus for 48h, and the qRT-PCR data indicated that the mRNA levels of CPNE5, TMBIM6, and ATPase family AAA domain-containing protein 3A (ATAD3A) decreased after RBM15 knockdown."
item642	REG00001	M6ATAR00065	Up	M6ADIS0053	.	33637694	hsa_circ_0005630 (circRAB11FIP1) promoted autophagy flux of ovarian cancer through DSC1 and miR-129. CircRAB11FIP1 can serve as the possible marker for EOC diagnosis and treatment. CircRAB11FIP1 regulated the mechanism of autophagy through m6A modification and direct binding to mRNA. CircRAB11FIP1 bound to the mRNA of FTO and promoted its expression. CircRAB11FIP1 directly bound to miR-129 and regulated its targets ATG7 and ATG14. CircRAB11FIP1 bound to desmocollin 1to facilitate its interaction with ATG101. CircRAB11FIP1 mediated mRNA expression levels of ATG5 and ATG7 depending on m6A.
item643	REG00001	M6ATAR00190	Up	M6ADIS0053	.	33637694	CircRAB11FIP1 promoted autophagy flux of ovarian cancer through DSC1 and miR-129. CircRAB11FIP1 can serve as the possible marker for EOC diagnosis and treatment. CircRAB11FIP1 regulated the mechanism of autophagy through m6A modification and direct binding to mRNA. CircRAB11FIP1 bound to the mRNA of FTO and promoted its expression. CircRAB11FIP1 directly bound to miR-129 and regulated its targets Ubiquitin-like modifier-activating enzyme ATG7 (ATG7) and ATG14. CircRAB11FIP1 bound to desmocollin 1to facilitate its interaction with ATG101. CircRAB11FIP1 mediated mRNA expression levels of ATG5 and ATG7 depending on m6A.
item644	REG00001	M6ATAR00189	Up	M6ADIS0053	.	33637694	CircRAB11FIP1 promoted autophagy flux of ovarian cancer through DSC1 and miR-129. CircRAB11FIP1 can serve as the possible marker for EOC diagnosis and treatment. CircRAB11FIP1 regulated the mechanism of autophagy through m6A modification and direct binding to mRNA. CircRAB11FIP1 bound to the mRNA of FTO and promoted its expression. CircRAB11FIP1 directly bound to miR-129 and regulated its targets ATG7 and ATG14. CircRAB11FIP1 bound to desmocollin 1to facilitate its interaction with ATG101. CircRAB11FIP1 mediated mRNA expression levels of Autophagy protein 5 (ATG5) and ATG7 depending on m6A.
item645	REG00001	M6ATAR00194	Up	M6ADIS0053	.	33637694	CircRAB11FIP1 promoted autophagy flux of ovarian cancer through DSC1 and miR-129. CircRAB11FIP1 can serve as the possible marker for EOC diagnosis and treatment. CircRAB11FIP1 regulated the mechanism of autophagy through m6A modification and direct binding to mRNA. CircRAB11FIP1 bound to the mRNA of FTO and promoted its expression. CircRAB11FIP1 directly bound to miR-129 and regulated its targets ATG7 and Beclin 1-associated autophagy-related key regulator (ATG14). CircRAB11FIP1 bound to desmocollin 1to facilitate its interaction with ATG101. CircRAB11FIP1 mediated mRNA expression levels of ATG5 and ATG7 depending on m6A.
item646	REG00001	M6ATAR00191	Up	M6ADIS0053	.	33637694	CircRAB11FIP1 promoted autophagy flux of ovarian cancer through DSC1 and miR-129. CircRAB11FIP1 can serve as the possible marker for EOC diagnosis and treatment. CircRAB11FIP1 regulated the mechanism of autophagy through m6A modification and direct binding to mRNA. CircRAB11FIP1 bound to the mRNA of FTO and promoted its expression. CircRAB11FIP1 directly bound to miR-129 and regulated its targets ATG7 and ATG14. CircRAB11FIP1 bound to desmocollin 1to facilitate its interaction with Autophagy-related protein 101 (ATG101). CircRAB11FIP1 mediated mRNA expression levels of ATG5 and ATG7 depending on m6A.
item647	REG00001	M6ATAR00034	.	M6ADIS0053	.	33637694	CircRAB11FIP1 promoted autophagy flux of ovarian cancer through DSC1 and hsa-miR-129-5p. CircRAB11FIP1 can serve as the possible marker for EOC diagnosis and treatment. CircRAB11FIP1 regulated the mechanism of autophagy through m6A modification and direct binding to mRNA. CircRAB11FIP1 bound to the mRNA of FTO and promoted its expression. CircRAB11FIP1 directly bound to miR-129 and regulated its targets ATG7 and ATG14. CircRAB11FIP1 bound to desmocollin 1to facilitate its interaction with ATG101. CircRAB11FIP1 mediated mRNA expression levels of ATG5 and ATG7 depending on m6A.
item648	REG00001	M6ATAR00231	.	M6ADIS0053	.	33637694	CircRAB11FIP1 promoted autophagy flux of ovarian cancer through Desmocollin-1 (DSC1) and miR-129. CircRAB11FIP1 can serve as the possible marker for EOC diagnosis and treatment. CircRAB11FIP1 regulated the mechanism of autophagy through m6A modification and direct binding to mRNA. CircRAB11FIP1 bound to the mRNA of FTO and promoted its expression. CircRAB11FIP1 directly bound to miR-129 and regulated its targets ATG7 and ATG14. CircRAB11FIP1 bound to desmocollin 1to facilitate its interaction with ATG101. CircRAB11FIP1 mediated mRNA expression levels of ATG5 and ATG7 depending on m6A.
item649	REG00001	M6ATAR00141	Up	M6ADIS0118	.	33639196	"m6A modification is co-regulated by METTL3 and FTO in cadmium-treated cells. Metastasis associated lung adenocarcinoma transcript 1 (MALAT1), LncRNA-PVT1 and m6A modification could be key nodes for cadmium-induced oxidative damage, and highlight their importance as promising preventive and therapeutic targets in cadmium toxicity."
item650	REG00001	M6ATAR00153	Up	M6ADIS0118	.	33639196	"m6A modification is co-regulated by METTL3 and FTO in cadmium-treated cells. LncRNA-MALAT1, Pvt1 oncogene (PVT1) and m6A modification could be key nodes for cadmium-induced oxidative damage, and highlight their importance as promising preventive and therapeutic targets in cadmium toxicity."
item651	REG00007	M6ATAR00141	Up	M6ADIS0118	.	33639196	"m6A modification is co-regulated by METTL3 and FTO in cadmium-treated cells. Metastasis associated lung adenocarcinoma transcript 1 (MALAT1), LncRNA-PVT1 and m6A modification could be key nodes for cadmium-induced oxidative damage, and highlight their importance as promising preventive and therapeutic targets in cadmium toxicity."
item652	REG00007	M6ATAR00153	Up	M6ADIS0118	.	33639196	"m6A modification is co-regulated by METTL3 and FTO in cadmium-treated cells. LncRNA-MALAT1, Pvt1 oncogene (PVT1) and m6A modification could be key nodes for cadmium-induced oxidative damage, and highlight their importance as promising preventive and therapeutic targets in cadmium toxicity."
item653	REG00007	M6ATAR00370	Down	M6ADIS0106	.	33648590	"Impaired METTL3 expression in dental pulp stem cells led to increasing cell senescence and apoptosis by interfering with the mitotic cell cycle in a m6A-dependent manner. The protein interaction network of differentially expressed genes identified Serine/threonine-protein kinase PLK1 (PLK1), a critical cycle modulator, as the target of METTL3-mediated m6A methylation in DPSCs."
item654	REG00007	M6ATAR00444	Down	.	.	33649236	"Linking mTORC1 signaling with m6A RNA methylation and demonstrates their roles in suppressing autophagy. Double-stranded RNA (dsRNA)-mediated depletion of either METTL3 or METTL14 increased the half-life of luciferase mRNA with either Serine/threonine-protein kinase ULK1 (ULK1/ATG1) or Atg8a 3' UTRs. WTAP stabilizes the interaction between the two METTL proteins, and RBM15/RBM15B have been proposed to recruit the MTC to its target transcripts."
item655	REG00006	M6ATAR00444	Down	.	.	33649236	"Linking mTORC1 signaling with m6A RNA methylation and demonstrates their roles in suppressing autophagy. Double-stranded RNA (dsRNA)-mediated depletion of either METTL3 or METTL14 increased the half-life of luciferase mRNA with either Serine/threonine-protein kinase ULK1 (ULK1/ATG1) or Atg8a 3' UTRs. WTAP stabilizes the interaction between the two METTL proteins, and RBM15/RBM15B have been proposed to recruit the MTC to its target transcripts."
item656	REG00007	M6ATAR00798	Down	.	.	33649236	"Linking mTORC1 signaling with m6A RNA methylation and demonstrates their roles in suppressing autophagy. Double-stranded RNA (dsRNA)-mediated depletion of either METTL3 or METTL14 increased the half-life of luciferase mRNA with either ATG1 or GABA type A receptor-associated protein (GABARAP/ATG8A) 3' UTRs. WTAP stabilizes the interaction between the two METTL proteins, and RBM15/RBM15B have been proposed to recruit the MTC to its target transcripts."
item657	REG00006	M6ATAR00798	Down	.	.	33649236	"Linking mTORC1 signaling with m6A RNA methylation and demonstrates their roles in suppressing autophagy. Double-stranded RNA (dsRNA)-mediated depletion of either METTL3 or METTL14 increased the half-life of luciferase mRNA with either ATG1 or GABA type A receptor-associated protein (GABARAP/ATG8A) type A receptor-associated protein (GABARAP/ATG8A) 3' UTRs. WTAP stabilizes the interaction between the two METTL proteins, and RBM15/RBM15B have been proposed to recruit the MTC to its target transcripts."
item658	.	.	.	M6ADIS0002	.	33649845	The present review summarizes the recent progress in research regarding the role of m6A in human cancer and discusses the influence of m6A on classic signaling pathways in malignant tumors.
item659	REG00001	M6ATAR00206	Up	.	.	33651996	FTO regulates myoblast proliferation by controlling G1/S-specific cyclin-D1 (CCND1) expression in an m6A-YTHDF2-dependent manner.
item660	REG00008	M6ATAR00206	Down	.	.	33651996	FTO regulates myoblast proliferation by controlling G1/S-specific cyclin-D1 (CCND1) expression in an m6A-YTHDF2-dependent manner.
item661	REG00009	M6ATAR00384	.	M6ADIS0112	.	33658830	"This study established the transcriptional map of m6A in MH7A cells and revealed the potential relationship between RNA methylation modification and rheumatoid arthritis related genes. The results suggested that m6A modification was associated with the occurrence and course of RA to some extent. The validations of WTAP, Receptor-interacting serine/threonine-protein kinase 2 (RIPK2), JAK3 and TNFRSF10A were in accordance with the m6A and RNA sequencing results."
item662	REG00009	M6ATAR00300	.	M6ADIS0112	.	33658830	"This study established the transcriptional map of m6A in MH7A cells and revealed the potential relationship between RNA methylation modification and rheumatoid arthritis related genes. The results suggested that m6A modification was associated with the occurrence and course of RA to some extent. The validations of WTAP, RIPK2, Tyrosine-protein kinase JAK3 (JAK3) and TNFRSF10A were in accordance with the m6A and RNA sequencing results."
item663	REG00009	M6ATAR00434	.	M6ADIS0112	.	33658830	"This study established the transcriptional map of m6A in MH7A cells and revealed the potential relationship between RNA methylation modification and rheumatoid arthritis related genes. The results suggested that m6A modification was associated with the occurrence and course of RA to some extent. The validations of WTAP, RIPK2, JAK3 and Tumor necrosis factor receptor superfamily member 10A (TNFRSF10A) were in accordance with the m6A and RNA sequencing results."
item664	REG00007	M6ATAR00124	Up	M6ADIS0105	.	33660100	"METTL3-mediated formation of EV microRNA 93 (MIR93), facilitated by m6A, is implicated in the aberrant cross-talk of epithelium-macrophages, indicating that this process is involved in the smoking-related emphysema. EV miR-93 was used as a novel risk biomarker for CS-induced emphysema. MiR-93 activated the JNK pathway by targeting dual-specificity phosphatase 2 (DUSP2), which elevated the levels of matrix metalloproteinase 9 (MMP9) and matrix metalloproteinase 12 (MMP12) and induced elastin degradation, leading to emphysema."
item665	REG00007	M6ATAR00232	Down	M6ADIS0105	.	33660100	"METTL3-mediated formation of EV miR-93, facilitated by m6A, is implicated in the aberrant cross-talk of epithelium-macrophages, indicating that this process is involved in the smoking-related emphysema. EV miR-93 was used as a novel risk biomarker for CS-induced emphysema. MiR-93 activated the JNK pathway by targeting Dual specificity protein phosphatase 2 (DUSP2), which elevated the levels of matrix metalloproteinase 9 (MMP9) and matrix metalloproteinase 12 (MMP12) and induced elastin degradation, leading to emphysema."
item666	REG00007	M6ATAR00335	Down	M6ADIS0105	.	33660100	"METTL3-mediated formation of EV miR-93, facilitated by m6A, is implicated in the aberrant cross-talk of epithelium-macrophages, indicating that this process is involved in the smoking-related emphysema. EV miR-93 was used as a novel risk biomarker for CS-induced emphysema. MiR-93 activated the JNK pathway by targeting dual-specificity phosphatase 2 (DUSP2), which elevated the levels of Matrix metalloproteinase-9 (MMP9) and matrix metalloproteinase 12 (MMP12) and induced elastin degradation, leading to emphysema."
item667	REG00007	M6ATAR00332	Down	M6ADIS0105	.	33660100	"METTL3-mediated formation of EV miR-93, facilitated by m6A, is implicated in the aberrant cross-talk of epithelium-macrophages, indicating that this process is involved in the smoking-related emphysema. EV miR-93 was used as a novel risk biomarker for CS-induced emphysema. MiR-93 activated the JNK pathway by targeting dual-specificity phosphatase 2 (DUSP2), which elevated the levels of matrix metalloproteinase 9 (MMP9) and Macrophage metalloelastase (MMP12) and induced elastin degradation, leading to emphysema."
item668	REG00007	M6ATAR00252	Down	M6ADIS0007	.	33676554	"METTL3 positively regulates F-box/WD repeat-containing protein 7 (FBXW7) expression and confirm the tumor-suppressive role of m6A-modified FBXW7, thus providing insight into its epigenetic regulatory mechanisms in lung adenocarcinoma initiation and development."
item669	.	M6ATAR00093	.	M6ADIS0061	.	33680969	LINC00857/miR-150-5p/E2F3 regulatory axis is taken as an alternative therapeutic target for treating pancreatic Cancer.
item670	.	M6ATAR00035	Up	M6ADIS0061	.	33680969	LINC00857/miR-150-5p/E2F3 regulatory axis is taken as an alternative therapeutic target for treating pancreatic Cancer.
item671	.	M6ATAR00235	Up	M6ADIS0061	.	33680969	LINC00857/miR-150-5p/E2F3 regulatory axis is taken as an alternative therapeutic target for treating pancreatic Cancer.
item672	REG00001	M6ATAR00136	Up	M6ADIS0001	.	33684100	"Loss of m6A RNA methylation and increased translation in human glioblastoma cells as well as a role for miRNAs in the modulation of m6A RNA demethylation in genes that are most efficiently translated during glioma stem cells differentiation. Ectopic expression of the RRACH-binding miR-145 induces loss of m6A, formation of FTO/AGO1/ILF3/microRNA 145 (MIR145) complexes on a clinically relevant tumor suppressor gene (CLIP3) and significant increase in its nascent translation."
item673	REG00001	M6ATAR00173	Up	M6ADIS0001	.	33684100	"Loss of m6A RNA methylation and increased translation in human glioblastoma cells as well as a role for miRNAs in the modulation of m6A RNA demethylation in genes that are most efficiently translated during glioma stem cells differentiation. Ectopic expression of the RRACH-binding miR-145 induces loss of m6A, formation of FTO/Protein argonaute-1 (AGO1)/ILF3/miR-145 complexes on a clinically relevant tumor suppressor gene (CLIP3) and significant increase in its nascent translation."
item674	REG00001	M6ATAR00295	Up	M6ADIS0001	.	33684100	"Loss of m6A RNA methylation and increased translation in human glioblastoma cells as well as a role for miRNAs in the modulation of m6A RNA demethylation in genes that are most efficiently translated during glioma stem cells differentiation. Ectopic expression of the RRACH-binding miR-145 induces loss of m6A, formation of FTO/AGO1/Interleukin enhancer-binding factor 3 (ILF3)/miR-145 complexes on a clinically relevant tumor suppressor gene (CLIP3) and significant increase in its nascent translation."
item675	REG00008	M6ATAR00405	Up	M6ADIS0067	.	33692441	YTHDF2-mediated LncRNA FENDRR degradation promotes cell proliferation by elevating Transcription factor SOX-4 (SOX4) expression in endometrioid endometrial carcinoma.
item676	REG00008	M6ATAR00096	Down	M6ADIS0067	.	33692441	YTHDF2-mediated LncRNA FOXF1 adjacent non-coding developmental regulatory RNA (FENDRR) degradation promotes cell proliferation by elevating SOX4 expression in endometrioid endometrial carcinoma.
item677	REG00024	.	.	M6ADIS0006	.	33708621	Hsa_circ_0007456 was validated to promote hepatocellular carcinoma cell proliferation by binding with hsa-miR-139-5p to promote YTHDF1 expression.
item678	REG00007	M6ATAR00260	Up	M6ADIS0006	M6ADRUG0032	33723389	"METTL3 can sensitise hepatocellular carcinoma cells to sorafenib through stabilising Forkhead box protein O3 (FOXO3) in an m6A-dependent manner and translated by YTHDF1, thereby inhibiting the transcription of autophagy-related genes, including ATG3, ATG5, ATG7, ATG12, and ATG16L1."
item679	REG00024	M6ATAR00260	Up	M6ADIS0006	M6ADRUG0032	33723389	"METTL3 can sensitise hepatocellular carcinoma cells to sorafenib through stabilising Forkhead box protein O3 (FOXO3) in an m6A-dependent manner and translated by YTHDF1, thereby inhibiting the transcription of autophagy-related genes, including ATG3, ATG5, ATG7, ATG12, and ATG16L1."
item680	REG00007	M6ATAR00188	Up	M6ADIS0006	M6ADRUG0032	33723389	"METTL3 can sensitise hepatocellular carcinoma cells to sorafenib through stabilising forkhead box class O3 (FOXO3) in an m6A-dependent manner and translated by YTHDF1, thereby inhibiting the transcription of autophagy-related genes, including Ubiquitin-like-conjugating enzyme ATG3 (ATG3), ATG5, ATG7, ATG12, and ATG16L1."
item681	REG00007	M6ATAR00189	Up	M6ADIS0006	M6ADRUG0032	33723389	"METTL3 can sensitise hepatocellular carcinoma cells to sorafenib through stabilising forkhead box class O3 (FOXO3) in an m6A-dependent manner and translated by YTHDF1, thereby inhibiting the transcription of autophagy-related genes, including ATG3, Autophagy protein 5 (ATG5), ATG12, and ATG16L1."
item682	REG00007	M6ATAR00190	Up	M6ADIS0006	M6ADRUG0032	33723389	"METTL3 can sensitise hepatocellular carcinoma cells to sorafenib through stabilising forkhead box class O3 (FOXO3) in an m6A-dependent manner and translated by YTHDF1, thereby inhibiting the transcription of autophagy-related genes, including ATG3, ATG5, Ubiquitin-like modifier-activating enzyme ATG7 (ATG7), ATG12, and ATG16L1."
item683	REG00007	M6ATAR00186	Up	M6ADIS0006	M6ADRUG0032	33723389	"METTL3 can sensitise hepatocellular carcinoma cells to sorafenib through stabilising forkhead box class O3 (FOXO3) in an m6A-dependent manner and translated by YTHDF1, thereby inhibiting the transcription of autophagy-related genes, including ATG3, ATG5, ATG7, Ubiquitin-like protein ATG12 (ATG12), and ATG16L1."
item684	REG00007	M6ATAR00161	Up	M6ADIS0006	M6ADRUG0032	33723389	"METTL3 can sensitise hepatocellular carcinoma cells to sorafenib through stabilising forkhead box class O3 (FOXO3) in an m6A-dependent manner and translated by YTHDF1, thereby inhibiting the transcription of autophagy-related genes, including ATG3, ATG5, ATG7, ATG12, and Autophagy-related protein 16-1 (ATG16L1)."
item685	REG00024	M6ATAR00188	Up	M6ADIS0006	M6ADRUG0032	33723389	"METTL3 can sensitise hepatocellular carcinoma cells to sorafenib through stabilising forkhead box class O3 (FOXO3) in an m6A-dependent manner and translated by YTHDF1, thereby inhibiting the transcription of autophagy-related genes, including Ubiquitin-like-conjugating enzyme ATG3 (ATG3), ATG5, ATG7, ATG12, and ATG16L1."
item686	REG00024	M6ATAR00189	Up	M6ADIS0006	M6ADRUG0032	33723389	"METTL3 can sensitise hepatocellular carcinoma cells to sorafenib through stabilising forkhead box class O3 (FOXO3) in an m6A-dependent manner and translated by YTHDF1, thereby inhibiting the transcription of autophagy-related genes, including ATG3, Autophagy protein 5 (ATG5), ATG7, ATG12, and ATG16L1."
item687	REG00024	M6ATAR00190	Up	M6ADIS0006	M6ADRUG0032	33723389	"METTL3 can sensitise hepatocellular carcinoma cells to sorafenib through stabilising forkhead box class O3 (FOXO3) in an m6A-dependent manner and translated by YTHDF1, thereby inhibiting the transcription of autophagy-related genes, including ATG3, ATG5, Ubiquitin-like modifier-activating enzyme ATG7 (ATG7), ATG12, and ATG16L1."
item688	REG00024	M6ATAR00186	Up	M6ADIS0006	M6ADRUG0032	33723389	"METTL3 can sensitise hepatocellular carcinoma cells to sorafenib through stabilising forkhead box class O3 (FOXO3) in an m6A-dependent manner and translated by YTHDF1, thereby inhibiting the transcription of autophagy-related genes, including ATG3, ATG5, ATG7, Ubiquitin-like protein ATG12 (ATG12), and ATG16L1."
item689	REG00024	M6ATAR00161	Up	M6ADIS0006	M6ADRUG0032	33723389	"METTL3 can sensitise hepatocellular carcinoma cells to sorafenib through stabilising forkhead box class O3 (FOXO3) in an m6A-dependent manner and translated by YTHDF1, thereby inhibiting the transcription of autophagy-related genes, including ATG3, ATG5, ATG7, ATG12, and Autophagy-related protein 16-1 (ATG16L1)."
item690	REG00007	M6ATAR00355	Up	M6ADIS0063	.	33730643	METTL3 regulates PM 2.5-induced cell injury by targeting Oxidative stress-induced growth inhibitor 1 (OSGIN1) in human airway epithelial cells.
item691	REG00007	.	.	M6ADIS0092	.	33740664	Muscle specific miRNAs are essential for skeletal muscle differentiation. METTL3 regulated the expressions of muscle specific miRNAs by multiple mechanisms.
item692	REG00007	M6ATAR00375	Down	M6ADIS0032	.	33741419	"METTL3/YTHDF2/Mutated in multiple advanced cancers 1 (PTEN) axis exerts a significant role in hypoxia induced PASMCs proliferation, providing a novel therapeutic target for hypoxic pulmonary hypertension."
item693	REG00008	M6ATAR00375	Down	M6ADIS0032	.	33741419	"METTL3/YTHDF2/Mutated in multiple advanced cancers 1 (PTEN) axis exerts a significant role in hypoxia induced PASMCs proliferation, providing a novel therapeutic target for hypoxic pulmonary hypertension."
item694	REG00007	M6ATAR00070	Up	M6ADIS0005	.	33741902	"METTL3-mediated m6A modification plays a key role in stabilizing the expression of hsa_circ_0081609 (circCUX1), thereby inhibiting the expression of caspase 1 and conferring the radiotherapy resistance of hypopharyngeal squamous cell carcinoma."
item695	REG00004	M6ATAR00131	.	M6ADIS0074	.	33746977	"Systematically analyzed 21 m6A regulators in adrenocortical carcinoma samples from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) database. Taking the intersection of these mRNAs and 21 m6A-related genes as potential functional molecules, these data indicated that 12 lncRNAs can dysregulate the behavior of microRNA 211 (MIR211) so that it promotes the expression of key m6A gene HNRNPA2B1."
item696	REG00007	M6ATAR00152	Up	M6ADIS0113	.	33748113	METTL3 regulates ossification of the posterior longitudinal ligament via the lncRNA X inactive specific transcript (XIST)/miR-302a-3p/USP8 axis.
item697	REG00007	M6ATAR00375	Down	M6ADIS0004	.	33749070	"The molecular mechanism underlying the effect of LINC00470 on chronic myelocytic leukaemia by reducing the Mutated in multiple advanced cancers 1 (PTEN) stability via RNA methyltransferase METTL3, thus leading to the inhibition of cell autophagy while promoting chemoresistance in CML."
item698	REG00007	M6ATAR00157	Up	M6ADIS0004	.	33749070	"The molecular mechanism underlying the effect of Long intergenic non-protein coding RNA 470 (LINC00470) on chronic myelocytic leukaemia by reducing the PTEN stability via RNA methyltransferase METTL3, thus leading to the inhibition of cell autophagy while promoting chemoresistance in CML."
item699	REG00007	M6ATAR00036	Up	M6ADIS0059	.	33754062	METTL3-induced Circ_1662 promoted colorectal cancer cell invasion and migration by accelerating YAP1 nuclear transport. Circ1662 enhanced CRC invasion and migration depending on YAP1 and SMAD3. This result implies that circ1662 is a new prognostic and therapeutic marker for CRC metastasis.
item700	REG00007	M6ATAR00451	Up	M6ADIS0059	.	33754062	METTL3-induced circ1662 promoted colorectal cancer cell invasion and migration by accelerating Transcriptional coactivator YAP1 (YAP1) nuclear transport. Circ1662 enhanced CRC invasion and migration depending on YAP1 and SMAD3. This result implies that circ1662 is a new prognostic and therapeutic marker for CRC metastasis.
item701	REG00007	M6ATAR00396	Down	M6ADIS0059	.	33754062	METTL3-induced circ1662 promoted colorectal cancer cell invasion and migration by accelerating YAP1 nuclear transport. Circ1662 enhanced CRC invasion and migration depending on YAP1 and Mothers against decapentaplegic homolog 3 (SMAD3). This result implies that circ1662 is a new prognostic and therapeutic marker for CRC metastasis.
item702	REG00014	M6ATAR00452	Up	M6ADIS0004	.	33763698	"Y-box-binding protein 1 (YBX1) selectively functions in regulating survival of myeloid leukemia cells. YBX1 interacts with insulin-like growth factor 2 messenger RNA (mRNA)-binding proteins (IGF2BPs) and stabilizes m6A-tagged RNA. YBX1 deficiency dysregulates the expression of apoptosis-related genes and promotes mRNA decay of MYC and BCL2 in an m6A-dependent manner, which contributes to the defective survival that results from deletion of YBX1."
item703	REG00013	M6ATAR00452	Up	M6ADIS0004	.	33763698	"Y-box-binding protein 1 (YBX1) selectively functions in regulating survival of myeloid leukemia cells. YBX1 interacts with insulin-like growth factor 2 messenger RNA (mRNA)-binding proteins (IGF2BPs) and stabilizes m6A-tagged RNA. YBX1 deficiency dysregulates the expression of apoptosis-related genes and promotes mRNA decay of MYC and BCL2 in an m6A-dependent manner, which contributes to the defective survival that results from deletion of YBX1."
item704	REG00012	M6ATAR00452	Up	M6ADIS0004	.	33763698	"Y-box-binding protein 1 (YBX1) selectively functions in regulating survival of myeloid leukemia cells. YBX1 interacts with insulin-like growth factor 2 messenger RNA (mRNA)-binding proteins (IGF2BPs) and stabilizes m6A-tagged RNA. YBX1 deficiency dysregulates the expression of apoptosis-related genes and promotes mRNA decay of MYC and BCL2 in an m6A-dependent manner, which contributes to the defective survival that results from deletion of YBX1."
item705	REG00014	M6ATAR00341	Up	M6ADIS0004	.	33763698	"YBX1 selectively functions in regulating survival of myeloid leukemia cells. YBX1 interacts with insulin-like growth factor 2 messenger RNA (mRNA)-binding proteins (IGF2BPs) and stabilizes m6A-tagged RNA. YBX1 deficiency dysregulates the expression of apoptosis-related genes and promotes mRNA decay of Myc proto-oncogene protein (MYC) and BCL2 in an m6A-dependent manner, which contributes to the defective survival that results from deletion of YBX1."
item706	REG00013	M6ATAR00341	Up	M6ADIS0004	.	33763698	"YBX1 selectively functions in regulating survival of myeloid leukemia cells. YBX1 interacts with insulin-like growth factor 2 messenger RNA (mRNA)-binding proteins (IGF2BPs) and stabilizes m6A-tagged RNA. YBX1 deficiency dysregulates the expression of apoptosis-related genes and promotes mRNA decay of Myc proto-oncogene protein (MYC) and BCL2 in an m6A-dependent manner, which contributes to the defective survival that results from deletion of YBX1."
item707	REG00012	M6ATAR00341	Up	M6ADIS0004	.	33763698	"YBX1 selectively functions in regulating survival of myeloid leukemia cells. YBX1 interacts with insulin-like growth factor 2 messenger RNA (mRNA)-binding proteins (IGF2BPs) and stabilizes m6A-tagged RNA. YBX1 deficiency dysregulates the expression of apoptosis-related genes and promotes mRNA decay of Myc proto-oncogene protein (MYC) and BCL2 in an m6A-dependent manner, which contributes to the defective survival that results from deletion of YBX1."
item708	REG00014	M6ATAR00196	Up	M6ADIS0004	.	33763698	"YBX1 selectively functions in regulating survival of myeloid leukemia cells. YBX1 interacts with insulin-like growth factor 2 messenger RNA (mRNA)-binding proteins (IGF2BPs) and stabilizes m6A-tagged RNA. YBX1 deficiency dysregulates the expression of apoptosis-related genes and promotes mRNA decay of MYC and Apoptosis regulator Bcl-2 (BCL2) in an m6A-dependent manner, which contributes to the defective survival that results from deletion of YBX1."
item709	REG00013	M6ATAR00196	Up	M6ADIS0004	.	33763698	"YBX1 selectively functions in regulating survival of myeloid leukemia cells. YBX1 interacts with insulin-like growth factor 2 messenger RNA (mRNA)-binding proteins (IGF2BPs) and stabilizes m6A-tagged RNA. YBX1 deficiency dysregulates the expression of apoptosis-related genes and promotes mRNA decay of MYC and Apoptosis regulator Bcl-2 (BCL2) in an m6A-dependent manner, which contributes to the defective survival that results from deletion of YBX1."
item710	REG00012	M6ATAR00196	Up	M6ADIS0004	.	33763698	"YBX1 selectively functions in regulating survival of myeloid leukemia cells. YBX1 interacts with insulin-like growth factor 2 messenger RNA (mRNA)-binding proteins (IGF2BPs) and stabilizes m6A-tagged RNA. YBX1 deficiency dysregulates the expression of apoptosis-related genes and promotes mRNA decay of MYC and Apoptosis regulator Bcl-2 (BCL2) in an m6A-dependent manner, which contributes to the defective survival that results from deletion of YBX1."
item711	REG00024	M6ATAR00439	Up	M6ADIS0057	.	33791305	YTHDF1 promoted Ubiquitin carboxyl-terminal hydrolase 14 (USP14) protein translation in an m6A-dependent manner. USP14 upregulation was positively correlated with YTHDF1 expression and indicated a poor prognosis in gastric cancer.
item712	REG00004	M6ATAR00295	Up	M6ADIS0048	.	33794982	"m6A-dependent effect of HNRNPA2B1 on regulating AKT signaling pathway and the correlation between HNRNPA2B1 and multiple myeloma cell growth. HNRNPA2B1 recognized the m6A sites of Interleukin enhancer-binding factor 3 (ILF3) and enhanced the stability of ILF3 mRNA transcripts, while AKT3 downregulation by siRNA abrogated the cellular proliferation induced by HNRNPA2B1 overexpression."
item713	REG00004	M6ATAR00176	Up	M6ADIS0048	.	33794982	"m6A-dependent effect of HNRNPA2B1 on regulating AKT signaling pathway and the correlation between HNRNPA2B1 and multiple myeloma cell growth. HNRNPA2B1 recognized the m6A sites of ILF3 and enhanced the stability of ILF3 mRNA transcripts, while RAC-gamma serine/threonine-protein kinase (AKT3) downregulation by siRNA abrogated the cellular proliferation induced by HNRNPA2B1 overexpression."
item714	REG00024	M6ATAR00382	Up	M6ADIS0008	.	33816306	The oncogenic role of YTHDF1 in cervical cancer by regulating E3 SUMO-protein ligase RanBP2 (RANBP2) expression and YTHDF1 represents a potential target for cervical cancer therapy.
item715	REG00025	M6ATAR00297	.	M6ADIS0006	.	33829656	"KDM5B regulates the YTHDF3/ITGA6 axis by inhibiting the expression of miR-448 to promote the occurrence of hepatocellular carcinoma. miR-448 could target YTHDF3 and inhibit the YTHDF3/Integrin alpha-6 (ITGA6) axis, thereby inhibiting the occurrence of HCC."
item716	.	.	.	M6ADIS0071	.	33830842	Integrated analysis of mRNA-m 6 A-protein profiles reveals novel insights into the mechanisms for cadmium-induced urothelial transformation. multi-omics analysis provided a comprehensive reference map of gene activity and revealed m6A signalling pathways crucial for Cd2+ carcinogenesis.
item717	REG00001	M6ATAR00347	.	M6ADIS0002	.	33846348	FTO deletion inhibited arsenic-induced tumorigenesis. Epidermis-specific FTO deletion prevented skin tumorigenesis induced by arsenic and UVB irradiation. E3 ubiquitin-protein ligase NEDD4-like (NEDD4L) was identified as the m6A-modified gene target of FTO. Arsenic stabilizes FTO protein through inhibiting p62-mediated selective autophagy. FTO-mediated dysregulation of mRNA m6A methylation as an epitranscriptomic mechanism to promote arsenic tumorigenicity. Arsenic suppresses p62 expression by downregulating the NF-kappaB pathway to upregulate FTO.
item718	REG00001	M6ATAR00347	.	M6ADIS0124	.	33846348	FTO deletion inhibited arsenic-induced tumorigenesis. Epidermis-specific FTO deletion prevented skin tumorigenesis induced by arsenic and UVB irradiation. E3 ubiquitin-protein ligase NEDD4-like (NEDD4L) was identified as the m6A-modified gene target of FTO. Arsenic stabilizes FTO protein through inhibiting p62-mediated selective autophagy. FTO-mediated dysregulation of mRNA m6A methylation as an epitranscriptomic mechanism to promote arsenic tumorigenicity. Arsenic suppresses p62 expression by downregulating the NF-kappaB pathway to upregulate FTO.
item719	REG00001	M6ATAR00410	Down	M6ADIS0002	.	33846348	FTO deletion inhibited arsenic-induced tumorigenesis. Epidermis-specific FTO deletion prevented skin tumorigenesis induced by arsenic and UVB irradiation. NEDD4L was identified as the m6A-modified gene target of FTO. Arsenic stabilizes FTO protein through inhibiting Sequestosome-1 (SQSTM1)-mediated selective autophagy. FTO-mediated dysregulation of mRNA m6A methylation as an epitranscriptomic mechanism to promote arsenic tumorigenicity. Arsenic suppresses p62 expression by downregulating the NF-kappaB pathway to upregulate FTO.
item720	REG00001	M6ATAR00410	Down	M6ADIS0124	.	33846348	FTO deletion inhibited arsenic-induced tumorigenesis. Epidermis-specific FTO deletion prevented skin tumorigenesis induced by arsenic and UVB irradiation. NEDD4L was identified as the m6A-modified gene target of FTO. Arsenic stabilizes FTO protein through inhibiting Sequestosome-1 (SQSTM1)-mediated selective autophagy. FTO-mediated dysregulation of mRNA m6A methylation as an epitranscriptomic mechanism to promote arsenic tumorigenicity. Arsenic suppresses p62 expression by downregulating the NF-kappaB pathway to upregulate FTO.
item721	REG00007	M6ATAR00389	Up	M6ADIS0059	M6ADRUG0048	33858476	Translocation protein SEC62 (SEC62) upregulated by the METTL3-mediated m6A modification promotes the stemness and chemoresistance of colorectal cancer by binding to beta-catenin and enhancing Wnt signalling. Depletion of Sec62 sensitized the CRC cells to 5-Fu or oxaliplatin treatment.
item722	REG00007	M6ATAR00389	Up	M6ADIS0059	M6ADRUG0005	33858476	Translocation protein SEC62 (SEC62) upregulated by the METTL3-mediated m6A modification promotes the stemness and chemoresistance of colorectal cancer by binding to beta-catenin and enhancing Wnt signalling. Depletion of Sec62 sensitized the CRC cells to 5-Fu or oxaliplatin treatment.
item723	REG00007	M6ATAR00037	Up	M6ADIS0065	.	33867838	CircMETTL3 promotes breast cancer progression through circMETTL3/hsa-miR-31-5p/CDK1 axis.
item724	REG00007	M6ATAR00209	Up	M6ADIS0065	.	33867838	CircMETTL3 promotes breast cancer progression through circMETTL3/miR-31-5p/Cyclin-dependent kinase 1 (CDK1) axis.
item725	REG00001	.	.	M6ADIS0046	M6ADRUG0029	33897884	"FTO-dependent m6A RNA methylation mediated the anti-leukemic actions of saikosaponin-d, thereby opening a window to develop SsD as an epitranscriptome-base drug for leukemia therapy. SsD showed a broadly-suppressed acute myeloid leukemia cell proliferation and promoted apoptosis and cell-cycle arrest both in vitro and in vivo."
item726	REG00007	M6ATAR00363	Up	M6ADIS0007	.	33898106	"METTL3 regulates the m6A modification to promote the maturation of miR-1246, which targets Paternally-expressed gene 3 protein (PEG3) to participate in occurrence and development of non-small cell lung cancer."
item727	REG00007	M6ATAR00109	Up	M6ADIS0007	.	33898106	"METTL3 regulates the m6A modification to promote the maturation of microRNA 1246 (MIR1246), which targets PEG3 to participate in occurrence and development of non-small cell lung cancer."
item728	REG00006	M6ATAR00440	Up	M6ADIS0006	.	33903120	"Methyltransferase-like 14 (Mettl14)-induced m6A modification participated in the regulation of Ubiquitin carboxyl-terminal hydrolase 48 (USP48) in hepatocellular carcinoma by maintaining USP48 mRNA stability. This work uncovers the tumor-suppressive function of the Mettl14-USP48-SIRT6 axis via modulation of glycolysis, providing new insights into the critical roles of metabolic activities in HCC and identifying an attractive target for future treatment studies."
item729	REG00006	M6ATAR00394	Up	M6ADIS0006	.	33903120	"Methyltransferase-like 14 (Mettl14)-induced m6A modification participated in the regulation of USP48 in hepatocellular carcinoma by maintaining USP48 mRNA stability. This work uncovers the tumor-suppressive function of the Mettl14-USP48-NAD-dependent protein deacetylase sirtuin-6 (SIRT6) axis via modulation of glycolysis, providing new insights into the critical roles of metabolic activities in HCC and identifying an attractive target for future treatment studies."
item730	REG00001	.	.	.	.	33905655	"As a straightforward and scarless m6A removal strategy, the demethylase-activated DNAzyme system offers a versatile toolbox for programmable gene regulation in synthetic biology. Based on a systematic investigation, the active DNAzyme configuration was potently disrupted by the site-specific incorporation of m6A modification and subsequently restored into the intact DNAzyme structure via the tunable FTO-specific removal of m6A-caging groups under a variety of conditions."
item731	REG00015	M6ATAR00270	Up	M6ADIS0065	.	33926554	KIAA1429 had the highest mutation frequency. Higher E3 ubiquitin-protein ligase Hakai (CBLL1) expression was associated with a better prognosis in breast cancer than lower CBLL1 expression.
item732	REG00006	M6ATAR00038	.	M6ADIS0128	.	33928080	"Circ_GFR-Alpha-1 promotes female germline stem cells self-renewal by acting as a ceRNA that sponges miR-449, leading to enhanced GFRalpha-1 expression and activation of the GDNF signaling pathway. circGFRalpha-1 acts as a ceRNA based on METTL14-mediated cytoplasmic export through the GGACU motif."
item733	REG00007	M6ATAR00141	Up	M6ADIS0001	.	33933553	METTL3 promoted the malignant progression of IDH-wildtype gliomas and revealed important insight into the upstream regulatory mechanism of Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) and NF-Kappa-B with a primary focus on m6A modification.
item734	REG00005	M6ATAR00345	Up	M6ADIS0007	.	33934179	"ALKBH5 knockdown, was able to inhibit malignant behavior of lung adenocarcinoma by regulating RMRP expression via demethylation. RMRP and ALKBH5 therefore represent promising therapeutic targets for lung adenocarcinoma."
item735	REG00014	M6ATAR00323	Up	M6ADIS0059	M6ADRUG0022	33948366	"IGF2BP3, directly bound to the m6A-modified region of ATP-dependent translocase ABCB1 (ABCB1) mRNA, thereby promoting the stability and expression of ABCB1 mRNA. The expression of IGF2BP3 and ABCB1 was strongly correlated with DOX sensitivity. Targeting IGF2BP3 was an important chemotherapeutic strategy for preventing MDR development in colorectal cancer."
item736	REG00007	M6ATAR00189	Up	M6ADIS0009	M6ADRUG0047	33968659	m6A methyltransferase METTL3 regulates autophagy and sensitivity to cisplatin by targeting Autophagy protein 5 (ATG5) in seminoma. The use of autophagy inhibitors 3-MA could reverse the protective effect of METTL3 on TCam-2 cells.
item737	REG00007	M6ATAR00189	Up	M6ADIS0009	M6ADRUG0059	33968659	m6A methyltransferase METTL3 regulates autophagy and sensitivity to cisplatin by targeting Autophagy protein 5 (ATG5) in seminoma. The use of autophagy inhibitors 3-MA could reverse the protective effect of METTL3 on TCam-2 cells.
item738	REG00005	M6ATAR00344	Up	M6ADIS0001	M6ADRUG0010	33975615	"In glioma, hsa_circ_0072083 could regulate Homeobox protein NANOG (NANOG) and ALKBH5 via targeting miR-1252-5p to control temozolomide resistance. circ_0072083 silence reduced NANOG expression via blocking ALKBH5-mediated demethylation."
item739	.	.	.	M6ADIS0046	.	34001273	The review discuss how m6A regulators are closely correlated with the clinical features of acute myeloid leukemia patients and serve as new biomarkers and therapeutic targets for acute myeloid leukemia.
item740	REG00005	M6ATAR00277	Down	M6ADIS0109	.	34044094	ALKBH5-dependent High mobility group protein B1 (HMGB1) expression mediates STING-interferon regulatory factor 3 innate immune response in radiation-induced liver diseases.
item741	REG00005	M6ATAR00419	Down	M6ADIS0109	.	34044094	ALKBH5-dependent HMGB1 expression mediates Stimulator of interferon genes protein (STING1)-interferon regulatory factor 3 innate immune response in radiation-induced liver diseases.
item742	REG00007	.	.	M6ADIS0006	.	34046411	"Make a clear summary of the known roles of METTL3 in hepatocellular carcinoma, and explicitly narrate the potential mechanisms for these roles."
item743	REG00005	M6ATAR00799	Up	M6ADIS0104	.	34048572	"ROS promotes ALKBH5 SUMOylation through activating ERK/EPHB2/JNK signaling, leading to inhibition of ALKBH5 m6A demethylase activity by blocking substrate accessibility. Post-translational modification of ALKBH5 regulates ROS-induced DNA damage response. ROS specifically promotes ALKBH5 but not FTO, METTL3 and METTL14 SUMOylation by enhancing the interaction of ALKBH5 and Ubiquitin conjugating enzyme E2 I (UBE2I/UBC9) and inhibiting the association between ALKBH5 and SENP1."
item744	REG00005	M6ATAR00800	Down	M6ADIS0104	.	34048572	"ROS promotes ALKBH5 SUMOylation through activating ERK/EPHB2/JNK signaling, leading to inhibition of ALKBH5 m6A demethylase activity by blocking substrate accessibility. Post-translational modification of ALKBH5 regulates ROS-induced DNA damage response. ROS specifically promotes ALKBH5 but not FTO, METTL3 and METTL14 SUMOylation by enhancing the interaction of ALKBH5 and UBC9 and inhibiting the association between ALKBH5 and SUMO specific peptidase 1 (SENP1)."
item745	.	M6ATAR00317	.	M6ADIS0041	.	34108665	RNA m6A modification orchestrates a LINE-1 type transposase domain-containing protein 1 (LINE-1/L1TD1)-host interaction that facilitates retrotransposition and contributes to long gene vulnerability.
item746	REG00022	M6ATAR00279	Down	M6ADIS0126	.	34131081	"Heat directly binds to Heat shock 70 kDa protein 1A (HSPA1A), thereby targeting stress genes in a trans-acting manner. Intriguingly, Heat is heavily methylated in the form of m6A. Heat mediates these effects via the nuclear m6A reader YTHDC1, forming a transcriptional silencing complex for stress genes. Reveals a crucial role of nuclear epitranscriptome in the transcriptional regulation of heat shock response."
item747	REG00007	M6ATAR00196	Up	M6ADIS0007	.	34132367	"METTL3 regulated cellular growth, survival and migration in non-small cell lung cancer. METTL3 promoted non-small cell lung cancer progression by modulating the level of Apoptosis regulator Bcl-2 (BCL2)."
item748	REG00023	.	Down	M6ADIS0060	.	34149792	"The m6A RNA methylation regulators, specifically YTHDC2 and METTL14, were significantly down-regulated and were potential prognostic biomarkers in rectal cancer."
item749	REG00006	.	Down	M6ADIS0060	.	34149792	"The m6A RNA methylation regulators, specifically YTHDC2 and METTL14, were significantly down-regulated and were potential prognostic biomarkers in rectal cancer."
item750	REG00007	M6ATAR00150	Down	M6ADIS0006	.	34163177	"Maternally expressed 3 (MEG3) regulates the expression of BTG2 through miR-544b, thus affecting the malignant behavior of hepatocellular carcinoma. METTL3 regulates the m6A modification of MEG3 and its expression."
item751	REG00005	M6ATAR00438	Up	M6ADIS0003	M6ADRUG0086	34169564	"ALKBH5 and Ubiquitin carboxyl-terminal hydrolase 1 (USP1) were upregulated in T-cell acute lymphoblastic leukemia, and ALKBH5-mediated m6A modification increased USP1 and Aurora B expression. Silencing USP1 increased CEM-C1 cell sensitivity to dexamethasone, reduced cell invasion, promoted cell apoptosis, and ameliorated glucocorticoid receptor (GR) expression."
item752	REG00005	M6ATAR00438	Up	M6ADIS0003	M6ADRUG0011	34169564	"ALKBH5 and Ubiquitin carboxyl-terminal hydrolase 1 (USP1) were upregulated in T-cell acute lymphoblastic leukemia, and ALKBH5-mediated m6A modification increased USP1 and Aurora B expression. Silencing USP1 increased CEM-C1 cell sensitivity to dexamethasone, reduced cell invasion, promoted cell apoptosis, and ameliorated glucocorticoid receptor (GR) expression."
item753	REG00001	M6ATAR00299	.	.	.	34212271	"FTO inhibits adipocytes apoptosis via reducing m6A epigenetic modification-mediated UPRmt.UPRmt-induced increase in PKR and eIF2-alpha phosphorylation, and ATF5-mediated upregulation of BAX expression promoted apoptosis. Furthermore, adipocytes apoptosis is inhibited by FTO-activated Tyrosine-protein kinase JAK2 (JAK2)/STAT3 signaling pathway ."
item754	REG00001	M6ATAR00418	.	.	.	34212271	"FTO inhibits adipocytes apoptosis via reducing m6A epigenetic modification-mediated UPRmt.UPRmt-induced increase in PKR and eIF2-alpha phosphorylation, and ATF5-mediated upregulation of BAX expression promoted apoptosis. Furthermore, adipocytes apoptosis is inhibited by FTO-activated JAK2/Signal transducer and activator of transcription 3 (STAT3) signaling pathway ."
item755	REG00008	M6ATAR00341	.	M6ADIS0065	M6ADRUG0039	34216543	"LCAT3 upregulation is attributable to m6A modification mediated by METTL3, leading to LCAT3 stabilization. Treated cells with tamoxifen to induce MYC activity. Highlights the therapeutic potential of RBPs by uncovering a critical role for YTHDF2 in counteracting the global increase of mRNA synthesis in Myc proto-oncogene protein (MYC)-driven breast cancers."
item756	REG00013	M6ATAR00039	Up	M6ADIS0100	.	34226535	IGF2BP2 physically interacted with AGO2 and increased more hsa-miR-133a-3p accumulation on its target site.m6A modification promoted the repression of specific miRNA during heart development and hypertrophy.
item757	.	M6ATAR00794	.	M6ADIS0066	.	34238292	"In ovarian cancer, a prognostic signature containing four LI-m6As (AC010894.3, ACAP2-IT1, CACNA1G-AS1, and UBA6-AS1) was constructed according to the LASSO Cox regression analysis of the 10 LI-m6As."
item758	.	M6ATAR00101	.	M6ADIS0066	.	34238292	"In ovarian cancer, a prognostic signature containing four LI-m6As (AC010894.3, ACAP2 intronic transcript 1 (ACAP2-IT1), CACNA1G-AS1, and UBA6-AS1) was constructed according to the LASSO Cox regression analysis of the 10 LI-m6As."
item759	.	M6ATAR00145	.	M6ADIS0066	.	34238292	"In ovarian cancer, a prognostic signature containing four LI-m6As (AC010894.3, ACAP2-IT1, CACNA1G antisense RNA 1 (CACNA1G-AS1), and UBA6-AS1) was constructed according to the LASSO Cox regression analysis of the 10 LI-m6As."
item760	.	M6ATAR00084	.	M6ADIS0066	.	34238292	"In ovarian cancer, a prognostic signature containing four LI-m6As (AC010894.3, ACAP2-IT1, CACNA1G-AS1, and UBA6 divergent transcript (UBA6-DT/UBA6-AS1)) was constructed according to the LASSO Cox regression analysis of the 10 LI-m6As."
item761	REG00007	M6ATAR00057	Up	M6ADIS0051	.	34245327	"METTL3-mediated hsa_circ_0004771 (circNRIP1) exhibits oncogenic roles in osteosarcoma by regulating FOXC2 via sponging miR-199a, which provides new ideas for the treatment of osteosarcoma."
item762	REG00007	M6ATAR00256	Up	M6ADIS0051	.	34245327	"METTL3-mediated circNRIP1 exhibits oncogenic roles in osteosarcoma by regulating Forkhead box protein C2 (FOXC2) via sponging miR-199a, which provides new ideas for the treatment of osteosarcoma."
item763	REG00007	M6ATAR00040	Up	M6ADIS0051	.	34245327	"METTL3-mediated circNRIP1 exhibits oncogenic roles in osteosarcoma by regulating FOXC2 via sponging hsa-miR-199a-5p, which provides new ideas for the treatment of osteosarcoma."
item764	REG00001	M6ATAR00254	Up	M6ADIS0013	.	34254281	"FTO induced the dysfunctions of GCs by upregulating Flotillin-2 (FLOT2), suggesting that FTO/FLOT2 plays a role in the pathophysiology of polycystic ovarian syndrome."
item765	REG00004	M6ATAR00175	Up	M6ADIS0065	M6ADRUG0039	34273466	"In breast cancer, modest stable overexpression of A2B1 in MCF-7 cells (MCF-7-A2B1 cells) resulted in tamoxifen and fulvestrant - resistance whereas knockdown of A2B1 in LCC9 and LY2 cells restored tamoxifen and fulvestrant, endocrine-sensitivity. MCF-7-A2B1 cells have increased ER-alpha and reduced miR-222-3p that targets ER-alpha. MCF-7-A2B1 have activated RAC-alpha serine/threonine-protein kinase (AKT1) and MAPK that depend on A2B1 expression and are growth inhibited by inhibitors of these pathways."
item766	REG00004	M6ATAR00327	Up	M6ADIS0065	M6ADRUG0039	34273466	"In breast cancer, modest stable overexpression of A2B1 in MCF-7 cells (MCF-7-A2B1 cells) resulted in tamoxifen and fulvestrant - resistance whereas knockdown of A2B1 in LCC9 and LY2 cells restored tamoxifen and fulvestrant, endocrine-sensitivity. MCF-7-A2B1 cells have increased ER-alpha and reduced miR-222-3p that targets ER-alpha. MCF-7-A2B1 have activated AKT and Mitogen-activated protein kinase 1 (MAPK/ERK2/MAPK1) that depend on A2B1 expression and are growth inhibited by inhibitors of these pathways."
item767	REG00004	M6ATAR00175	Up	M6ADIS0065	M6ADRUG0028	34273466	"In breast cancer, modest stable overexpression of A2B1 in MCF-7 cells (MCF-7-A2B1 cells) resulted in tamoxifen and fulvestrant- resistance whereas knockdown of A2B1 in LCC9 and LY2 cells restored tamoxifen and fulvestrant, endocrine-sensitivity. MCF-7-A2B1 cells have increased ER-alpha and reduced miR-222-3p that targets ER-alpha. MCF-7-A2B1 have activated RAC-alpha serine/threonine-protein kinase (AKT1) and MAPK that depend on A2B1 expression and are growth inhibited by inhibitors of these pathways."
item768	REG00004	M6ATAR00327	Up	M6ADIS0065	M6ADRUG0028	34273466	"In breast cancer, modest stable overexpression of A2B1 in MCF-7 cells (MCF-7-A2B1 cells) resulted in tamoxifen and fulvestrant- resistance whereas knockdown of A2B1 in LCC9 and LY2 cells restored tamoxifen and fulvestrant, endocrine-sensitivity. MCF-7-A2B1 cells have increased ER-alpha and reduced miR-222-3p that targets ER-alpha. MCF-7-A2B1 have activated AKT and Mitogen-activated protein kinase 1 (MAPK/ERK2/MAPK1) that depend on A2B1 expression and are growth inhibited by inhibitors of these pathways."
item769	REG00007	M6ATAR00041	Up	M6ADIS0007	.	34274028	"LCAT3 upregulation is attributable to N6-methyladenosine (m6A) modification mediated by methyltransferase like 3 (METTL3), leading to LCAT3 stabilization. LCAT3 as a novel oncogenic lncRNA in the lung, and validated the LCAT3-FUBP1-MYC axis as a potential therapeutic target for lung adenocarcinomas."
item770	REG00007	M6ATAR00262	Up	M6ADIS0007	.	34274028	"LCAT3 upregulation is attributable to N6-methyladenosine (m6A) modification mediated by methyltransferase like 3 (METTL3), leading to LCAT3 stabilization. LCAT3 as a novel oncogenic lncRNA in the lung, and validated the LCAT3-Far upstream element-binding protein 1 (FUBP1)-MYC axis as a potential therapeutic target for lung adenocarcinomas."
item771	REG00007	M6ATAR00341	Up	M6ADIS0007	.	34274028	"LCAT3 upregulation is attributable to N6-methyladenosine (m6A) modification mediated by methyltransferase like 3 (METTL3), leading to LCAT3 stabilization. LCAT3 as a novel oncogenic lncRNA in the lung, and validated the LCAT3-FUBP1-Myc proto-oncogene protein (MYC) axis as a potential therapeutic target for lung adenocarcinomas."
item772	REG00007	M6ATAR00195	Up	M6ADIS0043	.	34279591	"Knocking down METTL3 prevented Enterovirus 71-induced cell death and suppressed Enterovirus 71-induced expression of Apoptosis regulator BAX (BAX) while rescuing Bcl-2 expression after Enterovirus 71 infection. Knocking down METTL3 inhibited Enterovirus 71-induced expression of Atg5, Atg7 and LC3 II. Knocking down METTL3 inhibited Enterovirus 71-induced apoptosis and autophagy."
item773	REG00007	M6ATAR00196	Down	M6ADIS0043	.	34279591	"Knocking down METTL3 prevented Enterovirus 71-induced cell death and suppressed Enterovirus 71-induced expression of BAX while rescuing Apoptosis regulator Bcl-2 (BCL2) expression after Enterovirus 71 infection. Knocking down METTL3 inhibited Enterovirus 71-induced expression of Atg5, Atg7 and LC3 II. Knocking down METTL3 inhibited Enterovirus 71-induced apoptosis and autophagy."
item774	REG00007	M6ATAR00189	Up	M6ADIS0043	.	34279591	"Knocking down METTL3 prevented Enterovirus 71-induced cell death and suppressed Enterovirus 71-induced expression of Bax while rescuing Bcl-2 expression after Enterovirus 71 infection. Knocking down METTL3 inhibited Enterovirus 71-induced expression of Autophagy protein 5 (ATG5), Atg7 and LC3 II. Knocking down METTL3 inhibited Enterovirus 71-induced apoptosis and autophagy."
item775	REG00007	M6ATAR00190	Up	M6ADIS0043	.	34279591	"Knocking down METTL3 prevented Enterovirus 71-induced cell death and suppressed Enterovirus 71-induced expression of Bax while rescuing Bcl-2 expression after Enterovirus 71 infection. Knocking down METTL3 inhibited Enterovirus 71-induced expression of Atg5, Ubiquitin-like modifier-activating enzyme ATG7 (ATG7) and LC3 II. Knocking down METTL3 inhibited Enterovirus 71-induced apoptosis and autophagy."
item776	REG00007	M6ATAR00331	Up	M6ADIS0043	.	34279591	"Knocking down METTL3 prevented Enterovirus 71-induced cell death and suppressed Enterovirus 71-induced expression of Bax while rescuing Bcl-2 expression after Enterovirus 71 infection. Knocking down METTL3 inhibited Enterovirus 71-induced expression of Atg5, Atg7 and Microtubule-associated proteins 1A/1B light chain 3B (MAP1LC3B/LC3B-II). Knocking down METTL3 inhibited Enterovirus 71-induced apoptosis and autophagy."
item777	REG00007	.	.	M6ADIS0029	.	34286671	"Hsa-miR-302a-3p targets METTL3 and plays tumour suppressive roles in the proliferation, apoptosis, invasion, and migration of melanoma cells."
item778	REG00006	M6ATAR00081	Up	M6ADIS0057	.	34288797	"In gastric cancer, METTL14 was involved in the m6A modification of LINC01320 and induced the up-regulation of Long intergenic non-protein coding RNA 1320 (LINC01320)."
item779	REG00006	M6ATAR00131	Up	M6ADIS0047	.	34298254	"microRNA 211 (MIR211) is a novel tumor suppressor in T-cell lymphoblastic lymphoma,it regulated by METTL14. Targeting of miR-211/TCF12 axis is a potential treatment for T-cell lymphoblastic lymphoma patients."
item780	REG00007	.	.	M6ADIS0127	.	34298489	m6A RNA methylation has been defined and appears to affect DNA repair by modulation of translation.
item781	REG00013	M6ATAR00245	Up	M6ADIS0059	M6ADRUG0010	34309973	"IGF2BP2 activates the expression of Receptor tyrosine-protein kinase erbB-2 (ERBB2) by recognizing the m6A of YAP, thus affecting the cell cycle of colorectal cancer, inhibiting cell apoptosis, and promoting proliferation."
item782	REG00013	M6ATAR00451	Up	M6ADIS0059	M6ADRUG0010	34309973	"IGF2BP2 activates the expression of ErbB2 by recognizing the m6A of Transcriptional coactivator YAP1 (YAP1), thus affecting the cell cycle of colorectal cancer, inhibiting cell apoptosis, and promoting proliferation."
item783	.	.	.	.	.	34313542	Summarize the current understanding of the roles of RNA modifications in cell death mediation and discuss the prospects of such research.
item784	.	M6ATAR00104	.	M6ADIS0057	.	34332535	"m6A lncRNA is closely related to the occurrence and progression of gastric cancer. ACBD3 antisense RNA 1 (ACBD3-AS1) was overexpressed in tumor tissue. Naive B cell, Plasma cells, resting CD4 memory T cell were highly infiltrated tissues in cluster 2, while Macrophages M2, resting Mast cells, Monocytes, regulates T cells were lowly in cluster 1."
item785	REG00007	M6ATAR00326	Down	M6ADIS0001	M6ADRUG0010	34336690	"Two critical DNA repair genes (Methylated-DNA--protein-cysteine methyltransferase (MGMT) and APNG) were m6A-modified by METTL3, whereas inhibited by METTL3 silencing or DAA-mediated total methylation inhibition, which is crucial for METTL3-improved temozolomide resistance in glioblastoma cells."
item786	REG00007	M6ATAR00158	Down	M6ADIS0001	M6ADRUG0010	34336690	"Two critical DNA repair genes (MGMT and DNA-3-methyladenine glycosylase (ANPG/MPG)) were m6A-modified by METTL3, whereas inhibited by METTL3 silencing or DAA-mediated total methylation inhibition, which is crucial for METTL3-improved temozolomide resistance in glioblastoma cells."
item787	REG00013	M6ATAR00097	Up	M6ADIS0073	.	34340128	"IGF2BP2 loss inhibited cell proliferation, migration and invasion, and induced cell apoptosis and cell cycle arrest by down-regulating HOXD antisense growth-associated long non-coding RNA (HAGLR) expression in an m6A-dependent manner in thyroid cancer cells."
item788	.	M6ATAR00360	.	M6ADIS0070	.	34349798	"m6A-related prognostic lncRNA signature serves as a crucial mediator of the immune microenvironment in bladder cancer, representing promising therapeutic targets for improving immunotherapeutic efficacy. Cluster 1 was significantly correlated with poor prognosis, advanced clinical stage, higher Programmed cell death 1 ligand 1 (CD274/PD-L1) expression, a higher ESTIMATEScore and immuneScore, and distinct immune cell infiltration."
item789	.	M6ATAR00281	.	M6ADIS0001	M6ADRUG0079	34354698	Putative heat shock 70 kDa protein 7 (HSPA7) promoted macrophage infiltration and SPP1 expression via upregulating the YAP1 and LOX expression of glioblastoma stem cells in vitro and in clinical glioblastoma tumor samples. HSPA7 is expected to predict the ability of PD-1 inhibitors to respond to treatment in glioblastoma.
item790	.	M6ATAR00281	.	M6ADIS0001	M6ADRUG0080	34354698	Putative heat shock 70 kDa protein 7 (HSPA7) promoted macrophage infiltration and SPP1 expression via upregulating the YAP1 and LOX expression of glioblastoma stem cells in vitro and in clinical glioblastoma tumor samples. HSPA7 is expected to predict the ability of PD-1 inhibitors to respond to treatment in glioblastoma.
item791	REG00007	M6ATAR00140	Up	M6ADIS0004	.	34354942	METTL3-mediated m6A modification induced the aberrant expression of Nuclear paraspeckle assembly transcript 1 (NEAT1) in chronic myelocytic leukemia. Overexpression of NEAT1 inhibited cell viability and promoted the apoptosis of chronic myelocytic leukemia cells. miR-766-5p was upregulated in CML PBMCs and abrogated the effects of NEAT1 on cell viability and apoptosis of the chronic myelocytic leukemia cells.
item792	REG00007	M6ATAR00043	Up	M6ADIS0004	.	34354942	METTL3-mediated m6A modification induced the aberrant expression of NEAT1 in chronic myelocytic leukemia. Overexpression of NEAT1 inhibited cell viability and promoted the apoptosis of chronic myelocytic leukemia cells. hsa-miR-766-5p was upregulated in CML PBMCs and abrogated the effects of NEAT1 on cell viability and apoptosis of the chronic myelocytic leukemia cells.
item793	REG00008	M6ATAR00185	Down	M6ADIS0059	M6ADRUG0044	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Cyclic AMP-dependent transcription factor ATF-4 (ATF4) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition."
item794	REG00001	M6ATAR00185	.	M6ADIS0059	M6ADRUG0044	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Cyclic AMP-dependent transcription factor ATF-4 (ATF4) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition."
item795	REG00008	M6ATAR00185	Down	M6ADIS0059	M6ADRUG0082	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Cyclic AMP-dependent transcription factor ATF-4 (ATF4), which induced pro-survival autophagy during glutaminolysis inhibition."
item796	REG00008	M6ATAR00185	Down	M6ADIS0059	M6ADRUG0073	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Cyclic AMP-dependent transcription factor ATF-4 (ATF4), which induced pro-survival autophagy during glutaminolysis inhibition."
item797	REG00008	M6ATAR00185	Down	M6ADIS0059	M6ADRUG0063	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Cyclic AMP-dependent transcription factor ATF-4 (ATF4) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition."
item798	REG00008	M6ATAR00185	Down	M6ADIS0059	M6ADRUG0003	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Cyclic AMP-dependent transcription factor ATF-4 (ATF4) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition."
item799	REG00008	M6ATAR00185	Down	M6ADIS0059	M6ADRUG0064	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Cyclic AMP-dependent transcription factor ATF-4 (ATF4), which induced pro-survival autophagy during glutaminolysis inhibition."
item800	REG00001	M6ATAR00185	.	M6ADIS0059	M6ADRUG0082	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Cyclic AMP-dependent transcription factor ATF-4 (ATF4), which induced pro-survival autophagy during glutaminolysis inhibition."
item801	REG00001	M6ATAR00185	.	M6ADIS0059	M6ADRUG0073	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Cyclic AMP-dependent transcription factor ATF-4 (ATF4) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition."
item802	REG00001	M6ATAR00185	.	M6ADIS0059	M6ADRUG0063	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Cyclic AMP-dependent transcription factor ATF-4 (ATF4) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition."
item803	REG00001	M6ATAR00185	.	M6ADIS0059	M6ADRUG0003	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Cyclic AMP-dependent transcription factor ATF-4 (ATF4), which induced pro-survival autophagy during glutaminolysis inhibition."
item804	REG00001	M6ATAR00185	.	M6ADIS0059	M6ADRUG0064	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Cyclic AMP-dependent transcription factor ATF-4 (ATF4), which induced pro-survival autophagy during glutaminolysis inhibition."
item805	REG00008	M6ATAR00339	Up	M6ADIS0059	M6ADRUG0044	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition."
item806	REG00001	M6ATAR00339	.	M6ADIS0059	M6ADRUG0044	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition."
item807	REG00008	M6ATAR00339	Up	M6ADIS0059	M6ADRUG0082	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition."
item808	REG00008	M6ATAR00339	Up	M6ADIS0059	M6ADRUG0073	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition."
item809	REG00008	M6ATAR00339	Up	M6ADIS0059	M6ADRUG0063	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition."
item810	REG00008	M6ATAR00339	Up	M6ADIS0059	M6ADRUG0003	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition."
item811	REG00008	M6ATAR00339	Up	M6ADIS0059	M6ADRUG0064	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition."
item812	REG00001	M6ATAR00339	.	M6ADIS0059	M6ADRUG0082	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition."
item813	REG00001	M6ATAR00339	.	M6ADIS0059	M6ADRUG0073	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition."
item814	REG00001	M6ATAR00339	.	M6ADIS0059	M6ADRUG0063	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. Serine/threonine-protein kinase mTOR (MTOR) transcriptionally upregulated DDIT4 to suppress mTOR, which induced pro-survival autophagy during glutaminolysis inhibition."
item815	REG00001	M6ATAR00339	.	M6ADIS0059	M6ADRUG0003	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition."
item816	REG00001	M6ATAR00339	.	M6ADIS0059	M6ADRUG0064	34373753	"In colorectal cancer, Glutaminolysis inhibition upregulated ATF4 expression in an m6A-dependent manner to activate pro-survival autophagy through transcriptional activation of the mTOR inhibitor DDIT4. Determined the relationship between FTO alpha-ketoglutarate dependent dioxygenase (FTO), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), and ATF4. ATF4 transcriptionally upregulated DDIT4 to suppress Serine/threonine-protein kinase mTOR (MTOR), which induced pro-survival autophagy during glutaminolysis inhibition."
item817	REG00007	M6ATAR00144	Up	M6ADIS0006	M6ADRUG0032	34374933	"Identified the lncRNA NIFK antisense RNA 1 (NIFK-AS1) as being highly expressed in hepatocellular carcinoma tissues and cells, promotes disease progression and sorafenib resistance, and showed this up-regulation resulted from METTL3-dependent m6A methylation."
item818	REG00001	M6ATAR00362	Up	M6ADIS0001	M6ADRUG0010	34390075	Long noncoding RNA just proximal to X-inactive specific transcript facilitates aerobic glycolysis and temozolomide chemoresistance by promoting stability of PDH kinase 1 (PDK1) mRNA in an m6A-dependent manner in glioblastoma multiforme cells. JPX interacted with N6-methyladenosine (m6A) demethylase FTO alpha-ketoglutarate dependent dioxygenase (FTO) and enhanced FTO-mediated PDK1 mRNA demethylation.
item819	REG00013	M6ATAR00064	Up	M6ADIS0008	.	34392306	"m6A-modified hsa_circ_0000231 (circARHGAP12) interacts with IGF2BP2 to enhance FOXM1 mRNA stability, forming circARHGAP12/IGF2BP2/FOXM1 complex, thereby promoting the proliferation and migration of cervical cancer cells."
item820	REG00003	M6ATAR00134	.	M6ADIS0056	.	34395102	"HNRNPC, YTHDF, ZC3H13, YTHDC2, and METTL14 were dysregulated in esophageal cancer tissues. miR-186 interacted with HNRNPC and suppressed the expression of HNRNPC. Four miRNAs (microRNA 186 (MIR186), miR-320c, miR-320d, and miR-320b) were used to construct a prognostic signature, which could serve as a prognostic predictor independent from routine clinicopathological features."
item821	REG00003	M6ATAR00045	.	M6ADIS0056	.	34395102	"HNRNPC, YTHDF, ZC3H13, YTHDC2, and METTL14 were dysregulated in esophageal cancer tissues. miR-186 interacted with HNRNPC and suppressed the expression of HNRNPC. Four miRNAs (miR-186, hsa-miR-320c, miR-320d, and miR-320b) were used to construct a prognostic signature, which could serve as a prognostic predictor independent from routine clinicopathological features."
item822	REG00003	M6ATAR00046	.	M6ADIS0056	.	34395102	"HNRNPC, YTHDF, ZC3H13, YTHDC2, and METTL14 were dysregulated in esophageal cancer tissues. miR-186 interacted with HNRNPC and suppressed the expression of HNRNPC. Four miRNAs (miR-186, miR-320c, hsa-miR-320d, and miR-320b) were used to construct a prognostic signature, which could serve as a prognostic predictor independent from routine clinicopathological features."
item823	REG00003	M6ATAR00047	.	M6ADIS0056	.	34395102	"HNRNPC, YTHDF, ZC3H13, YTHDC2, and METTL14 were dysregulated in esophageal cancer tissues. miR-186 interacted with HNRNPC and suppressed the expression of HNRNPC. Four miRNAs (miR-186, miR-320c, miR-320d, and hsa-miR-320b) were used to construct a prognostic signature, which could serve as a prognostic predictor independent from routine clinicopathological features."
item824	REG00007	M6ATAR00141	Up	M6ADIS0065	.	34419065	"Silencing METTL3 down-regulate Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) and HMGA2 by sponging miR-26b, and finally inhibit EMT, migration and invasion in breast cancer, providing a theoretical basis for clinical treatment of breast cancer."
item825	.	M6ATAR00113	.	M6ADIS0006	.	34429653	The study demonstrated that the 9 m6A-related lncRNA signature serves as a novel predictor in the prognosis of hepatocellular Carcinoma and optimize (ICIs) therapy. Small nucleolar RNA host gene 4 (SNHG4) plays an oncogenic role in hepatocellular Carcinoma.
item826	REG00015	M6ATAR00460	Down	M6ADIS0009	M6ADRUG0047	34446080	VIRMA has an oncogenic role in germ cell tumor confirming our previous tissue-based study and is further involved in response to cisplatin by interfering with DNA repair. Enhanced response to cisplatin after VIRMA knockdown was related to significant increase in DNA damage (with higher Histone H2AX (H2AX) and GADD45B levels) and downregulation of XLF and MRE11.
item827	REG00015	M6ATAR00264	Down	M6ADIS0009	M6ADRUG0047	34446080	VIRMA has an oncogenic role in germ cell tumor confirming our previous tissue-based study and is further involved in response to cisplatin by interfering with DNA repair. Enhanced response to cisplatin after VIRMA knockdown was related to significant increase in DNA damage (with higher Gamma-H2AX and Negative growth regulatory protein MyD118 (GADD45B) levels) and downregulation of XLF and MRE11.
item828	REG00015	M6ATAR00462	Up	M6ADIS0009	M6ADRUG0047	34446080	VIRMA has an oncogenic role in germ cell tumor confirming our previous tissue-based study and is further involved in response to cisplatin by interfering with DNA repair. Enhanced response to cisplatin after VIRMA knockdown was related to significant increase in DNA damage (with higher Gamma-H2AX and GADD45B levels) and downregulation of Non-homologous end-joining factor 1 (NHEJ1/XLF) and MRE11.
item829	REG00015	M6ATAR00463	Up	M6ADIS0009	M6ADRUG0047	34446080	VIRMA has an oncogenic role in germ cell tumor confirming our previous tissue-based study and is further involved in response to cisplatin by interfering with DNA repair. Enhanced response to cisplatin after VIRMA knockdown was related to significant increase in DNA damage (with higher Gamma-H2AX and GADD45B levels) and downregulation of XLF and Double-strand break repair protein MRE11 (MRE11).
item830	REG00007	M6ATAR00801	Down	M6ADIS0120	.	34450538	SNHG4 was downregulated in the neonatal pneumonia patient serum and its overexpression could inhibit LPS induced inflammatory injury in human lung fibroblasts and mouse lung tissue. The molecular mechanism underlying this protective effect was achieved by suppression of METTL3-mediated m6A modification levels of YTHDF1-dependent Signal transducer and activator of transcription 2 (STAT2) mRNA.
item831	REG00024	M6ATAR00801	Down	M6ADIS0120	.	34450538	SNHG4 was downregulated in the neonatal pneumonia patient serum and its overexpression could inhibit LPS induced inflammatory injury in human lung fibroblasts and mouse lung tissue. The molecular mechanism underlying this protective effect was achieved by suppression of METTL3-mediated m6A modification levels of YTHDF1-dependent Signal transducer and activator of transcription 2 (STAT2) mRNA.
item832	REG00005	M6ATAR00049	.	M6ADIS0007	.	34480914	"In non-small cell lung cancer, m6A marks in mature hsa-miR-21-5p could directly affect its silencing potency towards target genes, which finally impaired its promotion to proliferation and motility. Depletion of the demethylase ALKBH5 altered the m6A abundance of miR-21-5p, thereby changing the expression levels of its target gene."
item833	REG00015	M6ATAR00017	Down	M6ADIS0102	.	34490238	"KIAA1429 is downregulated while ALKBH5 is upregulated in aortic tissues from aortic dissection patients. KIAA1429/ALKBH5-mediated m6A modifications can regulate the processing of hsa-miR-143-3p through interacting with the microprocessor protein DGCR8. KIAA1429 and ALKBH5 can oppositely regulate HASMC proliferation, HAEC apoptosis, and AD progression in AngII-infused mice via the miR-143-3p/DDX6 pathway."
item834	REG00005	M6ATAR00017	Down	M6ADIS0102	.	34490238	"KIAA1429 is downregulated while ALKBH5 is upregulated in aortic tissues from aortic dissection patients. KIAA1429/ALKBH5-mediated m6A modifications can regulate the processing of hsa-miR-143-3p through interacting with the microprocessor protein DGCR8. KIAA1429 and ALKBH5 can oppositely regulate HASMC proliferation, HAEC apoptosis, and AD progression in AngII-infused mice via the miR-143-3p/DDX6 pathway."
item835	REG00001	M6ATAR00141	Down	M6ADIS0070	.	34499008	"In bladder cancer, the changes in m6A methylation level mainly appeared at 5' untranslated region (5' UTR) of Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) and NOTCH1 transcripts, and at 3' UTR of CSNK2A2 and ITGA6 transcripts, responding to the overexpression of FTO. SFPQ could influence the FTO-mediated m6A RNA demethylation, eventually affecting the gene expression."
item836	REG00001	M6ATAR00351	Down	M6ADIS0070	.	34499008	"In bladder cancer, the changes in m6A methylation level mainly appeared at 5' untranslated region (5' UTR) of MALAT1 and Neurogenic locus notch homolog protein 1 (NOTCH1) transcripts, and at 3' UTR of CSNK2A2 and ITGA6 transcripts, responding to the overexpression of FTO. SFPQ could influence the FTO-mediated m6A RNA demethylation, eventually affecting the gene expression."
item837	REG00001	M6ATAR00391	.	M6ADIS0070	.	34499008	"In bladder cancer, the changes in m6A methylation level mainly appeared at 5' untranslated region (5' UTR) of MALAT1 and NOTCH1 transcripts, and at 3' UTR of CSNK2A2 and ITGA6 transcripts, responding to the overexpression of FTO. Splicing factor, proline- and glutamine-rich (SFPQ) could influence the FTO-mediated m6A RNA demethylation, eventually affecting the gene expression."
item838	REG00001	M6ATAR00221	Up	M6ADIS0070	.	34499008	"In bladder cancer, the changes in m6A methylation level mainly appeared at 5' untranslated region (5' UTR) of MALAT1 and NOTCH1 transcripts, and at 3' UTR of Casein kinase II subunit alpha' (CSNK2A2) and ITGA6 transcripts, responding to the overexpression of FTO. SFPQ could influence the FTO-mediated m6A RNA demethylation, eventually affecting the gene expression."
item839	REG00001	M6ATAR00297	Up	M6ADIS0070	.	34499008	"In bladder cancer, the changes in m6A methylation level mainly appeared at 5' untranslated region (5' UTR) of MALAT1 and NOTCH1 transcripts, and at 3' UTR of CSNK2A2 and Integrin alpha-6 (ITGA6) transcripts, responding to the overexpression of FTO. SFPQ could influence the FTO-mediated m6A RNA demethylation, eventually affecting the gene expression."
item840	REG00006	M6ATAR00432	Up	M6ADIS0117	.	34503454	"METTL14 could aggravated high glucose-induced glomerular endothelial cell injury and diabetic nephropathy through m6A modification of alpha-klotho. METTL14 silence decreased the levels of ROS, Tumor necrosis factor (TNF/TNF-alpha) and IL-6 and cell apoptosis."
item841	REG00022	M6ATAR00242	Down	M6ADIS0065	M6ADRUG0022	34511602	"Epithelial membrane protein 3 (EMP3) blocks Akt-mTOR signaling activation and induces autophagy. EMP3 downregulates YTHDC1, which at least in part mediates the effects of EMP3 on breast cancer cells. EMP3 sensitizes breast cancer cells to the DNA-damaging drug Adriamycin. EMP3 downregulation can be responsible for breast cancer chemoresistance."
item842	REG00008	.	.	M6ADIS0006	M6ADRUG0037	34512165	"The m6A model includes LRPPRC, YTHDF2, KIAA14219, and RBM15B, classified A-hepatocellular carcinoma patients into high/low-risk subtypes. The expression of Immunosuppressive cytokines DNMT1/EZH2 was up-regulated in A-hepatocellular carcinoma patients, and teniposide can be a potential therapeutic drug for A-hepatocellular carcinoma."
item843	REG00021	.	Up	M6ADIS0006	M6ADRUG0037	34512165	"The m6A model includes LRPPRC, YTHDF2, KIAA14219, and RBM15B, classified A-hepatocellular carcinoma patients into high/low-risk subtypes. The expression of Immunosuppressive cytokines DNMT1/EZH2 was up-regulated in A-hepatocellular carcinoma patients, and teniposide can be a potential therapeutic drug for A-hepatocellular carcinoma."
item844	REG00015	.	Up	M6ADIS0006	M6ADRUG0037	34512165	"The m6A model includes LRPPRC, YTHDF2, KIAA14219, and RBM15B, classified A-hepatocellular carcinoma patients into high/low-risk subtypes. The expression of Immunosuppressive cytokines DNMT1/EZH2 was up-regulated in A-hepatocellular carcinoma patients, and teniposide can be a potential therapeutic drug for A-hepatocellular carcinoma."
item845	REG00001	M6ATAR00264	Up	M6ADIS0092	.	34513292	"Negative growth regulatory protein MyD118 (GADD45B)-mediated m6A modification in Negative growth regulatory protein MyD118 (GADD45B) mRNA drives skeletal muscle differentiation by activating the p38 MAPK pathway, which provides a molecular mechanism for the regulation of myogenesis via RNA methylation."
item846	.	M6ATAR00367	.	M6ADIS0007	.	34517553	"In lung squamous cell carcinoma, seven m6A-related autophagy genes were screened to construct a prognostic model: CASP4, CDKN1A, DLC1, ITGB1, Serine/threonine-protein kinase PINK1, mitochondrial (PINK1), TP63, and EIF4EBP1."
item847	.	M6ATAR00383	.	M6ADIS0007	.	34517553	"In lung squamous cell carcinoma, seven m6A-related autophagy genes were screened to construct a prognostic model: CASP4, CDKN1A, Rho GTPase-activating protein 7 (DLC1), ITGB1, PINK1, TP63, and EIF4EBP1."
item848	.	M6ATAR00204	.	M6ADIS0007	.	34517553	"In lung squamous cell carcinoma, seven m6A-related autophagy genes were screened to construct a prognostic model: Caspase-4 (CASP4), CDKN1A, DLC1, ITGB1, PINK1, TP63, and EIF4EBP1."
item849	.	M6ATAR00298	.	M6ADIS0007	.	34517553	"In lung squamous cell carcinoma, seven m6A-related autophagy genes were screened to construct a prognostic model: CASP4, CDKN1A, DLC1, Integrin beta-1 (ITGB1), PINK1, TP63, and EIF4EBP1."
item850	.	M6ATAR00213	.	M6ADIS0007	.	34517553	"In lung squamous cell carcinoma, seven m6A-related autophagy genes were screened to construct a prognostic model: CASP4, Cyclin-dependent kinase inhibitor 1 (CDKN1A), DLC1, ITGB1, PINK1, TP63, and EIF4EBP1."
item851	.	M6ATAR00357	.	M6ADIS0007	.	34517553	"In lung squamous cell carcinoma, seven m6A-related autophagy genes were screened to construct a prognostic model: CASP4, CDKN1A, DLC1, ITGB1, PINK1, Tumor protein 63 (TP63), and EIF4EBP1."
item852	REG00007	M6ATAR00237	Up	M6ADIS0029	M6ADRUG0054	34530048	"METTL3 increased the m6A modification of Epidermal growth factor receptor (EGFR) mRNA in A375R cells, which promoted its translation efficiency. Inhibiting METTL3 function to restore PLX4032 sensitivity in patients with melanoma."
item853	REG00007	M6ATAR00141	Up	M6ADIS0028	M6ADRUG0056	34530916	"This study highlighted METTL3 as a tumor promoter in Thymic tumors and c-MYC as a promising target to be exploited for the treatment of TET. High expression of c-MYC protein is enabled by lncRNA Metastasis associated lung adenocarcinoma transcript 1 (MALAT1), which is methylated and delocalized by METTL3. Silencing of METTL3 combined with cisplatin or c-MYC inhibitor induces cell death in TET cells. Blocking of c-MYC by using JQ1 inhibitor cooperates with METTL3 depletion in the inhibition of proliferation and induction of cell death."
item854	REG00007	M6ATAR00141	Up	M6ADIS0028	M6ADRUG0047	34530916	"This study highlighted METTL3 as a tumor promoter in Thymic tumors and c-MYC as a promising target to be exploited for the treatment of TET. High expression of c-MYC protein is enabled by lncRNA Metastasis associated lung adenocarcinoma transcript 1 (MALAT1), which is methylated and delocalized by METTL3. Silencing of METTL3 combined with cisplatin or c-MYC inhibitor induces cell death in TET cells. Blocking of c-MYC by using JQ1 inhibitor cooperates with METTL3 depletion in the inhibition of proliferation and induction of cell death."
item855	REG00007	M6ATAR00146	Up	M6ADIS0059	M6ADRUG0005	34535128	The increased LBX2 antisense RNA 1 (LBX2-AS1) in CRC was mediated by METTL3-dependent m6A methylation. LBX2-AS1 serves as a therapeutic target and predictor of 5-FU benefit in colorectal cancer patients.
item856	.	M6ATAR00442	.	M6ADIS0002	.	34539785	"The role of Ubiquilin-4 (UBQLN4) in pan-cancer for the first time. Based on the comprehensive analysis of multiomics data, we identified UBQLN4 as a potential molecular biomarker for prognosis and treatment in oncotherapy."
item857	REG00007	M6ATAR00802	Up	M6ADIS0059	.	34544413	"Overexpression of LINC01605, regulated by SMYD2-EP300-mediated H3K27ac and H3K4me3 modifications, bound to METTL3 protein to promote m6A modification of Spectrin beta, non-erythrocytic 2 (SPTBN2) mRNA, leading to the development of colorectal cancer."
item858	REG00008	M6ATAR00151	Down	M6ADIS0056	.	34544449	"The elevated FTO in esophageal squamous cell carcinoma decreased m6A methylation of LINC00022 transcript, leading to the inhibition of Deleted in lymphocytic leukemia 2 (DLEU2/LINC00022) decay via the m6A reader YTHDF2."
item859	REG00001	M6ATAR00151	Down	M6ADIS0056	.	34544449	"The elevated FTO in esophageal squamous cell carcinoma decreased m6A methylation of Deleted in lymphocytic leukemia 2 (DLEU2/LINC00022) transcript, leading to the inhibition of LINC00022 decay via the m6A reader YTHDF2."
item860	REG00001	M6ATAR00213	.	M6ADIS0056	.	34544449	"The elevated FTO in esophageal squamous cell carcinoma decreased m6A methylation of LINC00022 transcript, leading to the inhibition of LINC00022 decay via the m6A reader YTHDF2. LINC00022 directly binds to Cyclin-dependent kinase inhibitor 1 (CDKN1A) protein and promotes its ubiquitination-mediated degradation, thereby facilitating cell-cycle progression and proliferation."
item861	REG00007	M6ATAR00386	Up	M6ADIS0107	.	34547464	"The upregulation of METTL3 and YTHDF1 induced by lipotoxicity contributes to the elevated expression level of Beclin-1 associated RUN domain containing protein (RUBCN/Rubicon) in an m6A-dependent manner, which inhibits the fusion of autophagosomes and lysosomes and further suppresses the clearance of LDs via lysosomes in nonalcoholic fatty liver disease."
item862	REG00024	M6ATAR00386	Up	M6ADIS0107	.	34547464	"The upregulation of METTL3 and YTHDF1 induced by lipotoxicity contributes to the elevated expression level of Beclin-1 associated RUN domain containing protein (RUBCN/Rubicon) in an m6A-dependent manner, which inhibits the fusion of autophagosomes and lysosomes and further suppresses the clearance of LDs via lysosomes in nonalcoholic fatty liver disease."
item863	.	M6ATAR00080	.	M6ADIS0006	.	34551796	"LncRNA activating regulator of DKK1 (LNCAROD) induces PKM2 upregulation via simultaneously enhancing SRSF3-mediated PKM switching to PKM2 and sponging miR-145-5p to increase PKM2 level, eventually increasing hepatocellular carcinoma cell aerobic glycolysis to participate in tumor malignancy and chemoresistance, especially under hypoxic microenvironment."
item864	REG00001	.	.	M6ADIS0002	.	34556998	"The FTO gene's research progress in tumors is reviewed, aiming to find new targets for molecular pathological diagnosis and molecular targeted therapy of tumors."
item865	REG00007	M6ATAR00306	Down	M6ADIS0119	M6ADRUG0045	34560125	m6A methylation was involved in oxidative stress-mediated apoptosis in the mechanism of colistin nephrotoxicity. METTL3-mediated m6A methylation modification is involved in colistin-induced nephrotoxicity through apoptosis mediated by Kelch-like ECH-associated protein 1 (KEAP1)/Nrf2 signaling pathway.
item866	REG00007	M6ATAR00348	Up	M6ADIS0119	M6ADRUG0045	34560125	m6A methylation was involved in oxidative stress-mediated apoptosis in the mechanism of colistin nephrotoxicity. METTL3-mediated m6A methylation modification is involved in colistin-induced nephrotoxicity through apoptosis mediated by Keap1/Nuclear factor erythroid 2-related factor 2 (NFE2L2) signaling pathway.
item867	REG00001	M6ATAR00098	Up	M6ADIS0008	.	34564982	"FTO-stabilized HOXC13 antisense RNA (HOXC13-AS) epigenetically up-regulated FZD6 and activated Wnt/beta-catenin signaling to drive cervical cancer proliferation, invasion, and EMT, suggesting HOXC13-AS as a potential target for cervical cancer treatment."
item868	.	M6ATAR00359	.	M6ADIS0059	.	34568334	"The study highlights a robust correlation between the level of cancer stemness and traits related to tumor heterogeneity, including the immune microenvironment, TMB, and the expression of m6A RNA methylation regulatory factors in colorectal cancer cells. A three-gene prognostic signature (PCNA-interacting partner (PARPBP), KNSTRN, and KIF2C) was explored together with specific clinical features to construct a nomogram, which was successfully validated in an external cohort."
item869	.	M6ATAR00307	.	M6ADIS0059	.	34568334	"The study highlights a robust correlation between the level of cancer stemness and traits related to tumor heterogeneity, including the immune microenvironment, TMB, and the expression of m6A RNA methylation regulatory factors in colorectal cancer cells. A three-gene prognostic signature (PARPBP, KNSTRN, and Kinesin-like protein KIF2C (KIF2C)) was explored together with specific clinical features to construct a nomogram, which was successfully validated in an external cohort."
item870	.	M6ATAR00395	.	M6ADIS0059	.	34568334	"The study highlights a robust correlation between the level of cancer stemness and traits related to tumor heterogeneity, including the immune microenvironment, TMB, and the expression of m6A RNA methylation regulatory factors in colorectal cancer cells. A three-gene prognostic signature (PARPBP, Small kinetochore-associated protein (KNSTRN), and KIF2C) was explored together with specific clinical features to construct a nomogram, which was successfully validated in an external cohort."
item871	REG00006	M6ATAR00393	Down	M6ADIS0117	M6ADRUG0022	34580283	"The elevated m6A RNA levels and the most upregulated METTL14 expression in kidneys of mice with adriamycin and diabetic nephropathy. METTL14-dependent RNA m6A modification contributes to podocyte injury through posttranscriptional regulation of NAD-dependent protein deacetylase sirtuin-1 (SIRT1) mRNA, which provide a potential approach for the diagnosis and treatment of podocytopathies."
item872	REG00007	M6ATAR00249	.	M6ADIS0001	M6ADRUG0010	34586728	Uncover the fundamental mechanisms underlying the interplay of m6 A RNA modification and histone modification in Temozolomide resistance and emphasize the therapeutic potential of targeting the SOX4/EZH2/METTL3 axis in the treatment of TMZ-resistant glioblastoma.
item873	REG00007	M6ATAR00094	Up	M6ADIS0008	.	34589576	"METTL3/FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) accelerates cervical cancer progression via a m6A-dependent modality, which serves as a potential therapeutic target for cervical cancer."
item874	REG00007	.	.	M6ADIS0089	.	34593014	METTL3 reduction-mediated m6A dysregulation likely contributes to neurodegeneration in Alzheimer's disease which can be a therapeutic target for Alzheimer's disease.
item875	REG00007	M6ATAR00199	Up	M6ADIS0107	.	34599880	"Liver-specific Mettl3 knockout mice exhibited global decrease in m6A on polyadenylated RNAs and pathologic features associated with nonalcoholic fatty liver disease. Studies in the M3LKO model indicated that METTL3 exhibits pleotropic function to maintain liver homeostasis by deregulating m6A profile and expression of the liver transcriptome. A significant decrease in total Brain and muscle ARNT-like 1 (Bmal1/ARNTL) and Clock mRNAs but an increase in their nuclear levels were observed in M3LKO livers, suggesting impaired nuclear export."
item876	REG00007	M6ATAR00459	Up	M6ADIS0107	.	34599880	"Liver-specific Mettl3 knockout mice exhibited global decrease in m6A on polyadenylated RNAs and pathologic features associated with nonalcoholic fatty liver disease. Studies in the M3LKO model indicated that METTL3 exhibits pleotropic function to maintain liver homeostasis by deregulating m6A profile and expression of the liver transcriptome. A significant decrease in total Bmal1 and Circadian locomoter output cycles protein kaput (CLOCK) mRNAs but an increase in their nuclear levels were observed in M3LKO livers, suggesting impaired nuclear export."
item877	.	M6ATAR00051	.	M6ADIS0058	.	34603397	"Identified 10 upregulated m6A regulators at both mRNA and protein levels, and 2,479 m6A-related lncRNAs in colon adenocarcinoma. Functional inference suggested that CTD-3184A7.4, RP11-458F8.4, and RP11-108L7.15 were positively correlated with the energy metabolism-related pathways, further suggesting that these lncRNAs were involved in energy metabolism-related pathways."
item878	.	M6ATAR00073	.	M6ADIS0058	.	34603397	"Identified 10 upregulated m6A regulators at both mRNA and protein levels, and 2,479 m6A-related lncRNAs in colon adenocarcinoma. Functional inference suggested that CTD-3184A7.4, Long intergenic non-protein coding RNA 2604 (LINC02604/RP11-458F8.4), and RP11-108L7.15 were positively correlated with the energy metabolism-related pathways, further suggesting that these lncRNAs were involved in energy metabolism-related pathways."
item879	.	M6ATAR00052	.	M6ADIS0058	.	34603397	"Identified 10 upregulated m6A regulators at both mRNA and protein levels, and 2,479 m6A-related lncRNAs in colon adenocarcinoma. Functional inference suggested that CTD-3184A7.4, RP11-458F8.4, and RP11-108L7.15 were positively correlated with the energy metabolism-related pathways, further suggesting that these lncRNAs were involved in energy metabolism-related pathways."
item880	REG00024	M6ATAR00197	Up	M6ADIS0006	M6ADRUG0032	34607160	Analyzed the effect of sorafenib on HSC ferroptosis and m6A modification in advanced fibrotic patients with hepatocellular carcinoma receiving sorafenib monotherapy. YTHDF1 promotes Beclin-1 (BECN1) mRNA stability and autophagy activation via recognizing the m6A binding site within BECN1 coding regions.
item881	REG00007	M6ATAR00102	Up	M6ADIS0057	.	34608273	"LV-sh-THAP7 antisense RNA 1 (THAP7-AS1) treatment could suppress gastric cancer growth. THAP7-AS1, transcriptionally activated by SP1 and then modified by METTL3-mediated m6A, exerts oncogenic functions, by promoting interaction between NLS and importin alpha-1 and then improving the CUL4B protein entry into the nucleus to repress the transcription of miR-22-3p and miR-320a."
item882	REG00006	M6ATAR00147	Down	M6ADIS0007	.	34624573	"HLA complex group 11 (HCG11) mediated by METTL14 inhibited the growth of lung adenocarcinoma via IGF2BP2/LATS1. The m6A modification of HCG11 promoted its nuclear exportation and binding by Insulin Like Growth Factor 2 MRNA Binding Protein 2 (IGF2BP2), resulting in increased stability."
item883	REG00013	M6ATAR00147	Up	M6ADIS0007	.	34624573	"HLA complex group 11 (HCG11) mediated by METTL14 inhibited the growth of lung adenocarcinoma via IGF2BP2/LATS1. The m6A modification of HCG11 promoted its nuclear exportation and binding by Insulin Like Growth Factor 2 MRNA Binding Protein 2 (IGF2BP2), resulting in increased stability."
item884	.	M6ATAR00345	.	M6ADIS0007	M6ADRUG0047	34628486	"m6A RNA methylation-mediated RMRP stability renders proliferation and progression of non-small cell lung cancer through regulating TGFBR1/SMAD2/SMAD3 pathway. RMRP promoted the cancer stem cells properties and epithelial mesenchymal transition, which promote the resistance to radiation therapy and cisplatin."
item885	REG00004	M6ATAR00327	Up	M6ADIS0058	.	34630502	hnRNPA2B1 promotes colon cancer progression via the MAPK pathway. hnRNPA2B1 is an upstream regulator of the ERK/Mitogen-activated protein kinase 1 (MAPK/ERK2/MAPK1) pathway and inhibition of MAPK signaling blocked the effects of hnRNPA2B1.
item886	REG00004	M6ATAR00244	Up	M6ADIS0058	.	34630502	hnRNPA2B1 promotes colon cancer progression via the MAPK pathway. hnRNPA2B1 is an upstream regulator of the Ephrin type-B receptor 2 (ERK/EPHB2)/MAPK pathway and inhibition of MAPK signaling blocked the effects of hnRNPA2B1.
item887	REG00007	M6ATAR00166	Up	M6ADIS0010	.	34631715	"Knockdown of METTL3 in clear cell renal cell carcinoma cell line impaired both cell migration capacity and tumor spheroid formation in soft fibrin gel, a mechanical method for selecting stem-cell-like tumorigenic cells. METTL3 knockdown cells and functional studies confirmed that translation of ATP-binding cassette sub-family D member 1 (ABCD1)."
item888	REG00013	M6ATAR00087	Up	M6ADIS0001	.	34645788	Cancer susceptibility 9 (CASC9)/IGF2BP2/HK2 axis promotes the aerobic glycolysis of glioblastoma multiforme.
item889	REG00022	M6ATAR00410	Up	M6ADIS0033	.	34657574	"In diabetes/diabetic skin, YTHDC1 interacted and cooperated with ELAVL1/HuR (ELAV like RNA binding protein 1) in modulating the expression of Sequestosome-1 (SQSTM1)."
item890	REG00022	M6ATAR00410	Up	M6ADIS0080	.	34657574	"In diabetes/diabetic skin, YTHDC1 interacted and cooperated with ELAVL1/HuR (ELAV like RNA binding protein 1) in modulating the expression of Sequestosome-1 (SQSTM1)."
item891	REG00007	M6ATAR00099	Up	M6ADIS0061	.	34658294	"METTL3 induced m6A hyper-methylation on the 3' UTR of LIFR antisense RNA 1 (LIFR-AS1) to enhance its mRNA stability and LIFR-AS1 could directly interact with miR-150-5p, thereby indirectly up-regulating VEGFA expressions within cells. A noval m6A-LIFR-AS1 axis promotes pancreatic cancer progression at least in part via regulation of the miR-150-5p/VEGFA axis, indicating that this regulatory axis can be a viable clinical target for the treatment of pancreatic cancer."
item892	REG00005	.	.	M6ADIS0057	.	34659574	"NcRNA, lncNRON, exhibits oncogenic roles in the progression of gastric cancer. NRON, as a possible additional regulatory subunit of the m6A eraser, strengthens the m6A recognition of RNAs by m6A eraser ALKBH5 to enhance Nanog mRNA stability and expression."
item893	REG00007	M6ATAR00377	Down	M6ADIS0059	.	34660259	"In colorectal cancer, n6-methyladenosine (m6A) subunit METTL3 increased PTTG3P expression by influencing its stability, while insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) could identify Putative pituitary tumor-transforming gene 3 protein (PTTG3P) m6A methylation status and bind to it."
item894	REG00013	M6ATAR00377	Up	M6ADIS0059	.	34660259	"In colorectal cancer, n6-methyladenosine (m6A) subunit METTL3 increased PTTG3P expression by influencing its stability, while insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) could identify Putative pituitary tumor-transforming gene 3 protein (PTTG3P) m6A methylation status and bind to it."
item895	REG00023	M6ATAR00053	Up	M6ADIS0077	.	34660707	YTHDC2/Circ_YTHDC2/TET2 pathway is an important target of metformin in preventing the progression of VSMCs dysfunction under high glucose.
item896	REG00008	.	.	M6ADIS0020	.	34664060	Germ cell-specific Ythdf2 mutants (Ythdf2-vKO) at a C57BL/6J background and demonstrated that YTHDF2 is essential for mouse spermatogenesis and fertility. Demonstrates the fundamental role of YTHDF2 during mouse spermatogenesis and provides a potential candidate for the diagnosis of male infertility with the oligoasthenoteratozoospermia syndrome.
item897	REG00005	M6ATAR00140	Down	M6ADIS0001	.	34670781	"Hypoxia-induced ALKBH5 erased m6A deposition from the lncRNA NEAT1, stabilizing the transcript and facilitating Nuclear paraspeckle assembly transcript 1 (NEAT1)-mediated paraspeckle assembly. Ectopic expression of CXCL8 in ALKBH5-deficient glioblastoma multiforme cells partially restored TAM recruitment and tumor progression."
item898	REG00008	M6ATAR00351	Down	.	.	34671198	"YTHDF2 inhibits Notch signaling by downregulating the Neurogenic locus notch homolog protein 1 (NOTCH1), HES1, and HES5 mRNA levels."
item899	REG00008	M6ATAR00272	Down	.	.	34671198	"YTHDF2 inhibits Notch signaling by downregulating the Notch1, Transcription factor HES-1 (HES1), and HES5 mRNA levels."
item900	REG00008	M6ATAR00273	Down	.	.	34671198	"YTHDF2 inhibits Notch signaling by downregulating the Notch1, HES1, and Transcription factor HES-5 (HES5) mRNA levels."
item901	REG00007	M6ATAR00458	Up	M6ADIS0019	.	34689175	METTL3 targets Intersectin-2 (ITSN2) for m6A modification and then enhances its stability to influence the oocytes meiosis. mRNA m6A modification in follicle development and coordination of RNA stabilization during oocyte growth.
item902	REG00007	M6ATAR00458	Up	M6ADIS0013	.	34689175	METTL3 targets Intersectin-2 (ITSN2) for m6A modification and then enhances its stability to influence the oocytes meiosis. mRNA m6A modification in follicle development and coordination of RNA stabilization during oocyte growth.
item903	REG00009	M6ATAR00067	Up	M6ADIS0070	M6ADRUG0047	34702726	"Circ0008399 bound WTAP to promote formation of the WTAP/METTL3/METTL14 m6A methyltransferase complex, reduce cisplatin sensitivity in bladder cancer, implicating the potential therapeutic value of targeting this axis."
item904	REG00007	M6ATAR00067	Up	M6ADIS0070	M6ADRUG0047	34702726	"Circ0008399 bound WTAP to promote formation of the WTAP/METTL3/METTL14 m6A methyltransferase complex, reduce cisplatin sensitivity in bladder cancer, implicating the potential therapeutic value of targeting this axis."
item905	REG00006	M6ATAR00067	Up	M6ADIS0070	M6ADRUG0047	34702726	"Circ0008399 bound WTAP to promote formation of the WTAP/METTL3/METTL14 m6A methyltransferase complex, reduce cisplatin sensitivity in bladder cancer, implicating the potential therapeutic value of targeting this axis."
item906	REG00007	M6ATAR00058	Up	M6ADIS0006	.	34703649	"In hepatocellular carcinoma, METTL3 could direct the formation of hsa_circ_0021427 (circHPS5), and specific m6A controlled the accumulation of circHPS5. YTHDC1 facilitated the cytoplasmic output of circHPS5 under m6A modification. CircHPS5 can act as a miR-370 sponge to regulate the expression of HMGA2 and further accelerate hepatocellular carcinoma cell tumorigenesis."
item907	REG00022	M6ATAR00058	Up	M6ADIS0006	.	34703649	"In hepatocellular carcinoma, METTL3 could direct the formation of circHPS5, and specific m6A controlled the accumulation of circHPS5. YTHDC1 facilitated the cytoplasmic output of hsa_circ_0021427 (circHPS5) under m6A modification. CircHPS5 can act as a miR-370 sponge to regulate the expression of HMGA2 and further accelerate hepatocellular carcinoma cell tumorigenesis."
item908	REG00007	M6ATAR00119	.	M6ADIS0006	.	34703649	"In hepatocellular carcinoma, METTL3 could direct the formation of circHPS5, and specific m6A controlled the accumulation of circHPS5. YTHDC1 facilitated the cytoplasmic output of circHPS5 under m6A modification. CircHPS5 can act as a microRNA 370 (MIR370) sponge to regulate the expression of HMGA2 and further accelerate hepatocellular carcinoma cell tumorigenesis."
item909	REG00022	M6ATAR00119	.	M6ADIS0006	.	34703649	"In hepatocellular carcinoma, METTL3 could direct the formation of circHPS5, and specific m6A controlled the accumulation of circHPS5. YTHDC1 facilitated the cytoplasmic output of circHPS5 under m6A modification. CircHPS5 can act as a microRNA 370 (MIR370) sponge to regulate the expression of HMGA2 and further accelerate hepatocellular carcinoma cell tumorigenesis."
item910	REG00007	M6ATAR00276	Up	M6ADIS0006	.	34703649	"In hepatocellular carcinoma, METTL3 could direct the formation of circHPS5, and specific m6A controlled the accumulation of circHPS5. YTHDC1 facilitated the cytoplasmic output of circHPS5 under m6A modification. CircHPS5 can act as a miR-370 sponge to regulate the expression of High mobility group protein HMGI-C (HMGA2) and further accelerate hepatocellular carcinoma cell tumorigenesis."
item911	REG00022	M6ATAR00276	Up	M6ADIS0006	.	34703649	"In hepatocellular carcinoma, METTL3 could direct the formation of circHPS5, and specific m6A controlled the accumulation of circHPS5. YTHDC1 facilitated the cytoplasmic output of circHPS5 under m6A modification. CircHPS5 can act as a miR-370 sponge to regulate the expression of High mobility group protein HMGI-C (HMGA2) and further accelerate hepatocellular carcinoma cell tumorigenesis."
item912	REG00007	M6ATAR00190	Down	M6ADIS0110	.	34706873	"In osteoarthritis METTL3-mediated m6A modification decreased the expression of autophagy-related 7, an E-1 enzyme crucial for the formation of autophagosomes, by attenuating its RNA stability. Silencing METTL3 enhanced autophagic flux and inhibited Ubiquitin-like modifier-activating enzyme ATG7 (ATG7) expression in OA-FLS."
item913	REG00007	M6ATAR00430	Up	M6ADIS0110	.	34706873	"In osteoarthritis METTL3-mediated m6A modification decreased the expression of Thioredoxin (TXN/SASP), an E-1 enzyme crucial for the formation of autophagosomes, by attenuating its RNA stability. Silencing METTL3 enhanced autophagic flux and inhibited SASP expression in OA-FLS."
item914	REG00025	M6ATAR00294	Up	M6ADIS0037	.	34709120	"N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, Interleukin-1 beta (IL1B) and TNF-alpha secretion."
item915	REG00025	M6ATAR00432	Up	M6ADIS0037	.	34709120	"N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and Tumor necrosis factor (TNF/TNF-alpha) secretion."
item916	REG00025	M6ATAR00175	Up	M6ADIS0037	.	34709120	"N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, RAC-alpha serine/threonine-protein kinase (AKT1), and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion."
item917	REG00025	M6ATAR00425	Up	M6ADIS0037	.	34709120	"N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited Transcription factor p65 (RELA), IL-1-beta and TNF-alpha secretion."
item918	REG00025	M6ATAR00327	Up	M6ADIS0037	.	34709120	"N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, Mitogen-activated protein kinase 1 (MAPK/ERK2/MAPK1), AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion."
item919	REG00025	M6ATAR00327	Up	M6ADIS0037	.	34709120	"N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, Mitogen-activated protein kinase 1 (MAPK/ERK2/MAPK1), AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion."
item920	REG00025	M6ATAR00330	Up	M6ADIS0037	.	34709120	"N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated Mitogen-activated protein kinase 14 (p38/MAPK14), ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion."
item921	REG00013	M6ATAR00294	Up	M6ADIS0037	.	34709120	"N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, Interleukin-1 beta (IL1B) and TNF-alpha secretion."
item922	REG00013	M6ATAR00432	Up	M6ADIS0037	.	34709120	"N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and Tumor necrosis factor (TNF/TNF-alpha) secretion."
item923	REG00013	M6ATAR00175	Up	M6ADIS0037	.	34709120	"N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, RAC-alpha serine/threonine-protein kinase (AKT1), and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion."
item924	REG00013	M6ATAR00425	Up	M6ADIS0037	.	34709120	"N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited Transcription factor p65 (RELA), IL-1-beta and TNF-alpha secretion."
item925	REG00013	M6ATAR00328	Up	M6ADIS0037	.	34709120	"N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, Mitogen-activated protein kinase 3 (ERK1/MAPK3), AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion."
item926	REG00013	M6ATAR00327	Up	M6ADIS0037	.	34709120	"N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, Mitogen-activated protein kinase 1 (MAPK/ERK2/MAPK1), AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion."
item927	REG00013	M6ATAR00330	Up	M6ADIS0037	.	34709120	"N6-methyladenosine (m6A) methylation modification is implicated in the pathogenesis of lung ischemia-reperfusion injury. YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated Mitogen-activated protein kinase 14 (p38/MAPK14), ERK1/2, AKT, and NF-Kappa-B pathways in BEAS-2B cells, and inhibited p-p65, IL-1-beta and TNF-alpha secretion."
item928	REG00001	M6ATAR00457	Up	M6ADIS0084	.	34713923	"FTO modification of N6 -methyladenosine is associated with myocardial cell energy metabolism disorder. FTO reduced the m6A level of Sarcoplasmic/endoplasmic reticulum calcium ATPase 2 (SERCA2a/ATP2A2) mRNA through demethylation, thus promoting SERCA2a expression, maintaining calcium homeostasis, and improving energy metabolism of H/R cardiomyocytes."
item929	REG00001	M6ATAR00115	Up	M6ADIS0070	.	34725345	"FTO promoted bladder cancer cell proliferation, migration and invasion via the FTO/microRNA 576 (MIR576)/CDK6 pathways in an m6A-dependent manner."
item930	REG00001	M6ATAR00212	Up	M6ADIS0070	.	34725345	"FTO promoted bladder cancer cell proliferation, migration and invasion via the FTO/miR-576/Cyclin-dependent kinase 6 (CDK6) pathways in an m6A-dependent manner."
item931	REG00007	M6ATAR00192	Down	M6ADIS0002	.	34729106	"m6A modification regulates ATM mRNA metabolism and ATM downstream signaling, which illustrates the importance of m6A modification-related molecules for being used as therapeutic targets in DNA damage-related diseases. METTL3 disrupts the ATM stability via m6A modification, thereby affecting the DNA-damage response."
item932	REG00007	M6ATAR00360	.	M6ADIS0007	.	34734017	"This study revealed that m6A methylation is closely related to the poor prognosis of non-small cell lung cancer patients via interference with the TIME, which suggests that m6A plays a role in optimizing individualized immunotherapy management and improving prognosis. The expression levels of METTL3, FTO and YTHDF1 in non-small cell lung cancer were changed. Patients in Cluster 1 had lower immunoscores, higher Programmed cell death 1 ligand 1 (CD274/PD-L1) expression, and shorter overall survival compared to patients in Cluster 2. The hallmarks of the Myelocytomatosis viral oncogene (MYC) targets, E2 transcription Factor (E2F) targets were significantly enriched."
item933	REG00007	M6ATAR00341	.	M6ADIS0007	.	34734017	"This study revealed that m6A methylation is closely related to the poor prognosis of non-small cell lung cancer patients via interference with the TIME, which suggests that m6A plays a role in optimizing individualized immunotherapy management and improving prognosis. The expression levels of METTL3, FTO and YTHDF1 in non-small cell lung cancer were changed. Patients in Cluster 1 had lower immunoscores, higher programmed death-ligand 1 (PD-L1) expression, and shorter overall survival compared to patients in Cluster 2. The Myc proto-oncogene protein (MYC) targets, E2 transcription Factor (E2F) targets were significantly enriched."
item934	REG00024	M6ATAR00341	.	M6ADIS0007	.	34734017	"This study revealed that m6A methylation is closely related to the poor prognosis of non-small cell lung cancer patients via interference with the TIME, which suggests that m6A plays a role in optimizing individualized immunotherapy management and improving prognosis. The expression levels of METTL3, FTO and YTHDF1 in non-small cell lung cancer were changed. Patients in Cluster 1 had lower immunoscores, higher programmed death-ligand 1 (PD-L1) expression, and shorter overall survival compared to patients in Cluster 2. The Myc proto-oncogene protein (MYC) targets, E2 transcription Factor (E2F) targets were significantly enriched."
item935	REG00001	M6ATAR00341	.	M6ADIS0007	.	34734017	"This study revealed that m6A methylation is closely related to the poor prognosis of non-small cell lung cancer patients via interference with the TIME, which suggests that m6A plays a role in optimizing individualized immunotherapy management and improving prognosis. The expression levels of METTL3, FTO and YTHDF1 in non-small cell lung cancer were changed. Patients in Cluster 1 had lower immunoscores, higher programmed death-ligand 1 (PD-L1) expression, and shorter overall survival compared to patients in Cluster 2. The Myc proto-oncogene protein (MYC) targets, E2 transcription Factor (E2F) targets were significantly enriched."
item936	REG00007	M6ATAR00234	.	M6ADIS0007	.	34734017	"This study revealed that m6A methylation is closely related to the poor prognosis of non-small cell lung cancer patients via interference with the TIME, which suggests that m6A plays a role in optimizing individualized immunotherapy management and improving prognosis. The expression levels of METTL3, FTO and YTHDF1 in non-small cell lung cancer were changed. Patients in Cluster 1 had lower immunoscores, higher programmed death-ligand 1 (PD-L1) expression, and shorter overall survival compared to patients in Cluster 2. The hallmarks of the Myelocytomatosis viral oncogene (MYC) targets, Transcription factor E2F1 (E2F1) targets were significantly enriched."
item937	REG00024	M6ATAR00234	.	M6ADIS0007	.	34734017	"This study revealed that m6A methylation is closely related to the poor prognosis of non-small cell lung cancer patients via interference with the TIME, which suggests that m6A plays a role in optimizing individualized immunotherapy management and improving prognosis. The expression levels of METTL3, FTO and YTHDF1 in non-small cell lung cancer were changed. Patients in Cluster 1 had lower immunoscores, higher programmed death-ligand 1 (PD-L1) expression, and shorter overall survival compared to patients in Cluster 2. The hallmarks of the Myelocytomatosis viral oncogene (MYC) targets, Transcription factor E2F1 (E2F1) targets were significantly enriched."
item938	REG00001	M6ATAR00234	.	M6ADIS0007	.	34734017	"This study revealed that m6A methylation is closely related to the poor prognosis of non-small cell lung cancer patients via interference with the TIME, which suggests that m6A plays a role in optimizing individualized immunotherapy management and improving prognosis. The expression levels of METTL3, FTO and YTHDF1 in non-small cell lung cancer were changed. Patients in Cluster 1 had lower immunoscores, higher programmed death-ligand 1 (PD-L1) expression, and shorter overall survival compared to patients in Cluster 2. The hallmarks of the Myelocytomatosis viral oncogene (MYC) targets, Transcription factor E2F1 (E2F1) targets were significantly enriched."
item939	REG00024	M6ATAR00360	.	M6ADIS0007	.	34734017	"This study revealed that m6A methylation is closely related to the poor prognosis of non-small cell lung cancer patients via interference with the TIME, which suggests that m6A plays a role in optimizing individualized immunotherapy management and improving prognosis. The expression levels of METTL3, FTO and YTHDF1 in non-small cell lung cancer were changed. Patients in Cluster 1 had lower immunoscores, higher Programmed cell death 1 ligand 1 (CD274/PD-L1) expression, and shorter overall survival compared to patients in Cluster 2. The hallmarks of the Myelocytomatosis viral oncogene (MYC) targets, E2 transcription Factor (E2F) targets were significantly enriched."
item940	REG00001	M6ATAR00360	.	M6ADIS0007	.	34734017	"This study revealed that m6A methylation is closely related to the poor prognosis of non-small cell lung cancer patients via interference with the TIME, which suggests that m6A plays a role in optimizing individualized immunotherapy management and improving prognosis. The expression levels of METTL3, FTO and YTHDF1 in non-small cell lung cancer were changed. Patients in Cluster 1 had lower immunoscores, higher Programmed cell death 1 ligand 1 (CD274/PD-L1) expression, and shorter overall survival compared to patients in Cluster 2. The hallmarks of the Myelocytomatosis viral oncogene (MYC) targets, E2 transcription Factor (E2F) targets were significantly enriched."
item941	REG00013	M6ATAR00112	Up	M6ADIS0059	.	34743750	"The critical modulation network underlying m6A readers stabilizes lncRNAs, and they jointly promote mitochondrial energy metabolism in the pathogenesis of colorectal cancer. N6-methyladenosine reader stabilizes the ZFAS1/OLA1 axis. Thus, direct interaction between the KH3-4 domain of IMP2 and ZFAS1 where IMP2 serves as a reader for m6A-modified ZFAS1 and promotes the RNA stability of ZFAS1 is critical for CRC development."
item942	REG00013	M6ATAR00354	Up	M6ADIS0059	.	34743750	"The critical modulation network underlying m6A readers stabilizes lncRNAs, and they jointly promote mitochondrial energy metabolism in the pathogenesis of colorectal cancer. N6-methyladenosine reader stabilizes the ZFAS1/OLA1 axis. Thus, direct interaction between the KH3-4 domain of IMP2 and ZFAS1 where IMP2 serves as a reader for m6A-modified ZFAS1 and promotes the RNA stability of ZFAS1 is critical for CRC development."
item943	REG00009	M6ATAR00167	.	M6ADIS0066	.	34745121	"Putative C->U-editing enzyme APOBEC-4 (APOBEC4) was found to be significantly correlated with m6A regulators such as WTAP, METTL14, ZC3H13, RBM15B, and FMR1. APOBEC3A was identified as a protective factor from comprehensive analyses based on the immune microenvironment and genomic instability of ovarian cancer. APOBEC3A had the potential to serve as a promising prognostic biomarker for foretelling the survival and immunotherapy response of ovarian cancer patients."
item944	REG00006	M6ATAR00167	.	M6ADIS0066	.	34745121	"Putative C->U-editing enzyme APOBEC-4 (APOBEC4) was found to be significantly correlated with m6A regulators such as WTAP, METTL14, ZC3H13, RBM15B, and FMR1. APOBEC3A was identified as a protective factor from comprehensive analyses based on the immune microenvironment and genomic instability of ovarian cancer. APOBEC3A had the potential to serve as a promising prognostic biomarker for foretelling the survival and immunotherapy response of ovarian cancer patients."
item945	REG00026	M6ATAR00167	.	M6ADIS0066	.	34745121	"Putative C->U-editing enzyme APOBEC-4 (APOBEC4) was found to be significantly correlated with m6A regulators such as WTAP, METTL14, ZC3H13, RBM15B, and FMR1. APOBEC3A was identified as a protective factor from comprehensive analyses based on the immune microenvironment and genomic instability of ovarian cancer. APOBEC3A had the potential to serve as a promising prognostic biomarker for foretelling the survival and immunotherapy response of ovarian cancer patients."
item946	REG00021	M6ATAR00167	.	M6ADIS0066	.	34745121	"Putative C->U-editing enzyme APOBEC-4 (APOBEC4) was found to be significantly correlated with m6A regulators such as WTAP, METTL14, ZC3H13, RBM15B, and FMR1. APOBEC3A was identified as a protective factor from comprehensive analyses based on the immune microenvironment and genomic instability of ovarian cancer. APOBEC3A had the potential to serve as a promising prognostic biomarker for foretelling the survival and immunotherapy response of ovarian cancer patients."
item947	REG00029	M6ATAR00167	.	M6ADIS0066	.	34745121	"Putative C->U-editing enzyme APOBEC-4 (APOBEC4) was found to be significantly correlated with m6A regulators such as WTAP, METTL14, ZC3H13, RBM15B, and FMR1. APOBEC3A was identified as a protective factor from comprehensive analyses based on the immune microenvironment and genomic instability of ovarian cancer. APOBEC3A had the potential to serve as a promising prognostic biomarker for foretelling the survival and immunotherapy response of ovarian cancer patients."
item948	REG00007	M6ATAR00225	Down	M6ADIS0107	.	34758326	"The contribution of METTL3-mediated m6A modification of DNA damage-inducible transcript 4 protein (DDIT4) mRNA to macrophage metabolic reprogramming in non-alcoholic fatty liver disease and obesity. In METTL3-deficient macrophages, there is a significant downregulation of mammalian target of rapamycin (mTOR) and nuclear factor Kappa-B (NF-Kappa-B) pathway activity in response to cellular stress and cytokine stimulation, which can be restored by knockdown of DDIT4."
item949	REG00007	M6ATAR00225	Down	M6ADIS0083	.	34758326	"The contribution of METTL3-mediated m6A modification of DNA damage-inducible transcript 4 protein (DDIT4) mRNA to macrophage metabolic reprogramming in non-alcoholic fatty liver disease and obesity. In METTL3-deficient macrophages, there is a significant downregulation of mammalian target of rapamycin (mTOR) and nuclear factor Kappa-B (NF-Kappa-B) pathway activity in response to cellular stress and cytokine stimulation, which can be restored by knockdown of DDIT4."
item950	REG00007	M6ATAR00339	Up	M6ADIS0107	.	34758326	"The contribution of METTL3-mediated m6A modification of Ddit4 mRNA to macrophage metabolic reprogramming in non-alcoholic fatty liver disease and obesity. In METTL3-deficient macrophages, there is a significant downregulation of Serine/threonine-protein kinase mTOR (MTOR) and nuclear factor Kappa-B (NF-Kappa-B) pathway activity in response to cellular stress and cytokine stimulation, which can be restored by knockdown of DDIT4."
item951	REG00007	M6ATAR00054	Up	M6ADIS0083	.	34758326	"The contribution of METTL3-mediated m6A modif ication of Ddit4 mRNA to macrophage metabolic reprogramming in non-alcoholic fatty liver disease and obesity. In METTL3-deficient macrophages, there is a significant downregulation of mammalian target of rapamycin (mTOR) and Nuclear factor NF-kappa-B p105 subunit (NF-Kappa-B/NFKB1) pathway activity in response to cellular stress and cytokine stimulation, which can be restored by knockdown of DDIT4."
item952	REG00007	M6ATAR00339	Up	M6ADIS0107	.	34758326	"The contribution of METTL3-mediated m6A modification of Ddit4 mRNA to macrophage metabolic reprogramming in non-alcoholic fatty liver disease and obesity. In METTL3-deficient macrophages, there is a significant downregulation of Serine/threonine-protein kinase mTOR (MTOR) and nuclear factor Kappa-B (NF-Kappa-B) pathway activity in response to cellular stress and cytokine stimulation, which can be restored by knockdown of DDIT4."
item953	REG00007	M6ATAR00054	Up	M6ADIS0083	.	34758326	"The contribution of Nuclear factor NF-kappa-B p105 subunit (NF-Kappa-B/NFKB1)-mediated m6A modification of Ddit4 mRNA to macrophage metabolic reprogramming in non-alcoholic fatty liver disease and obesity. In METTL3-deficient macrophages, there is a significant downregulation of mammalian target of rapamycin (mTOR) and Nuclear factor NF-kappa-B p105 subunit (NF-Kappa-B/NFKB1) pathway activity in response to cellular stress and cytokine stimulation, which can be restored by knockdown of DDIT4."
item954	REG00005	M6ATAR00435	Up	M6ADIS0048	.	34759347	ALKBH5 promoted multiple myeloma cell growth and survival through TNF receptor-associated factor 1 (TRAF1)-mediated activation of NF-Kappa-B and MAPK signaling pathways.
item955	.	M6ATAR00289	.	M6ADIS0029	M6ADRUG0042	34763233	"In skin cutaneous melanoma, drug sensitivity analysis indicated that the high expression of Interferon-induced 54 kDa protein (IFIT2) was sensitive to dasatinib drug. The expressing levels of IFITs were found to be positively correlated with the level of immune cell infiltrates, immune biomarkers and m6A regulators."
item956	REG00005	M6ATAR00132	.	M6ADIS0059	.	34786052	"ALKBH5 plays an antitumor role in colorectal cancer by modulating the FOXO3/microRNA 21 (MIR21)/SPRY2 axis, which not only suggests a regulatory effect between ALKBH5 and FOXO3, but also provides a new therapeutic direction for colorectal cancer."
item957	REG00005	M6ATAR00260	Down	M6ADIS0059	.	34786052	"ALKBH5 plays an antitumor role in colorectal cancer by modulating the Forkhead box protein O3 (FOXO3)/miR-21/SPRY2 axis, which not only suggests a regulatory effect between ALKBH5 and FOXO3, but also provides a new therapeutic direction for colorectal cancer."
item958	REG00005	M6ATAR00409	Up	M6ADIS0059	.	34786052	"ALKBH5 plays an antitumor role in colorectal cancer by modulating the FOXO3/miR-21/Protein sprouty homolog 2 (SPRY2) axis, which not only suggests a regulatory effect between ALKBH5 and FOXO3, but also provides a new therapeutic direction for colorectal cancer."
item959	REG00008	M6ATAR00140	Down	M6ADIS0010	.	34813676	"In renal cell carcinoma, YTHDF2 accelerated the degradation of Nuclear paraspeckle assembly transcript 1 (NEAT1)_1 by selectively recognizing METTL14-mediated m6A marks on Nuclear paraspeckle assembly transcript 1 (NEAT1)_1."
item960	REG00006	M6ATAR00140	Down	M6ADIS0010	.	34813676	"In renal cell carcinoma, YTHDF2 accelerated the degradation of Nuclear paraspeckle assembly transcript 1 (NEAT1)_1 by selectively recognizing METTL14-mediated m6A marks on Nuclear paraspeckle assembly transcript 1 (NEAT1)_1."
item961	.	.	.	M6ADIS0006	.	34825870	"Discuss the roles of the regulators in the progression and prognosis of hepatocellular carcinoma, and summarize the clinical association between m6A modification and hepatocellular carcinoma, so as to provide more valuable information for clinical treatment."
item962	REG00009	M6ATAR00163	Up	M6ADIS0006	.	34828353	"WTAP/LKB1/AMPK subunit alpha-1 (AMPK/PRKAA1) axis in hepatocellular carcinoma cells acted as a key regulator, linking m6A with autophagy. WTAP-mediated m6A modification plays an important role in the regulation of autophagy in hepatocellular carcinoma cells, which provides a promising target for the treatment of hepatocellular carcinoma."
item963	REG00009	M6ATAR00420	Up	M6ADIS0006	.	34828353	"WTAP/Serine/threonine-protein kinase STK11 (STK11/LKB1)/AMPK axis in hepatocellular carcinoma cells acted as a key regulator, linking m6A with autophagy. WTAP-mediated m6A modification plays an important role in the regulation of autophagy in hepatocellular carcinoma cells, which provides a promising target for the treatment of hepatocellular carcinoma."
item964	REG00020	M6ATAR00342	Down	M6ADIS0059	.	34842457	RBM15 silencing inhibited the CRC growth and metastasis in vitro and in vivo. RBM15 mediated m6A methylation modification of Myeloid differentiation primary response protein MyD88 (MYD88) mRNA in colorectal cancer cells.
item965	REG00006	M6ATAR00470	Down	M6ADIS0109	.	34847358	"METTL14 promotes DNA damage-inducible transcript 3 protein (DDIT3/CHOP) mRNA decay through its 3' UTR N6-methyladenosine (m6A) to inhibit its downstream pro-apoptotic target gene expression, suppress ER proteotoxic liver disease. UPR induces METTL14 expression by competing against the HRD1-ER-associated degradation (ERAD) machinery to block METTL14 ubiquitination and degradation."
item966	.	M6ATAR00083	.	M6ADIS0007	.	34849026	Apoptotic BCL2L1-antisense long non-coding RNA (ABALON) acted as a competing endogenous RNA by sponging miR-139-3p and indirectly regulated the expression of NOB1 in the occurrence of lung cancer.
item967	.	M6ATAR00055	.	M6ADIS0007	.	34849026	ABALON acted as a competing endogenous RNA by sponging hsa-miR-139-3p and indirectly regulated the expression of NOB1 in the occurrence of lung cancer.
item968	.	M6ATAR00350	.	M6ADIS0007	.	34849026	ABALON acted as a competing endogenous RNA by sponging miR-139-3p and indirectly regulated the expression of RNA-binding protein NOB1 (NOB1) in the occurrence of lung cancer.
item969	REG00008	M6ATAR00154	Up	M6ADIS0027	.	34850551	"ALKBH5 mediates KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) expression via an m6A-YTHDF2-dependent manner and KCNQ1OT1 could directly bind to HOXA9 to further regulate the proliferation, invasion and metastasis of laryngeal squamous cell carcinoma cells."
item970	REG00005	M6ATAR00154	Up	M6ADIS0027	.	34850551	"ALKBH5 mediates KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) expression via an m6A-YTHDF2-dependent manner and KCNQ1OT1 could directly bind to HOXA9 to further regulate the proliferation, invasion and metastasis of laryngeal squamous cell carcinoma cells."
item971	REG00005	M6ATAR00082	Up	M6ADIS0061	.	34853296	"ALKBH5-mediated m6A demethylation enhanced the stability of KCNK15-AS1. In pancreatic cancer, KCNK15 and WISP2 antisense RNA 1 (KCNK15-AS1) bound to KCNK15 to inhibit its translation, and interacted with MDM2 to induce REST ubiquitination, which eventually facilitated PTEN transcription to inactivate AKT pathway."
item972	REG00005	M6ATAR00175	.	M6ADIS0061	.	34853296	"ALKBH5-mediated m6A demethylation enhanced the stability of KCNK15-AS1. In pancreatic cancer, KCNK15-AS1 bound to KCNK15 to inhibit its translation, and interacted with MDM2 to induce REST ubiquitination, which eventually facilitated PTEN transcription to inactivate RAC-alpha serine/threonine-protein kinase (AKT1) pathway."
item973	REG00005	M6ATAR00375	.	M6ADIS0061	.	34853296	"ALKBH5-mediated m6A demethylation enhanced the stability of KCNK15-AS1. In pancreatic cancer, KCNK15-AS1 bound to KCNK15 to inhibit its translation, and interacted with MDM2 to induce REST ubiquitination, which eventually facilitated Mutated in multiple advanced cancers 1 (PTEN) transcription to inactivate AKT pathway."
item974	REG00007	M6ATAR00056	Up	M6ADIS0007	.	34858987	METTL3/SNHG1/hsa-miR-140-3p/UBE2C axis plays a crucial role in cancer progression and the immune response in non-small cell lung cancer.
item975	REG00007	M6ATAR00117	Up	M6ADIS0007	.	34858987	METTL3/Small nucleolar RNA host gene 1 (SNHG1)/miR-140-3p/UBE2C axis plays a crucial role in cancer progression and the immune response in non-small cell lung cancer.
item976	REG00022	M6ATAR00449	Down	M6ADIS0001	.	34863175	YTHDC1 inhibited glioma proliferation by reducing the expression of Vacuolar protein-sorting-associated protein 25 (VPS25).
item977	REG00007	M6ATAR00222	Down	M6ADIS0039	.	34863249	"SAM not only played a compensatory role, but also led to m6A modification changes in neural tube development and regulation. Ethionine affected m6A modification by reducing SAM metabolism. METTL3 is enriched in HT-22 cells, and METTL3 knockdown reduces cell proliferation and increases apoptosis through suppressing Wnt/Catenin beta-1 (CTNNB1/Beta-catenin) signaling pathway. Overexpression of ALKBH5 can only inhibit cell proliferation, but cannot promote cell apoptosis."
item978	REG00005	M6ATAR00222	.	M6ADIS0039	.	34863249	"SAM not only played a compensatory role, but also led to m6A modification changes in neural tube development and regulation. Ethionine affected m6A modification by reducing SAM metabolism. METTL3 is enriched in HT-22 cells, and METTL3 knockdown reduces cell proliferation and increases apoptosis through suppressing Wnt/Catenin beta-1 (CTNNB1/Beta-catenin) signaling pathway. Overexpression of ALKBH5 can only inhibit cell proliferation, but cannot promote cell apoptosis."
item979	REG00009	M6ATAR00122	Up	M6ADIS0065	M6ADRUG0022	34866525	LncRNA DLGAP1-AS1 promotes BC ADR-resistance through WTAP/DLGAP1 antisense RNA 1 (DLGAP1-AS1)/miR-299-3p feedback loop in breast cancer.
item980	REG00007	M6ATAR00069	Up	M6ADIS0006	.	34888309	"In hepatocellular carcinoma, hsa_circ_0058493 contained m6A methylation sites and that METTL3 mediated the degree of methylation modification of hsa_circ_0058493. YTHDC1 could bind to hsa_circ_0058493 and promote its intracellular localization from the nucleus to the cytoplasm."
item981	REG00022	M6ATAR00069	Up	M6ADIS0006	.	34888309	"In hepatocellular carcinoma, hsa_circ_0058493 contained m6A methylation sites and that METTL3 mediated the degree of methylation modification of hsa_circ_0058493. YTHDC1 could bind to hsa_circ_0058493 and promote its intracellular localization from the nucleus to the cytoplasm."
item982	REG00006	M6ATAR00288	Down	M6ADIS0055	.	34900689	"The study identified the mechanism by which rapamycin affects autophagy via regulating METTL14, which provides a new idea for a potential targeted therapy for oral squamous cell carcinoma. METTL14 mediated Eukaryotic translation initiation factor 4 gamma 1 (EIF4G1) expression via m6A modification and regulated autophagy levels and biological functions in oral squamous cell carcinoma."
item983	REG00008	.	.	M6ADIS0006	.	34900723	"In hepatocellular carcinoma, CASC11 decreased UBE2T N6-methyladenosine (m6A) level via recruiting ALKBH5. CASC11 inhibited the association between UBE2T mRNA and m6A reader protein YTHDF2."
item984	REG00005	.	.	M6ADIS0006	.	34900723	"In hepatocellular carcinoma, CASC11 decreased UBE2T N6-methyladenosine (m6A) level via recruiting ALKBH5. CASC11 inhibited the association between UBE2T mRNA and m6A reader protein YTHDF2."
item985	.	M6ATAR00429	.	M6ADIS0112	M6ADRUG0027	34902811	"In rheumatoid arthritis fibroblast-like synoviocytes, m6A methylation-mediated gene Protein-glutamine gamma-glutamyltransferase 2 (TGM2) served as a promoter of RA-FLS proliferation by inducing DNA replication and cell cycle transition and inhibiting apoptosis through activating NF-Kappa-B signaling. TGM2 can be an attractive target and Sar was a novel anti-RA drug."
item986	REG00023	.	.	.	.	34910909	YTHDC2 regulates the pachytene stage by perpetuating a meiotic transcriptome and preventing microtubule network changes that could lead to telomere clustering.
item987	REG00009	M6ATAR00374	Down	M6ADIS0017	M6ADRUG0026	34921949	"AcSDKP in liver fibrosis via m6A modification and Hedgehog pathway, which helps us to shed light on the molecular mechanism in liver fibrosis progression. WTAP targeted the 3'-UTR of Protein patched homolog 1 (PTCH1) mRNA, and administration of AcSDKP reduced the stability of Ptch1 mRNA."
item988	REG00001	.	.	M6ADIS0010	.	34921979	MicroRNA 155 is overexpressed in renal cell carcinoma and functions as an oncogenic role by repressing the FTO expression and increased m6A level.
item989	REG00011	M6ATAR00479	.	M6ADIS0068	.	23435425	"ELF3 is a member of the ETS family of transcription factors, is a repressor of Androgen receptor (AR) transcriptional activity. Modulation of ELF3 expression and/or AR/ELF3 interaction has utility in the treatment of PC."
item990	REG00011	M6ATAR00396	.	M6ADIS0117	.	31150422	"Elf3 plays an important role in the process of phenotypic alterations of podocyte induced by the activation of TGF-beta signals. Elf3 protein levels in patients with DN (R2 = 0.7259) were useful as an early non-invasive marker for podocyte injuries in DN. The epithelium-specific transcription factor, Elf3 was induced by AGE stimulation and, subsequently, upregulated RII expression in cultured podocytes. Induction of Elf3 and activation of RII-Mothers against decapentaplegic homolog 3 (SMAD3) signaling, leading to a decrease in WT1 expression, were observed in podocytes in diabetic human kidneys."
item991	REG00011	M6ATAR00480	.	M6ADIS0117	.	31150422	"Elf3 plays an important role in the process of phenotypic alterations of podocyte induced by the activation of TGF-beta signals. Elf3 protein levels in patients with DN (R2 = 0.7259) were useful as an early non-invasive marker for podocyte injuries in DN. The epithelium-specific transcription factor, Elf3 was induced by AGE stimulation and, subsequently, upregulated RII expression in cultured podocytes. Induction of Elf3 and activation of RII-Smad3 signaling, leading to a decrease in Wilms tumor protein (WT1) expression, were observed in podocytes in diabetic human kidneys."
item992	REG00018	.	.	M6ADIS0065	.	33357433	METTL5 expression is elevated in breast cancer patient samples and is required for growth of several breast cancer cell lines.
item993	REG00018	M6ATAR00481	Up	M6ADIS0067	.	35166644	"Knocking down METTL5 could significantly activate apoptosis and inhibit endometrial carcinoma(EC) development via MMR administration.METTL5 expression in UCEC tumor tissue was increased, and UCEC patients with high METTL5 expression had worse prognostic outcomes. METTL5 knockdown induced the DNA mismatch repair protein Msh2 (MSH2), MSH6 and PMS2 expression in MMR."
item994	REG00018	M6ATAR00482	Up	M6ADIS0067	.	35166644	"Knocking down METTL5 could significantly activate apoptosis and inhibit endometrial carcinoma(EC) development via MMR administration.METTL5 expression in UCEC tumor tissue was increased, and UCEC patients with high METTL5 expression had worse prognostic outcomes. METTL5 knockdown induced the MSH2, DNA mismatch repair protein Msh6 (MSH6) and PMS2 expression in MMR."
item995	REG00018	M6ATAR00483	Up	M6ADIS0067	.	35166644	"Knocking down METTL5 could significantly activate apoptosis and inhibit endometrial carcinoma(EC) development via MMR administration.METTL5 expression in UCEC tumor tissue was increased, and UCEC patients with high METTL5 expression had worse prognostic outcomes. METTL5 knockdown induced the MSH2, MSH6 and Mismatch repair endonuclease PMS2 (PMS2) expression in MMR."
item996	REG00019	M6ATAR00484	Up	M6ADIS0001	.	35064112	This study NKAP knockdown induced cell death in glioblastoma cells. NKAP acted as a new ferroptosis suppressor by binding to m6A and then promoting Cystine/glutamate transporter (SLC7A11) mRNA splicing and maturation.
item997	REG00007	M6ATAR00485	.	M6ADIS0007	M6ADRUG0090	35070958	"The participation of Metformin decreased the bindings of DNMT3a/b to the METTL3 promoter with the help of the readers of NKAP and HNRNPA2B1.the mediation of m6A formation on pri-Let-7b processing increased the mature microRNA let-7b (MIRLET7B), whose key role is to suppress the Notch signaling and to re-captivate the Osimertinib treatment.The findings open up future drug development, targeting this pathway for lung cancer patients."
item998	REG00019	M6ATAR00485	.	M6ADIS0007	M6ADRUG0007	35070958	"The participation of Metformin decreased the bindings of DNMT3a/b to the METTL3 promoter with the help of the readers of NKAP and HNRNPA2B1.the mediation of m6A formation on pri-Let-7b processing increased the mature microRNA let-7b (MIRLET7B), whose key role is to suppress the Notch signaling and to re-captivate the Osimertinib treatment.The findings open up future drug development, targeting this pathway for lung cancer patients."
item999	REG00004	M6ATAR00485	.	M6ADIS0007	M6ADRUG0007	35070958	"The participation of Metformin decreased the bindings of DNMT3a/b to the METTL3 promoter with the help of the readers of NKAP and HNRNPA2B1.the mediation of m6A formation on pri-Let-7b processing increased the mature microRNA let-7b (MIRLET7B), whose key role is to suppress the Notch signaling and to re-captivate the Osimertinib treatment.The findings open up future drug development, targeting this pathway for lung cancer patients."
item1000	REG00030	M6ATAR00486	.	M6ADIS0053	.	32642286	"IGFBP3 was shown to function as a suppressor of invasion in epithelial ovarian cancer (EOC). IGFBP3 could activate Thrombospondin-1 (THBS1) through promoter regulation mainly via an intracellular signaling pathway, such angiogenesis-regulating ability represents a major function of IGFBP3 as an onco-suppressor in the pathogenesis of ovarian cancer."
item1001	REG00030	M6ATAR00341	.	M6ADIS0001	.	33023892	"YTHDF2 depletion downregulated IGFBP3 mRNA and protein levels, without affecting its mRNA stability. YTHDF2 regulated IGFBP3 levels via Myc proto-oncogene protein (MYC) in glioblastoma stem cells."
item1002	REG00030	M6ATAR00291	.	M6ADIS0007	M6ADRUG0047	28330997	Overexpression of IGFBP3 induced apoptosis and enhanced cisplatin response in vitro and confirmed that the suppression is in part by blocking Insulin-like growth factor I (IGF1) signaling. IGFBP3 is effective in lung cancer cells with high IGF1 signaling activity and imply that relevant biomarkers are essential in selecting lung cancer patients for IGF1-targeted therapy.
item1003	REG00030	M6ATAR00487	.	M6ADIS0051	.	33188835	Higher IGFBP-3 levels in osteosarcoma tissue compared with normal healthy tissue. IGFBP-3 treatment of two human osteosarcoma cell lines promoted cell migration and upregulated levels of Vascular cell adhesion protein 1 (VCAM1) expression via PI3K/Akt and AP-1 signaling.
item1004	REG00031	M6ATAR00451	Up	M6ADIS0007	.	32106857	YTHDF1 promoted Transcriptional coactivator YAP1 (YAP1) mRNA translation by interacting with eIF3a in NSCLC.
item1005	REG00031	.	.	M6ADIS0007	.	34648968	"The eIF3A R803K mutation promotes small cell lung cancer chemotherapy resistance by inducing senescence. Furthermore, a senolytic drug, fisetin, can reverse chemotherapy resistance mediated by the eIF3A R803K mutation."
item1006	REG00031	M6ATAR00488	.	M6ADIS0132	.	29286129	Pregulation of eIF3a mRNA and protein and in human keloid tissues compared with in normal tissues. Knockdown of eIF3a inhibited KF proliferation induced by Transforming growth factor beta-1 proprotein (TGFB1).
item1007	REG00032	.	.	M6ADIS0133	.	21191016	CBLL1 acts in concert with the ubiquitin proteasome system to mediate West Nile virus (WNV) infection internalization.
item1008	REG00032	.	.	M6ADIS0002	.	34764728	KIF26B elevates m6A RNA methylation via enhancing ZC3H13/CBLL1 nuclear localization. KIF26B-SRF forms a positive feedback loop facilitating tumor growth.
item1009	REG00032	M6ATAR00334	.	M6ADIS0007	.	31124298	"CBLL1 was frequently upregulated in non-small lung cancer (NSCLC) tissues compared to the adjacent nontumor tissues. CBLL1 knockdown inhibited cell invasion via increased E-cadherin protein expression, and decreased expression of 72 kDa type IV collagenase (MMP2) and MMP9 in NSCLC cell lines."
item1010	REG00032	M6ATAR00335	.	M6ADIS0007	.	31124298	"CBLL1 was frequently upregulated in non-small lung cancer (NSCLC) tissues compared to the adjacent nontumor tissues. CBLL1 knockdown inhibited cell invasion via increased E-cadherin protein expression, and decreased expression of MMP2 and Matrix metalloproteinase-9 (MMP9) in NSCLC cell lines."
item1011	REG00033	.	Up	M6ADIS0006	.	30737498	"ZCCHC4 protein is overexpressed in hepatocellular carcinoma tumors, and ZCCHC4 knockout significantly reduces tumor size in a xenograft mouse model."
item1012	REG00007	M6ATAR00171	Down	M6ADIS0001	M6ADRUG0076	28297667	"Knockdown of METTL3 or METTL14 induced changes in mRNA m6A enrichment and altered mRNA expression of genes (e.g., Meltrin-beta (ADAM19)) with critical biological functions in GSCs. Treatment with <span>MA2, a chemical inhibitor of FTO, dramatically suppressed GSC-induced tumorigenesis and prolonged lifespan in GSC-grafted animals."
item1013	REG00006	M6ATAR00171	Down	M6ADIS0001	M6ADRUG0076	28297667	"Knockdown of METTL3 or METTL14 induced changes in mRNA m6A enrichment and altered mRNA expression of genes (e.g., Meltrin-beta (ADAM19)) with critical biological functions in GSCs. Treatment with <span>MA2, a chemical inhibitor of FTO, dramatically suppressed GSC-induced tumorigenesis and prolonged lifespan in GSC-grafted animals."
item1014	REG00001	.	.	M6ADIS0083	.	29771336	"FTO fails to bind to its own promoter that promotes FTO expression in the hypothalamus of high-fat diet-induced obese and 48-h fasting mice, suggesting a disruption of the stable expression of this gene.ketogenic diet-derived ketone body <span>beta-hydroxybutyrate (BHB) transiently increases FTO expression in both mouse hypothalamus and cultured cells."
item1015	REG00001	.	.	M6ADIS0095	M6ADRUG0076	29875633	"<span>MA2, which is a highly selective inhibitor of FTO, has a protective effect and improves the viability of HEI-OC1 cells after <span>cisplatin treatment, and they provide new insights into potential therapeutic targets for the amelioration of cisplatin-induced ototoxicity."
item1016	REG00001	M6ATAR00410	Down	.	M6ADRUG0044	30046135	"The m6A changes caused by FTO influence the stability of ULK1 transcripts, likely through a YTHDF2-dependent manner.Under both basal and <span>rapamycin-induced autophagy conditions, depletion of FTO significantly reduced the formation of GFP-LC3B puncta. The level of Sequestosome-1 (SQSTM1)/SQSTM1 (an autophagy substrate) was higher in FTO-knockdown cells than that in control cells. FTO specifically upregulates the ULK1 protein abundance. ULK1 mRNA undergoes m6A modification in the 3'-UTR and the m6A-marked ULK1 transcripts can further be targeted for degradation by YTHDF2."
item1017	REG00001	M6ATAR00444	Up	.	M6ADRUG0044	30046135	"The m6A changes caused by FTO influence the stability of ULK1 transcripts, likely through a YTHDF2-dependent manner.Under both basal and <span>rapamycin-induced autophagy conditions, depletion of FTO significantly reduced the formation of GFP-LC3B puncta. The level of p62/SQSTM1 (an autophagy substrate) was higher in FTO-knockdown cells than that in control cells. FTO specifically upregulates the Serine/threonine-protein kinase ULK1 (ULK1) protein abundance. ULK1 mRNA undergoes m6A modification in the 3'-UTR and the m6A-marked ULK1 transcripts can further be targeted for degradation by YTHDF2."
item1018	REG00008	M6ATAR00444	Up	.	M6ADRUG0044	30046135	"The m6A changes caused by FTO influence the stability of ULK1 transcripts, likely through a YTHDF2-dependent manner.Under both basal and <span>rapamycin-induced autophagy conditions, depletion of FTO significantly reduced the formation of GFP-LC3B puncta. The level of p62/SQSTM1 (an autophagy substrate) was higher in FTO-knockdown cells than that in control cells. FTO specifically upregulates the Serine/threonine-protein kinase ULK1 (ULK1) protein abundance. ULK1 mRNA undergoes m6A modification in the 3'-UTR and the m6A-marked ULK1 transcripts can further be targeted for degradation by YTHDF2."
item1019	REG00001	.	.	M6ADIS0046	.	30991027	FTO is a druggable target and that targeting FTO by small-molecule inhibitors<span>(FB23 and FB23-2) holds potential to treat acute myeloid leukemia.
item1020	REG00001	.	.	M6ADIS0046	.	30991027	FTO is a druggable target and that targeting FTO by small-molecule inhibitors<span>(FB23 and FB23-2) holds potential to treat acute myeloid leukemia.
item1021	REG00015	M6ATAR00209	Up	M6ADIS0065	M6ADRUG0005	31285549	KIAA1429 acts as an oncogenic factor in breast cancer by regulating CDK1 in an N6-methyladenosine-independent manner.<span>5'-fluorouracil was found to be very effective in reducing the expression of KIAA1429 and Cyclin-dependent kinase 1 (CDK1) in breast cancer.
item1022	REG00006	.	.	M6ADIS0085	M6ADRUG0039	31369074	"METTL14 deficiency in beta-cells induces glucose intolerance and a decrease in insulin secretion.To define the role of m6A in regulating the beta-cell function, the study generated beta-cell METTL14-specific knockout (beta-KO) mice by <span>tamoxifen administration. beta-cell mass in beta-KO mice was related to beta-cell proliferation and also observed elevated mRNA and protein levels of Ire1-alpha and sXBP-1 in beta-KO islets."
item1023	REG00008	M6ATAR00293	Down	M6ADIS0006	.	31735169	YTHDF2 processed the decay of m6A-containing Interleukin-11 (IL11) and serpin family E member 2 (SERPINE2) mRNAs. YTHDF2 transcription succumbed to hypoxia-inducible factor-2-alpha (HIF-2-alpha). Administration of a HIF-2-alpha antagonist <span>(PT2385) restored YTHDF2-programed epigenetic machinery and repressed liver cancer.
item1024	REG00008	M6ATAR00266	Down	M6ADIS0006	.	31735169	YTHDF2 processed the decay of m6A-containing interleukin 11 (IL11) and Glia-derived nexin (SERPINE2) mRNAs. YTHDF2 transcription succumbed to hypoxia-inducible factor-2-alpha (HIF-2-alpha). Administration of a HIF-2-alpha antagonist <span>(PT2385) restored YTHDF2-programed epigenetic machinery and repressed liver cancer.
item1025	REG00001	M6ATAR00348	Up	M6ADIS0130	.	31923814	"<span>DEHP worsened testicular histology, decreased testosterone concentrations, downregulated expression of spermatogenesis inducers, enhanced oxidative stress, inhibited the Nuclear factor erythroid 2-related factor 2 (NFE2L2)-mediated antioxidant pathway, and increased apoptosis in testes. DEHP is a common environmental endocrine disrupting chemical that induces male reproductive disorders. Additionally, DEHP increased global levels of m6A RNA modification and altered the expression of two important RNA methylation modulator genes, FTO and YTHDC2."
item1026	REG00023	M6ATAR00348	.	M6ADIS0130	.	31923814	"<span>DEHP worsened testicular histology, decreased testosterone concentrations, downregulated expression of spermatogenesis inducers, enhanced oxidative stress, inhibited the Nuclear factor erythroid 2-related factor 2 (NFE2L2)-mediated antioxidant pathway, and increased apoptosis in testes. DEHP is a common environmental endocrine disrupting chemical that induces male reproductive disorders. Additionally, DEHP increased global levels of m6A RNA modification and altered the expression of two important RNA methylation modulator genes, FTO and YTHDC2."
item1027	REG00007	M6ATAR00325	Up	M6ADIS0072	.	32017066	"METTL3-mediated m6A RNA methylation modulates uveal melanoma cell proliferation, migration, and invasion by targeting Hepatocyte growth factor receptor (c-Met/MET). <span>Cycloleucine (Cyc) was used to block m6 A methylation in UM cells."
item1028	.	.	.	M6ADIS0042	.	32294948	Regulation of <span>resveratrol is essential for the inhibition of AFB1-induced oxidative stress and liver injury. The objective of this study was to investigate the effects of AFB1 and resveratrol in m6A RNA methylation and their crosstalk in the regulation of hepatic function in mice.
item1029	.	.	.	M6ADIS0042	.	32294948	Regulation of resveratrol is essential for the inhibition of AFB1-induced oxidative stress and liver injury. The objective of this study was to investigate the effects of <span>AFB1 and resveratrol in m6A RNA methylation and their crosstalk in the regulation of hepatic function in mice.
item1030	REG00007	M6ATAR00249	Up	M6ADIS0007	.	32373962	"<span>Simvastatin induces METTL3 down-regulation in lung cancer tissues, which further influences EMT via m6A modification on Histone-lysine N-methyltransferase EZH2 (EZH2) mRNA and thus inhibits the malignant progression of lung cancer."
item1031	REG00020	M6ATAR00023	Down	M6ADIS0109	M6ADRUG0044	32518161	"Mammalian target of rapamycin complex 1 (mTORC1) pathway is highly activated in rbm15-deficient hepatocytes. <span>Rapamycin treatment partially restored normal hepatic gene expression as well as the nuclear location of the transcription factor Hnf4a. Taken together, these results reveal an unexpected role of Rbm15 in liver maturation."
item1032	REG00001	M6ATAR00316	Down	M6ADIS0046	.	32531268	"Genetic depletion and pharmacological inhibition of FTO dramatically attenuate leukemia stem/initiating cell self-renewal and reprogram immune response by suppressing expression of immune checkpoint genes, especially Leukocyte immunoglobulin-like receptor subfamily B member 4 (LILRB4). FTO inhibitors, such as <span>rhein, meclofenamic acid (MA), MO-I-500, fluorescein, and R-2HG, can inhibit acute myeloid leukemia cell viability. CS1 and CS2 displayed a much higher efficacy in inhibiting AML cell viability."
item1033	REG00001	M6ATAR00316	Down	M6ADIS0046	M6ADRUG0006	32531268	"Genetic depletion and pharmacological inhibition of FTO dramatically attenuate leukemia stem/initiating cell self-renewal and reprogram immune response by suppressing expression of immune checkpoint genes, especially Leukocyte immunoglobulin-like receptor subfamily B member 4 (LILRB4). FTO inhibitors, such as rhein, <span>meclofenamic acid (MA), MO-I-500, fluorescein, and R-2HG, can inhibit acute myeloid leukemia cell viability. CS1 and CS2 displayed a much higher efficacy in inhibiting AML cell viability."
item1034	REG00001	M6ATAR00316	Down	M6ADIS0046	.	32531268	"Genetic depletion and pharmacological inhibition of FTO dramatically attenuate leukemia stem/initiating cell self-renewal and reprogram immune response by suppressing expression of immune checkpoint genes, especially Leukocyte immunoglobulin-like receptor subfamily B member 4 (LILRB4). FTO inhibitors, such as rhein, meclofenamic acid (MA), <span>MO-I-500, fluorescein, and R-2HG, can inhibit acute myeloid leukemia cell viability. CS1 and CS2 displayed a much higher efficacy in inhibiting AML cell viability."
item1035	REG00001	M6ATAR00316	Down	M6ADIS0046	.	32531268	"Genetic depletion and pharmacological inhibition of FTO dramatically attenuate leukemia stem/initiating cell self-renewal and reprogram immune response by suppressing expression of immune checkpoint genes, especially Leukocyte immunoglobulin-like receptor subfamily B member 4 (LILRB4). FTO inhibitors, such as rhein, meclofenamic acid (MA), MO-I-500, <span>fluorescein, and R-2HG, can inhibit acute myeloid leukemia cell viability. CS1 and CS2 displayed a much higher efficacy in inhibiting AML cell viability."
item1036	REG00001	M6ATAR00316	Down	M6ADIS0046	M6ADRUG0066	32531268	"Genetic depletion and pharmacological inhibition of FTO dramatically attenuate leukemia stem/initiating cell self-renewal and reprogram immune response by suppressing expression of immune checkpoint genes, especially Leukocyte immunoglobulin-like receptor subfamily B member 4 (LILRB4). FTO inhibitors, such as rhein, meclofenamic acid (MA), MO-I-500, fluorescein, and <span>R-2HG, can inhibit acute myeloid leukemia cell viability. CS1 and CS2 displayed a much higher efficacy in inhibiting AML cell viability."
item1037	REG00001	M6ATAR00316	Down	M6ADIS0046	.	32531268	"Genetic depletion and pharmacological inhibition of FTO dramatically attenuate leukemia stem/initiating cell self-renewal and reprogram immune response by suppressing expression of immune checkpoint genes, especially Leukocyte immunoglobulin-like receptor subfamily B member 4 (LILRB4). FTO inhibitors, such as rhein, meclofenamic acid (MA), MO-I-500, fluorescein, and R-2HG, can inhibit acute myeloid leukemia cell viability. CS1 and <span>CS2 displayed a much higher efficacy in inhibiting AML cell viability."
item1038	REG00001	M6ATAR00316	Down	M6ADIS0046	.	32531268	"Genetic depletion and pharmacological inhibition of FTO dramatically attenuate leukemia stem/initiating cell self-renewal and reprogram immune response by suppressing expression of immune checkpoint genes, especially Leukocyte immunoglobulin-like receptor subfamily B member 4 (LILRB4). FTO inhibitors, such as rhein, meclofenamic acid (MA), MO-I-500, fluorescein, and R-2HG, can inhibit acute myeloid leukemia cell viability. <span>CS1 and CS2 displayed a much higher efficacy in inhibiting AML cell viability."
item1039	REG00005	M6ATAR00141	Up	M6ADIS0025	.	32656611	"ALKBH5 could up-regulate Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) expression by demethylation. Furthermore, <span>dexmedetomidine inhibited the expression of ALKBH5 in LPS-treated HK-2 cells. Dexmedetomidine suppressed the biological behavior of HK-2 cells treated with LPS by inhibiting the expression of ALKBH5 in vitro, which provides potential targets for the prevention and treatment of sepsis-induced kidney injury. Dexmedetomidine suppressed the biological behavior of HK-2 cells treated with LPS by inhibiting the expression of ALKBH5 in vitro, which provides potential targets for the prevention and treatment of sepsis-induced kidney injury."
item1040	REG00007	M6ATAR00175	Up	M6ADIS0056	.	32825955	"METTL3 plays a carcinogenic role in human EC progression partially through RAC-alpha serine/threonine-protein kinase (AKT1) signaling pathways, suggesting that METTL3 serves as a potential therapeutic target for esophageal cancer therapy. A <span>double-effect inhibitor (BEZ235) inhibited AKT and mTOR phosphorylation and hindered the effect of METTL3 overexpression on the proliferation and migration of Eca-109 and KY-SE150 cells."
item1041	REG00001	.	.	M6ADIS0034	.	33010548	The inhibition of FTO-mediated up-regulation of m6A could be involved in MEHP-induced Leydig cell apoptosis.
item1042	REG00008	M6ATAR00341	Up	M6ADIS0001	M6ADRUG0099	33023892	"The m6A reader YTHDF2 stabilized Myc proto-oncogene protein (MYC) mRNA specifically in cancer stem cells. Given the challenge of targeting MYC, YTHDF2 presents a therapeutic target to perturb MYC signaling in glioblastoma. The IGF1/IGF1R inhibitor <span>linsitinib preferentially targeted YTHDF2-expressing cells, inhibiting GSC viability without affecting NSCs and impairing in vivo glioblastoma growth. YTHDF2 links RNA epitranscriptomic modifications and GSC growth, laying the foundation for the YTHDF2-MYC-IGFBP3 axis as a specific and novel therapeutic target in glioblastoma."
item1043	REG00014	M6ATAR00341	Up	M6ADIS0001	M6ADRUG0099	33023892	"The m6A reader YTHDF2 stabilized Myc proto-oncogene protein (MYC) mRNA specifically in cancer stem cells. Given the challenge of targeting MYC, YTHDF2 presents a therapeutic target to perturb MYC signaling in glioblastoma. The IGF1/IGF1R inhibitor <span>linsitinib preferentially targeted YTHDF2-expressing cells, inhibiting GSC viability without affecting NSCs and impairing in vivo glioblastoma growth. YTHDF2 links RNA epitranscriptomic modifications and GSC growth, laying the foundation for the YTHDF2-MYC-IGFBP3 axis as a specific and novel therapeutic target in glioblastoma."
item1044	REG00007	M6ATAR00358	Up	M6ADIS0011	M6ADRUG0044	33090698	METTL3 promotes the progression of retinoblastoma through Phosphatidylinositol 3-kinase regulatory subunit beta (PI3K-p85/PIK3R2)/AKT/mTOR pathways in vitro and in vivo. METTL3 has an impact on the PI3K-AKT-mTOR-P70S6K/4EBP1 pathway. The cell proliferation results show that the stimulatory function of METTL3 is lost after <span>rapamycin treatment.
item1045	REG00007	M6ATAR00175	Up	M6ADIS0011	M6ADRUG0044	33090698	METTL3 promotes the progression of retinoblastoma through PI3K/RAC-alpha serine/threonine-protein kinase (AKT1)/mTOR pathways in vitro and in vivo. METTL3 has an impact on the PI3K-AKT-mTOR-P70S6K/4EBP1 pathway. The cell proliferation results show that the stimulatory function of METTL3 is lost after <span>rapamycin treatment.
item1046	REG00007	M6ATAR00339	Up	M6ADIS0011	M6ADRUG0044	33090698	METTL3 promotes the progression of retinoblastoma through PI3K/AKT/Serine/threonine-protein kinase mTOR (MTOR) pathways in vitro and in vivo. METTL3 has an impact on the PI3K-AKT-mTOR-P70S6K/4EBP1 pathway. The cell proliferation results show that the stimulatory function of METTL3 is lost after <span>rapamycin treatment.
item1047	REG00007	M6ATAR00313	Up	M6ADIS0011	M6ADRUG0044	33090698	METTL3 promotes the progression of retinoblastoma through PI3K/AKT/mTOR pathways in vitro and in vivo. METTL3 has an impact on the PI3K-AKT-mTOR-Ribosomal protein S6 kinase beta-1 (RPS6KB1/p70S6K)/4EBP1 pathway. The cell proliferation results show that the stimulatory function of METTL3 is lost after <span>rapamycin treatment.
item1048	REG00007	M6ATAR00159	Down	M6ADIS0011	M6ADRUG0044	33090698	METTL3 promotes the progression of retinoblastoma through PI3K/AKT/mTOR pathways in vitro and in vivo. METTL3 has an impact on the PI3K-AKT-mTOR-P70S6K/eIF4E-binding protein 1 (4EBP1/EIF4EBP1) pathway. The cell proliferation results show that the stimulatory function of METTL3 is lost after <span>rapamycin treatment.
item1049	.	M6ATAR00356	.	M6ADIS0058	.	33205006	"Colon cancer cell lines, either WiDr homozygous for missense-mutated Cellular tumor antigen p53 (TP53/p53) (R273H) or SW48/TP53-Dox bearing heterozygous TP53 mutant (R273H), display drug resistance with increased ceramide glycosylation. Increased Gb3-cSrc complex in GEMs of membranes in response to anticancer drug induced cell stress promotes expression of p53 mutant proteins and accordant cancer drug resistance. <span>Genz-161 effectively inhibited GCS activity, and substantially suppressed the elevated Gb3 levels seen in GEMs of p53-mutant cells exposed to doxorubicin."
item1050	REG00001	M6ATAR00196	.	M6ADIS0065	.	33505967	"Studies of the aberrant expression of m6A mediators in breast cancer revealed that they were associated with different BC subtypes and functions, such as proliferation, apoptosis, stemness, the cell cycle, migration, and metastasis, through several factors and signaling pathways, such as Apoptosis regulator Bcl-2 (BCL2) and the PI3K/Akt pathway, among others. Fat mass and obesity-associated protein (FTO) was identified as the first m6A demethylase, and a series of <span>inhibitors that target FTO were reported to have potential for the treatment of BC by inhibiting cell proliferation and promoting apoptosis."
item1051	REG00001	M6ATAR00196	.	M6ADIS0065	.	33505967	"Studies of the aberrant expression of m6A mediators in breast cancer revealed that they were associated with different BC subtypes and functions, such as proliferation, apoptosis, stemness, the cell cycle, migration, and metastasis, through several factors and signaling pathways, such as Apoptosis regulator Bcl-2 (BCL2) and the PI3K/Akt pathway, among others. Fat mass and obesity-associated protein (FTO) was identified as the first m6A demethylase, and a series of <span>inhibitors that target FTO were reported to have potential for the treatment of BC by inhibiting cell proliferation and promoting apoptosis."
item1052	REG00001	M6ATAR00196	.	M6ADIS0065	.	33505967	"Studies of the aberrant expression of m6A mediators in breast cancer revealed that they were associated with different BC subtypes and functions, such as proliferation, apoptosis, stemness, the cell cycle, migration, and metastasis, through several factors and signaling pathways, such as Apoptosis regulator Bcl-2 (BCL2) and the PI3K/Akt pathway, among others. Fat mass and obesity-associated protein (FTO) was identified as the first m6A demethylase, and a series of <span>inhibitors that target FTO were reported to have potential for the treatment of BC by inhibiting cell proliferation and promoting apoptosis."
item1053	REG00001	M6ATAR00196	.	M6ADIS0065	M6ADRUG0066	33505967	"Studies of the aberrant expression of m6A mediators in breast cancer revealed that they were associated with different BC subtypes and functions, such as proliferation, apoptosis, stemness, the cell cycle, migration, and metastasis, through several factors and signaling pathways, such as Apoptosis regulator Bcl-2 (BCL2) and the PI3K/Akt pathway, among others. Fat mass and obesity-associated protein (FTO) was identified as the first m6A demethylase, and a series of <span>inhibitors that target FTO were reported to have potential for the treatment of BC by inhibiting cell proliferation and promoting apoptosis."
item1054	REG00001	M6ATAR00196	.	M6ADIS0065	.	33505967	"Studies of the aberrant expression of m6A mediators in breast cancer revealed that they were associated with different BC subtypes and functions, such as proliferation, apoptosis, stemness, the cell cycle, migration, and metastasis, through several factors and signaling pathways, such as Apoptosis regulator Bcl-2 (BCL2) and the PI3K/Akt pathway, among others. Fat mass and obesity-associated protein (FTO) was identified as the first m6A demethylase, and a series of <span>inhibitors that target FTO were reported to have potential for the treatment of BC by inhibiting cell proliferation and promoting apoptosis."
item1055	REG00001	M6ATAR00196	.	M6ADIS0065	M6ADRUG0006	33505967	"Studies of the aberrant expression of m6A mediators in breast cancer revealed that they were associated with different BC subtypes and functions, such as proliferation, apoptosis, stemness, the cell cycle, migration, and metastasis, through several factors and signaling pathways, such as Apoptosis regulator Bcl-2 (BCL2) and the PI3K/Akt pathway, among others. Fat mass and obesity-associated protein (FTO) was identified as the first m6A demethylase, and a series of <span>inhibitors that target FTO were reported to have potential for the treatment of BC by inhibiting cell proliferation and promoting apoptosis."
item1056	REG00001	M6ATAR00196	.	M6ADIS0065	.	33505967	"Studies of the aberrant expression of m6A mediators in breast cancer revealed that they were associated with different BC subtypes and functions, such as proliferation, apoptosis, stemness, the cell cycle, migration, and metastasis, through several factors and signaling pathways, such as Apoptosis regulator Bcl-2 (BCL2) and the PI3K/Akt pathway, among others. Fat mass and obesity-associated protein (FTO) was identified as the first m6A demethylase, and a series of <span>inhibitors that target FTO were reported to have potential for the treatment of BC by inhibiting cell proliferation and promoting apoptosis."
item1057	REG00001	M6ATAR00196	.	M6ADIS0065	.	33505967	"Studies of the aberrant expression of m6A mediators in breast cancer revealed that they were associated with different BC subtypes and functions, such as proliferation, apoptosis, stemness, the cell cycle, migration, and metastasis, through several factors and signaling pathways, such as Apoptosis regulator Bcl-2 (BCL2) and the PI3K/Akt pathway, among others. Fat mass and obesity-associated protein (FTO) was identified as the first m6A demethylase, and a series of <span>inhibitors that target FTO were reported to have potential for the treatment of BC by inhibiting cell proliferation and promoting apoptosis."
item1058	REG00001	M6ATAR00196	.	M6ADIS0065	.	33505967	"Studies of the aberrant expression of m6A mediators in breast cancer revealed that they were associated with different BC subtypes and functions, such as proliferation, apoptosis, stemness, the cell cycle, migration, and metastasis, through several factors and signaling pathways, such as Apoptosis regulator Bcl-2 (BCL2) and the PI3K/Akt pathway, among others. Fat mass and obesity-associated protein (FTO) was identified as the first m6A demethylase, and a series of <span>inhibitors that target FTO were reported to have potential for the treatment of BC by inhibiting cell proliferation and promoting apoptosis."
item1059	REG00001	M6ATAR00196	.	M6ADIS0065	.	33505967	"Studies of the aberrant expression of m6A mediators in breast cancer revealed that they were associated with different BC subtypes and functions, such as proliferation, apoptosis, stemness, the cell cycle, migration, and metastasis, through several factors and signaling pathways, such as Apoptosis regulator Bcl-2 (BCL2) and the PI3K/Akt pathway, among others. Fat mass and obesity-associated protein (FTO) was identified as the first m6A demethylase, and a series of <span>inhibitors that target FTO were reported to have potential for the treatment of BC by inhibiting cell proliferation and promoting apoptosis."
item1060	.	.	.	M6ADIS0128	.	33763421	"Accumulating evidence has demonstrated that <span>lipopolysaccharide (LPS) compromises female reproduction, especially oocyte maturation and competence. <span>MV can protect oocytes from LPS-induced meiotic defects in part by reducing oxidative stress and maintaining m6A levels. LPS reduced m6A levels in oocytes, but MV restored these epigenetic modifications."
item1061	.	.	.	M6ADIS0128	.	33763421	"Accumulating evidence has demonstrated that <span>lipopolysaccharide (LPS) compromises female reproduction, especially oocyte maturation and competence. <span>MV can protect oocytes from LPS-induced meiotic defects in part by reducing oxidative stress and maintaining m6A levels. LPS reduced m6A levels in oocytes, but MV restored these epigenetic modifications."
item1062	REG00009	M6ATAR00185	Up	M6ADIS0097	.	33819187	"Myocardial infarction (MI) is one of the leading causes of death. WTAP promoted myocardial I/R injury through promoting ER stress and cell apoptosis by regulating m6A modification of Cyclic AMP-dependent transcription factor ATF-4 (ATF4) mRNA. H/R effects on ER stress and apoptosis were all blocked by silencing of WTAP, promoted by WTAP overexpression, and ameliorated by administration of ER stress inhibitor, <span>4-PBA."
item1063	REG00007	.	.	M6ADIS0046	.	33902106	"Inhibition of METTL3 by <span>STM2457 targets key stem cell populations of acute myeloid leukaemia and reverses the AML phenotype, preventing or slowing the development of AML in re-transplantation experiments."
item1064	REG00001	.	.	M6ADIS0036	.	33926120	"Inhibition of m6A RNA demethylation by small-molecule drugs, as presented here, has therapeutic potential and provides tools for the identification of disease-modifying m6A RNAs in neurogenesis and neuroregeneration. Small-molecule inhibitors of the RNA m6A demethylases FTO potently support the survival of dopamine neurons."
item1065	REG00001	M6ATAR00288	Up	M6ADIS0055	M6ADRUG0044	33972683	"<span>Rapamycin inhibited FTO activity, and directly targeted Eukaryotic translation initiation factor 4 gamma 1 (EIF4G1) transcripts and mediated their expression in an m6A-dependent manner in oral squamous cell carcinoma. After FTO silencing, YTHDF2 captured eIF4G1 transcripts containing m6A, resulting in mRNA degradation and decreased expression of eIF4G1 protein, thereby promoting autophagy and reducing tumor occurrence."
item1066	REG00008	M6ATAR00288	Down	M6ADIS0055	M6ADRUG0044	33972683	"<span>Rapamycin inhibited FTO activity, and directly targeted Eukaryotic translation initiation factor 4 gamma 1 (EIF4G1) transcripts and mediated their expression in an m6A-dependent manner in oral squamous cell carcinoma. After FTO silencing, YTHDF2 captured eIF4G1 transcripts containing m6A, resulting in mRNA degradation and decreased expression of eIF4G1 protein, thereby promoting autophagy and reducing tumor occurrence."
item1067	REG00022	M6ATAR00048	Up	.	M6ADRUG0039	34450044	"Direct suppression of m6A modification of S-mu-GLT (SugLT) or of m6A reader YTHDC1 reduces CSR. METTL3 enzyme-catalyzed N6-methyladenosine (m6A) RNA modification drives recognition and 3' end processing of S-mu-GLT by the RNA exosome, promoting class switch recombination and suppressing chromosomal translocations. <span>Tamoxifen affects the role of METTL3 in B cell development."
item1068	REG00001	.	.	M6ADIS0089	.	34491720	"Perturbed m6A signaling can be contributing to Alzheimer's disease pathogenesis, likely by compromising astrocyte bioenergetics. <span>MO-I-500, a novel pharmacological inhibitor of FTO, can strongly reduce the adverse effects of STZ. STZ-treated astrocytes expressed significantly higher levels of m6A demethylase FTO and m6A reader YTHDF1."
item1069	REG00024	.	.	M6ADIS0089	.	34491720	"Perturbed m6A signaling can be contributing to Alzheimer's disease pathogenesis, likely by compromising astrocyte bioenergetics. <span>MO-I-500, a novel pharmacological inhibitor of FTO, can strongly reduce the adverse effects of STZ. STZ-treated astrocytes expressed significantly higher levels of m6A demethylase FTO and m6A reader YTHDF1."
item1070	REG00007	M6ATAR00196	Up	M6ADIS0179	.	34530171	"Mettl3 inhibitor, <span>S-adenosylhomocysteine promoted the apoptosis and autophagy of chondrocytes with inflammation in vitro and aggravated the degeneration of chondrocytes and subchondral bone in monosodium iodoacetate (MIA) induced temporomandibular joint osteoarthritis mice in vivo. Bcl2 protein interacted with Beclin1 protein in chondrocytes induced by TNF-alpha stimulation. Mettl3 inhibits the apoptosis and autophagy of chondrocytes in inflammation through m6A/Ythdf1/Apoptosis regulator Bcl-2 (BCL2) signal axis which provides promising therapeutic strategy for temporomandibular joint osteoarthritis."
item1071	REG00024	M6ATAR00196	Up	M6ADIS0179	.	34530171	"Mettl3 inhibitor, <span>S-adenosylhomocysteine promoted the apoptosis and autophagy of chondrocytes with inflammation in vitro and aggravated the degeneration of chondrocytes and subchondral bone in monosodium iodoacetate (MIA) induced temporomandibular joint osteoarthritis mice in vivo. Bcl2 protein interacted with Beclin1 protein in chondrocytes induced by TNF-alpha stimulation. Mettl3 inhibits the apoptosis and autophagy of chondrocytes in inflammation through m6A/Ythdf1/Apoptosis regulator Bcl-2 (BCL2) signal axis which provides promising therapeutic strategy for temporomandibular joint osteoarthritis."
item1072	REG00007	M6ATAR00432	Up	M6ADIS0179	.	34530171	"Mettl3 inhibitor, <span>S-adenosylhomocysteine promoted the apoptosis and autophagy of chondrocytes with inflammation in vitro and aggravated the degeneration of chondrocytes and subchondral bone in monosodium iodoacetate (MIA) induced temporomandibular joint osteoarthritis mice in vivo. Bcl2 protein interacted with Beclin1 protein in chondrocytes induced by Tumor necrosis factor (TNF/TNF-alpha) stimulation. Mettl3 inhibits the apoptosis and autophagy of chondrocytes in inflammation through m6A/Ythdf1/Bcl2 signal axis which provides promising therapeutic strategy for temporomandibular joint osteoarthritis."
item1073	REG00007	M6ATAR00432	Up	M6ADIS0049	.	34530171	"Mettl3 inhibitor, <span>S-adenosylhomocysteine promoted the apoptosis and autophagy of chondrocytes with inflammation in vitro and aggravated the degeneration of chondrocytes and subchondral bone in monosodium iodoacetate (MIA) induced temporomandibular joint osteoarthritis mice in vivo. Bcl2 protein interacted with Beclin1 protein in chondrocytes induced by Tumor necrosis factor (TNF/TNF-alpha) stimulation. Mettl3 inhibits the apoptosis and autophagy of chondrocytes in inflammation through m6A/Ythdf1/Bcl2 signal axis which provides promising therapeutic strategy for temporomandibular joint osteoarthritis."
item1074	REG00024	M6ATAR00432	Up	M6ADIS0179	.	34530171	"Mettl3 inhibitor, <span>S-adenosylhomocysteine promoted the apoptosis and autophagy of chondrocytes with inflammation in vitro and aggravated the degeneration of chondrocytes and subchondral bone in monosodium iodoacetate (MIA) induced temporomandibular joint osteoarthritis mice in vivo. Bcl2 protein interacted with Beclin1 protein in chondrocytes induced by Tumor necrosis factor (TNF/TNF-alpha) stimulation. Mettl3 inhibits the apoptosis and autophagy of chondrocytes in inflammation through m6A/Ythdf1/Bcl2 signal axis which provides promising therapeutic strategy for temporomandibular joint osteoarthritis."
item1075	REG00024	M6ATAR00432	Up	M6ADIS0049	.	34530171	"Mettl3 inhibitor, <span>S-adenosylhomocysteine promoted the apoptosis and autophagy of chondrocytes with inflammation in vitro and aggravated the degeneration of chondrocytes and subchondral bone in monosodium iodoacetate (MIA) induced temporomandibular joint osteoarthritis mice in vivo. Bcl2 protein interacted with Beclin1 protein in chondrocytes induced by Tumor necrosis factor (TNF/TNF-alpha) stimulation. Mettl3 inhibits the apoptosis and autophagy of chondrocytes in inflammation through m6A/Ythdf1/Bcl2 signal axis which provides promising therapeutic strategy for temporomandibular joint osteoarthritis."
item1076	REG00007	M6ATAR00196	Up	M6ADIS0049	.	34530171	"Mettl3 inhibitor, <span>S-adenosylhomocysteine promoted the apoptosis and autophagy of chondrocytes with inflammation in vitro and aggravated the degeneration of chondrocytes and subchondral bone in monosodium iodoacetate (MIA) induced temporomandibular joint osteoarthritis mice in vivo. Bcl2 protein interacted with Beclin1 protein in chondrocytes induced by TNF-alpha stimulation. Mettl3 inhibits the apoptosis and autophagy of chondrocytes in inflammation through m6A/Ythdf1/Apoptosis regulator Bcl-2 (BCL2) signal axis which provides promising therapeutic strategy for temporomandibular joint osteoarthritis."
item1077	REG00024	M6ATAR00196	Up	M6ADIS0049	.	34530171	"Mettl3 inhibitor, <span>S-adenosylhomocysteine promoted the apoptosis and autophagy of chondrocytes with inflammation in vitro and aggravated the degeneration of chondrocytes and subchondral bone in monosodium iodoacetate (MIA) induced temporomandibular joint osteoarthritis mice in vivo. Bcl2 protein interacted with Beclin1 protein in chondrocytes induced by TNF-alpha stimulation. Mettl3 inhibits the apoptosis and autophagy of chondrocytes in inflammation through m6A/Ythdf1/Apoptosis regulator Bcl-2 (BCL2) signal axis which provides promising therapeutic strategy for temporomandibular joint osteoarthritis."
item1078	REG00001	.	.	M6ADIS0059	M6ADRUG0002	34869024	<span>Berberine effectively decreased m6A methylation by decreasing beta-catenin and subsequently increased FTO suggests a role of Berberine in modulating stemness and malignant behaviors in colorectal cancer.
item1079	REG00005	M6ATAR00413	.	M6ADIS0097	.	34879293	"<span>IOX1, which is an inhibitor of ALKBH5, was loaded on HSSS to form HSSS-I, which could effectively ameliorate cardiac dysfunction in acute myocardial infarction. The surface-modified bioengineered ferritin nanocage targeted the dying cells in the infarct area under the guidance of Scavenger receptor class F member 1 (SCARF1). These cells were then phagocytosed through recognition of their TfR1 receptor."
item1080	REG00005	M6ATAR00427	.	M6ADIS0097	.	34879293	"<span>IOX1, which is an inhibitor of ALKBH5, was loaded on HSSS to form HSSS-I, which could effectively ameliorate cardiac dysfunction in acute myocardial infarction. The surface-modified bioengineered ferritin nanocage targeted the dying cells in the infarct area under the guidance of Scarf1. These cells were then phagocytosed through recognition of their Transferrin receptor protein 1 (TFRC) receptor."
item1081	.	.	.	M6ADIS0090	.	31436138	This is the first study to show that stroke alters the cerebral m6A epitranscriptome which has functional implications in post-stroke pathophysiology.
item1082	REG00024	M6ATAR00754	Up	M6ADIS0032	.	33465322	YTHDF1 promotes PASMC proliferation and pulmonary hypertension by enhancing Melanoma-associated antigen D1 (MAGED1) translation.
item1083	REG00025	M6ATAR00206	.	.	.	35112553	Dysfunction of Ythdf3 and Mettl3 results in the translational defect of G1/S-specific cyclin-D1 (CCND1). Ythdf3 and Mettl3 regulates HSCs by transmitting m6A RNA methylation on the 5'UTR of Ccnd1.
item1084	REG00007	M6ATAR00017	Up	M6ADIS0096	.	35066738	"METTL3 promoted DGCR8 binding to pri-miR-143-3p through m6A modification, thus enhancing hsa-miR-143-3p expression to inhibit PRKCE transcription and further aggravating cardiomyocyte pyroptosis and MI/R injury."
item1085	REG00007	M6ATAR00770	Down	M6ADIS0096	.	35066738	"METTL3 promoted DGCR8 binding to pri-miR-143-3p through m6A modification, thus enhancing miR-143-3p expression to inhibit Protein kinase C epsilon (PRKCE) transcription and further aggravating cardiomyocyte pyroptosis and MI/R injury."
item1086	REG00025	M6ATAR00222	Up	M6ADIS0072	.	35110680	"YTHDF3 enhances Catenin beta-1 (CTNNB1/Beta-catenin) translation through recognizing and binding the m6A peaks on CTNNB1 mRNA.m6A reading protein YTHDF3 promotes the translation of the target transcript CTNNB1, contributing to ocular melanoma propagation and migration through m6A methylation."
item1087	REG00013	M6ATAR00393	.	M6ADIS0057	.	35502827	IGF2BP2 regulated GC the proliferation/migration through recognizing the m6A modification sites of NAD-dependent protein deacetylase sirtuin-1 (SIRT1) mRNA.
item1088	REG00007	M6ATAR00714	Down	M6ADIS0057	.	33758320	"METTL3 promotes translation of SPHK2 mRNA via an m6A-YTHDF1-dependent manner. Functionally, SPHK2 facilitates GC cell proliferation, migration and invasion by inhibiting Krueppel-like factor 2 (KLF2) expression."
item1089	REG00007	M6ATAR00778	Up	M6ADIS0057	.	33758320	"METTL3 promotes translation of Sphingosine kinase 2 (SPHK2) mRNA via an m6A-YTHDF1-dependent manner. Functionally, SPHK2 facilitates GC cell proliferation, migration and invasion by inhibiting KLF2 expression."
item1090	REG00024	M6ATAR00451	Up	M6ADIS0170	.	34990050	YTHDF1 knockdown alleviated the progression of renal fibrosis both in cultured cells induced by transforming growth factor-beta administration and in the UUO mouse model. Transcriptional coactivator YAP1 (YAP1) was accordingly down-regulated when YTHDF1 was inhibited.
item1091	REG00007	M6ATAR00049	Up	M6ADIS0170	.	34164910	METTL3-m6A-miR-21-5p-SPRY1/ERK/NF-kB axis in obstructive renal fibrosis and provides a deeper understanding of renal fibrosis.
item1092	REG00006	.	.	M6ADIS0061	M6ADRUG0024	34458141	Suppression of METTL14 obviously increased the sensitivity of gemcitabine in resistant cells. This study suggested that METTL14 is a potential target for chemotherapy resistance in pancreatic cancer.
item1093	REG00007	M6ATAR00341	Up	M6ADIS0169	.	33852874	"Mettl3 activates the cyst-promoting c-Myc and cAMP pathways through enhanced Myc proto-oncogene protein (MYC) and Avpr2 mRNA m6A modification and translation. Thus, Mettl3 promotes Autosomal dominant polycystic kidney disease and links methionine utilization to epitranscriptomic activation of proliferation and cyst growth."
item1094	REG00007	M6ATAR00783	Up	M6ADIS0099	.	35704246	Silencing METTL3 inhibited m6A level and decreased the binding of DGCR8 to pri-miR-375 and further limited hsa-miR-375-3p expression. METTL3-mediated m6A modification promoted VSMC phenotype transformation and made Atherosclerosis (AS) plaques more vulnerable via the miR-375-3p/PDK1 axis.
item1095	.	M6ATAR00260	.	M6ADIS0013	.	32869942	Altered m6 A modification was involved in up-regulated expression of Forkhead box protein O3 (FOXO3) mRNA in the luteinized granulosa cells from non-obese polycystic ovary syndrome patients following controlled ovarian hyperstimulation.
item1096	REG00007	M6ATAR00757	Up	M6ADIS0059	.	35700773	"METTL3 promoted Class E basic helix-loop-helix protein 41 (BHLHE41) expression in m6A-dependent manner, which subsequently induced CXCL1 transcription to enhance MDSC migration in vitro. METTL3 as a potential therapeutic target for CRC immunotherapy whose inhibition reverses immune suppression through m6A-BHLHE41-CXCL1 axis."
item1097	REG00009	M6ATAR00784	.	M6ADIS0168	.	35304463	"Subsequent loss- and gain-of-function experiments reveal WTAP is increased in senescent nucleus pulposus cells, and significantly promotes Long intergenic non-protein coding RNA 657 (NORAD) m6A modification. This study shows interruption of NORAD m6A modification or the NORAD/PUMILIO/E2F3 axis could serve as a potential therapeutic target to inhibit the senescence of NPCs and development of intervertebral disc degeneration(IVDD)."
item1098	REG00025	M6ATAR00260	Up	M6ADIS0125	.	30591559	"YTHDF3 as a negative regulator of antiviral immunity through the translational promotion of Forkhead box protein O3 (FOXO3) mRNA under homeostatic conditions, adding insight into the networks of RNA-binding protein-RNA interactions in homeostatically maintaining host antiviral immune function and preventing inflammatory response."
item1099	REG00005	M6ATAR00567	Down	M6ADIS0055	.	35395767	ALKBH5 overexpression inhibits RIG-I-mediated IFN-Alpha secretion through the IKK-Epsilon/TBK1/IRF3 pathway. Upregulation of AKLBH5 negatively correlates with RIG-I-like receptor 1 (RIG-I) and IFN-Alpha expression in head and neck squamous cell carcinoma (HNSCC) patients.
item1100	REG00005	.	.	M6ADIS0056	.	34876920	ALKBH5 as a demethylase was lowly expressed in cancer progression of esophageal squamous cell carcinoma (ESCC) and acts as a crucial component in ESCC progression.
item1101	REG00007	M6ATAR00785	Up	M6ADIS0161	.	35210391	"Enhanced METTL3 promoted the m6A methylation in total RNAs and inhibited neuropathic pain (NP) progression. Mechanistically, METTL3 accelerated microRNA 150 (MIR150) maturation via mediating m6A methylation of primiR-150 at locus 498, cooperating with the ""m6A reader"" YTHDF2. Therefore, the METTL3/miR-150/BDNF pathway is a promising therapeutic target for NP patients."
item1102	REG00001	.	.	M6ADIS0175	.	32531187	FTO regulates pathological ocular angiogenesis by controlling endothelial cell function in an m6A-YTHDF2-dependent manner. Pathological ocular angiogenesis commonly results in visual impairment or even blindness.
item1103	.	M6ATAR00756	.	M6ADIS0072	.	33601055	"Beta-site APP-cleaving enzyme 2 (BACE2) presented an increased level of N6-methyladenosine (m6A) RNA methylation, which led to the upregulation of BACE2 mRNA. This study provides a novel pattern of BACE2-mediated intracellular calcium release in ocular melanoma progression."
item1104	REG00007	M6ATAR00781	Up	M6ADIS0169	.	33852874	"Mettl3 activates the cyst-promoting c-Myc and cAMP pathways through enhanced c-Myc and Vasopressin V2 receptor (Avpr2/V2R) mRNA m6A modification and translation. Thus, Mettl3 promotes Autosomal dominant polycystic kidney disease and links methionine utilization to epitranscriptomic activation of proliferation and cyst growth."
item1105	REG00009	.	.	M6ADIS0173	.	32281240	"WTAP has been identified as a key subunit of the m6A methyltransferase complex, was down-regulated in brain arteriovenous malformations (AVMs) lesions."
item1106	REG00005	.	.	M6ADIS0167	.	35718974	"Functionally, the overexpression of ALKBH5 promoted apoptosis and inhibited the proliferation of T cells. ALKBH5 expression is downregulated in systemic lupus erythematosus (SLE) patients and could affect the apoptosis and proliferation of T cells."
item1107	.	M6ATAR00786	.	M6ADIS0006	.	34858996	"m6A methylation triggers the upregulation of Non-protein coding RNA 106 (LINC00106), which promotes the stemness and metastasis properties in HCC cells by sponging let7f, thereby resulting in periostin activation. The findings indicate the potential of LINC00106 as a diagnostic marker and therapeutic target for HCC."
item1108	REG00005	M6ATAR00780	Up	.	.	33387482	"UGT2B7 mRNA and protein levels in Huh-7 cells were significantly increased by double knockdown of METTL3 and METTL14, whereas those were decreased by knockdown of FTO or ALKBH5, suggesting that m6A modification downregulates UGT2B7 expression. RNA methylation posttranscriptionally controls hepatic UDP-glucuronosyltransferase 2B7 (UGT2B7) expression."
item1109	REG00007	M6ATAR00780	Down	.	.	33387482	"UGT2B7 mRNA and protein levels in Huh-7 cells were significantly increased by double knockdown of METTL3 and METTL14, whereas those were decreased by knockdown of FTO or ALKBH5, suggesting that m6A modification downregulates UGT2B7 expression. RNA methylation posttranscriptionally controls hepatic UDP-glucuronosyltransferase 2B7 (UGT2B7) expression."
item1110	REG00006	M6ATAR00780	Down	.	.	33387482	"UGT2B7 mRNA and protein levels in Huh-7 cells were significantly increased by double knockdown of METTL3 and METTL14, whereas those were decreased by knockdown of FTO or ALKBH5, suggesting that m6A modification downregulates UGT2B7 expression. RNA methylation posttranscriptionally controls hepatic UDP-glucuronosyltransferase 2B7 (UGT2B7) expression."
item1111	REG00001	M6ATAR00780	Up	.	.	33387482	"UGT2B7 mRNA and protein levels in Huh-7 cells were significantly increased by double knockdown of METTL3 and METTL14, whereas those were decreased by knockdown of FTO or ALKBH5, suggesting that m6A modification downregulates UGT2B7 expression. RNA methylation posttranscriptionally controls hepatic UDP-glucuronosyltransferase 2B7 (UGT2B7) expression."
item1112	REG00007	M6ATAR00774	Down	M6ADIS0171	.	34616359	"METTL3 knock-down experiment revealed that expressions of SOCS family members Suppressor of cytokine signaling 1 (SOCS1), SOCS2, SOCS4, SOCS5, and SOCS6 were increased after METTL3 knock-down. It indicated that METTL3 is involved in the development of Graves' disease (GD) by inducing mRNA m6A methylation modification of SOCS family members."
item1113	REG00007	M6ATAR00401	Down	M6ADIS0171	.	34616359	"METTL3 knock-down experiment revealed that expressions of SOCS family members SOCS1, Suppressor of cytokine signaling 2 (SOCS2), SOCS4, SOCS5, and SOCS6 were increased after METTL3 knock-down. It indicated that METTL3 is involved in the development of Graves' disease (GD) by inducing mRNA m6A methylation modification of SOCS family members."
item1114	REG00007	M6ATAR00776	Down	M6ADIS0171	.	34616359	"METTL3 knock-down experiment revealed that expressions of SOCS family members SOCS1, SOCS2, Suppressor of cytokine signaling 4 (SOCS4), SOCS5, and SOCS6 were increased after METTL3 knock-down. It indicated that METTL3 is involved in the development of Graves' disease (GD) by inducing mRNA m6A methylation modification of SOCS family members."
item1115	REG00007	.	.	M6ADIS0015	.	32755566	METTL3 knockout in vivo decreased avascular area and pathological neovascular tufts in an oxygen-induced retinopathy model and inhibited alkali burn-induced corneal neovascularization.
item1116	REG00007	M6ATAR00775	Down	M6ADIS0171	.	34616359	"METTL3 knock-down experiment revealed that expressions of SOCS family members SOCS1, SOCS2, SOCS4, Suppressor of cytokine signaling 5 (SOCS5), and SOCS6 were increased after METTL3 knock-down. It indicated that METTL3 is involved in the development of Graves' disease (GD) by inducing mRNA m6A methylation modification of SOCS family members."
item1117	REG00007	M6ATAR00777	Down	M6ADIS0171	.	34616359	"METTL3 knock-down experiment revealed that expressions of SOCS family members SOCS1, SOCS2, SOCS4, SOCS5, and Suppressor of cytokine signaling 6 (SOCS6) were increased after METTL3 knock-down. It indicated that METTL3 is involved in the development of Graves' disease (GD) by inducing mRNA m6A methylation modification of SOCS family members."
item1118	REG00005	M6ATAR00768	Up	M6ADIS0135	.	35142084	"ALKBH5 demethylates and stabilizes Hdac4 mRNA. Histone deacetylase 4 (HDAC4) interacts with and deacetylates FoxO3, resulting in a significant increase in FoxO3 expression. These results suggest that ALKBH5 is a potential therapeutic target for neurogenic muscle atrophy."
item1119	REG00012	.	.	M6ADIS0007	.	34974052	"NNK is a Group 1 human carcinogen, as classified by the International Agency for Research of Cancer (IARC), and plays a significant role in lung carcinogenesis. However IGF2BP1 is involved in the NNK-induced malignant transformation of Beas-2B cells, via m6A modification."
item1120	REG00001	M6ATAR00341	Down	M6ADIS0002	.	33966037	Wnt/Beta-catenin-mediated FTO downregulation and underscored the role of m6A modifications of Myc proto-oncogene protein (MYC) mRNA in regulating tumor cell glycolysis and growth.
item1121	REG00007	M6ATAR00524	Up	.	.	34825733	Mettl3 promotes oxLDL-triggered inflammation through interacting with Transcription factor ISGF-3 components p91/p84 (Stat1) protein and mRNA in RAW264.7 macrophages.
item1122	REG00005	M6ATAR00787	.	M6ADIS0006	.	34916222	"CircCPSF6 was dominated by ALKBH5-mediated demethylation, followed by the recognization and destabilization by YTHDF2. Meanwhile, circCPSF6 was upregulated in HCC specimens, and elevated hsa_circ_0000417 (circCPSF6) expression served as an independent prognostic factor for worse survival of patients with HCC."
item1123	REG00015	M6ATAR00758	Up	M6ADIS0007	.	35730068	"Knockdown of KIAA1429 significantly decreased the m6A levels of Protein BTG2 (BTG2) mRNA, leading to enhanced YTHDF2-dependent BTG2 mRNA stability and promoted the expression of BTG2; thus, participating in the tumorigenesis of LUAD."
item1124	REG00007	M6ATAR00788	Up	M6ADIS0172	.	34930676	METTL3 resulted in the upregulation of AGAP2-AS1 in psoriasis. LOC10013.776 (AGAP2-AS1) is upregulated in the skin tissue of psoriasis patients and m6A methylation was involved in its upregulation.
item1125	REG00020	M6ATAR00782	.	M6ADIS0006	.	34707107	RBM15-mediated m6A modification contributed to a post-transcriptional activation of Yes tyrosine kinase (YES/YES1) in an IGF2BP1-dependent manner. RBM15-mediated m6A modification facilitate the progression of HCC via the IGF2BP1-YES1-MAPK axis.
item1126	REG00005	M6ATAR00451	Up	M6ADIS0097	.	33456585	"ALKBH5-mediated m6A demethylation improved the mRNA stability of YTH N6-methyladenosine RNA-binding protein 1 (YTHDF1), thereby increasing its expression, which consequently promoted the translation of Transcriptional coactivator YAP1 (YAP1).This finding suggests a novel potential therapeutic strategy for myocardial infarction cardiac regeneration."
item1127	REG00007	M6ATAR00130	Up	M6ADIS0100	.	35836108	"METTL3 positively modulates the pri-miR-221/222 maturation process in an m6A-dependent manner and subsequently activates Wnt/Beta-catenin signaling by inhibiting DKK2, thus promoting Ang-II-induced cardiac hypertrophy."
item1128	REG00007	M6ATAR00129	Up	M6ADIS0100	.	35836108	"METTL3 positively modulates the pri-miR221/pri-miR-222 maturation process in an m6A-dependent manner and subsequently activates Wnt/Beta-catenin signaling by inhibiting DKK2, thus promoting Ang-II-induced cardiac hypertrophy."
item1129	REG00024	M6ATAR00237	Up	M6ADIS0006	.	35233828	YTHDF1 regulates the translation of Epidermal growth factor receptor (EGFR) mRNA via binding m6 A sites in the 3'-UTR of EGFR transcript. YTHDF1 is upregulated in ICC and associated with shorter survival of ICC patients.
item1130	REG00007	.	.	M6ADIS0173	.	32384926	"The expression level of METTL3 was reduced in the larger pathological tissues of cerebral arteriovenous malformation (AVM). Moreover, knockdown of METTL3 significantly affected angiogenesis of the human endothelial cells."
item1131	REG00001	M6ATAR00222	Up	M6ADIS0055	.	34853532	"FTO expression was significantly upregulated in HNSCC datasets and tissues. FTO expression was significantly correlated with Catenin beta-1 (CTNNB1/Beta-catenin) expression. Moreover, it exerted a tumorigenic effect by increasing CTNNB1 expression in an m6A-dependent manner."
item1132	REG00005	M6ATAR00213	Down	M6ADIS0007	.	35318440	"The expression of Cyclin-dependent kinase inhibitor 1 (CDKN1A) or TIMP3 was increased by ALKBH5 knockdown. In conclusions, the ALKBH5-IGF2BPs axis promotes cell proliferation and tumorigenicity, which in turn causes the unfavorable prognosis of NSCLC."
item1133	REG00005	M6ATAR00431	Down	M6ADIS0007	.	35318440	"The expression of CDKN1A (p21) or Metalloproteinase inhibitor 3 (TIMP3) was increased by ALKBH5 knockdown. In conclusions, the ALKBH5-IGF2BPs axis promotes cell proliferation and tumorigenicity, which in turn causes the unfavorable prognosis of NSCLC."
item1134	REG00001	M6ATAR00774	Up	M6ADIS0117	.	35731980	"Mechanistically, the FTO/Suppressor of cytokine signaling 1 (SOCS1)/JAK-STAT axis promotes diabetic kidney disease(DKD) pathogenesis via promoting inflammation. Moreover, FTO expression is significantly decreased in DKD, and overexpression of FTO can dramatically alleviate kidney inflammation."
item1135	REG00007	M6ATAR00766	Up	M6ADIS0056	.	34094960	L-glutamine amidohydrolase (GLS2) as a downstream target of METTL3. These findings uncover METTL3/GLS2 signaling as a potential therapeutic target in antimetastatic strategies against esophageal Squamous Cell Carcinoma(ESCC).
item1136	REG00007	M6ATAR00791	Up	M6ADIS0061	.	35758158	"hsa-miR-380-3p was enriched with m6A modifications, and elimination of m6A modifications by deleting METTL3 and METTL14 synergistically suppressed miR-380-3p expressions in pancreatic cancer cells."
item1137	REG00007	M6ATAR00762	Down	M6ADIS0059	.	35012593	"m6A and METTL3 levels were substantially elevated in colorectal carcinoma(CRC) tissues, METTL3 knockdown substantially reduced the m6A level of Protein crumbs homolog 3 (CRB3), and inhibited the degradation of CRB3 mRNA to increase CRB3 expression. METTL3 regulated the progression of CRC by regulating the m6A-CRB3-Hippo pathway."
item1138	REG00006	M6ATAR00791	Up	M6ADIS0061	.	35758158	"hsa-miR-380-3p was enriched with m6A modifications, and elimination of m6A modifications by deleting METTL3 and METTL14 synergistically suppressed miR-380-3p expressions in pancreatic cancer cells."
item1139	REG00007	M6ATAR00401	Down	M6ADIS0058	.	32705223	An increased level of METTL3 may maintain the tumorigenicity of colon cancer cells by suppressing Suppressor of cytokine signaling 2 (SOCS2).
item1140	REG00007	M6ATAR00792	Up	M6ADIS0065	.	33795252	"Specifically, increased METTL3 methylated KRT7-AS at A877 to increase the stability of a KRT7-AS/KRT7 mRNA duplex via IGF2BP1/HuR complexes. m6A promotes breast cancer lung metastasis by increasing the stability of a KRT7-AS/KRT7 mRNA duplex and translation of KRT7."
item1141	REG00007	M6ATAR00769	Up	M6ADIS0065	.	33795252	"Specifically, increased METTL3 methylated KRT7-AS at A877 to increase the stability of a KRT7-AS/Keratin, type II cytoskeletal 7 (KRT7) mRNA duplex via IGF2BP1/HuR complexes. m6A promotes breast cancer lung metastasis by increasing the stability of a KRT7-AS/KRT7 mRNA duplex and translation of KRT7."
item1142	.	M6ATAR00759	.	M6ADIS0058	.	31849331	"m6A methylation participated in the upregulation of CBX8 by maintaining Chromobox protein homolog 8 (CBX8) mRNA stability. Upon m6A methylation-induced upregulation, CBX8 interacts with KMT2b and Pol II to promote LGR5 expression in a noncanonical manner, which contributes to increased cancer stemness and decreased chemosensitivity in colon cancer."
item1143	REG00008	M6ATAR00755	Down	M6ADIS0065	.	34213887	"The increased expression of Cyclic-AMP-dependent transcription factor ATF-3 (ATF3) in tamoxifen-resistant cells arises from the decreased expression of the m6A reader protein YTHDF2 and the ensuing elevated stability of ATF3 mRNA, which ultimately promotes the translation of ATF3. ATF3 as a candidate therapeutic target for mitigating drug resistance in breast cancer cells."
item1144	REG00024	.	.	M6ADIS0058	M6ADRUG0047	33614908	"YTHDF1-promoted cisplatin resistance, contributing to overcoming chemoresistant colon cancers."
item1145	REG00007	M6ATAR00175	Down	M6ADIS0046	.	33932138	"Downregulated METTL3 expression in AML-MSCs induced an increase in RAC-alpha serine/threonine-protein kinase (AKT1) protein, resulting in enhanced MSC adipogenesis, thereby contributing to chemoresistance in acute myeloid leukaemia (AML) cells."
item1146	REG00025	M6ATAR00763	.	M6ADIS0059	.	35708211	YTHDF3 was highly expressed in oxaliplatin-resistant (OXAR) CRC tissues and cells. YTHDF3 as a novel hallmark and revealed the molecular mechanism of YTHDF3 on gene translation via coordination with Tyrosine-protein kinase EIF2AK2 (eIF2AK2/p68) in OXAR CRC cells.
item1147	REG00008	M6ATAR00214	Down	M6ADIS0006	M6ADRUG0047	35696608	"The role of YTHDF2 in tumourigenesis and cisplatin-desensitising function by promoting the degradation of Cyclin-dependent kinase inhibitor 1B (CDKN1B/p27) mRNA in an m6 A-dependent manner. YTHDF2 exhibits tumour oncogenic and cisplatin-desensitising properties, which offer insight into the development of novel combination therapeutic strategies for intrahepatic cholangiocarcinoma."
item1148	REG00020	.	.	M6ADIS0141	.	34301919	Knockdown of RBM15 remarkably suppressed the expression levels of multitarget genes related to programmed cell death and inflammatory response. These findings indicate that RBM15 can serve as a target for the treatment of COVID-19.
item1149	REG00007	M6ATAR00772	Up	M6ADIS0174	M6ADRUG0107	35032557	"METTL3, and the YTHDF1/eEF-1 complex mediate the translation of Multidrug resistance-associated protein 1 (MRP1/ABCC1) mRNA in an m6A-dependent manner to regulate the intracellular concentration of imatinib and drug resistance of gastrointestinal stromal tumor (GIST)."
item1150	REG00007	M6ATAR00771	Up	M6ADIS0059	.	35832094	"METTL3 enhances the expression of Lactate dehydrogenase A (LDHA), which catalyzes the conversion of pyruvate to lactate, to trigger glycolysis and 5-FU resistance. METTL3/LDHA axis-induced glucose metabolism is a potential therapy target to overcome 5-FU resistance in CRC cells."
item1151	REG00001	M6ATAR00444	Up	M6ADIS0057	M6ADRUG0047	35730319	"Knockdown of FTO reversed cisplatin resistance of SGC-7901/DDP cells both in vitro and in vivo, which was attributed to the inhibition of Serine/threonine-protein kinase ULK1 (ULK1)-mediated autophagy. These findings indicate that the FTO/ULK1 axis exerts crucial roles in cisplatin resistance of gastric cancer."
item1152	REG00007	M6ATAR00249	Up	M6ADIS0120	.	34476922	METTL3 promotes inflammation and cell apoptosis in a pediatric pneumonia model by regulating Histone-lysine N-methyltransferase EZH2 (EZH2).
item1153	REG00007	.	.	.	.	35104016	"HGHF-induced ferroptosis in osteoblasts is the main cause of osteoporosis in diabetes mellitus (DM) via activation of METTL3/ASK1-p38 signaling pathway, and inhibition of ferroptosis in osteoblasts provide a potential therapeutic strategy for diabetic osteoporosis."
item1154	REG00007	.	.	.	.	32749150	"The expression level of METTL3 positively correlated with molecular markers and infiltration level of CD8+ and CD4+ T cells and natural killer cells. In sum, These findings identified that METTL3 can be used as an independent prognostic marker in patients with testicular germ cell tumors (TGCTs)."
item1155	REG00007	M6ATAR00767	Up	M6ADIS0176	.	34491359	"METTL3 promotes tumor growth and hormone secretion by increasing expression of Guanine nucleotide-binding protein G (GNAS) and GADD45-Gamma in a m6A-dependent manner. Thus, METTL3 and the methylated RNAs constitute suitable targets for clinical treatment of Pituitary growth hormone-secreting-pituitary adenomas(GH-PAs)."
item1156	REG00007	M6ATAR00765	Up	M6ADIS0176	.	34491359	"METTL3 promotes tumor growth and hormone secretion by increasing expression of GNAS and Cytokine-responsive protein CR6 (GADD45-Gamma) in a m6A-dependent manner. Thus, METTL3 and the methylated RNAs constitute suitable targets for clinical treatment of Pituitary growth hormone-secreting-pituitary adenomas(GH-PAs)."
item1157	REG00007	M6ATAR00773	Up	M6ADIS0059	M6ADRUG0005	35856434	"METTL3 augmented 5 FU induced DNA damage and overcame 5 FU resistance in HCT 8R cells, which could be mimicked by inhibition of RAD51-associated protein 1 (RAD51AP1). The present study revealed that the METTL3/RAD51AP1 axis plays an important role in the acquisition of 5 FU resistance in CRC."
item1158	REG00007	M6ATAR00761	Down	M6ADIS0107	.	34893641	"Mechanistically, METTL3 directly binds to the promoters of the Platelet glycoprotein 4 (CD36) genes and recruits HDAC1/2 to induce deacetylation of H3K9 and H3K27 in their promoters, thus suppressing Cd36 and Ccl2 transcription. METTL3 negatively regulates hepatic Cd36 and Ccl2 gene transcription via a histone modification pathway for protection against Nonalcoholic steatohepatitis(NASH) progression."
item1159	REG00013	M6ATAR00779	.	M6ADIS0001	.	34954129	The gene expression of Serine/arginine-rich splicing factor 7 (SRSF7) is positively correlated with glioblastoma (GBM) cell-specific m6A methylation. The two m6A sites on PDZ-binding kinase (PBK) are regulated by SRSF7 and partially mediate the effects of SRSF7 in GBM cells through recognition by IGF2BP2.
item1160	REG00007	M6ATAR00760	Down	M6ADIS0107	.	34893641	"Mechanistically, METTL3 directly binds to the promoters of the Cd36 and Monocyte chemotactic and activating factor (CCL2) genes and recruits HDAC1/2 to induce deacetylation of H3K9 and H3K27 in their promoters, thus suppressing Cd36 and Ccl2 transcription. METTL3 negatively regulates hepatic Cd36 and Ccl2 gene transcription via a histone modification pathway for protection against Nonalcoholic steatohepatitis(NASH) progression."
item1161	REG00007	M6ATAR00325	Up	M6ADIS0007	M6ADRUG0030	33491264	"METTL3 combines with Hepatocyte growth factor receptor (c-Met/MET) and causes the PI3K/AKT signalling pathway to be manipulated, which affects the sensitivity of lung cancer cells to gefitinib. METTL3 knockdown promotes apoptosis and inhibits proliferation of lung cancer cells."
item1162	REG00007	M6ATAR00793	Up	M6ADIS0059	.	35030640	"hsa_circ_0000677 and its downstream target ABCC1 were upregulated in CRC cells, induced by the METTL3-mediated m6 A modification of circ_0000677 and SUMO1-mediated SUMOylation of METTL3. This work provided a new strategy for the therapeutic treatment of CRC."
item1163	REG00007	.	.	M6ADIS0145	.	35685469	"METTL3 knockdown suppressed the HSV-1 intermediate early and early genes (ICP0, ICP8 and UL23) and late genes (VP16, UL44, UL49 and ICP47). The components of m6A modification machinery, particularly m6A initiator METTL3 and reader YTHDF3, would be potential important targets for combating herpes virus type 1 (HSV-1) infections."
item1164	REG00001	M6ATAR00764	Up	M6ADIS0059	.	35297218	"Targeting FTO significantly suppresses cancer cell growth and enhances chemotherapy sensitivity, which not only mediating the balance of intracellular ROS by regulating Glucose-6-phosphate dehydrogenase (G6PD) expression, but also maintaining genome instability by regulating PARP1 expression. These findings shed light on new molecular mechanisms of CRC development and treatments mediated by m6A modification."
item1165	REG00001	M6ATAR00551	Up	M6ADIS0059	.	35297218	"Targeting FTO significantly suppresses cancer cell growth and enhances chemotherapy sensitivity, which not only mediating the balance of intracellular ROS by regulating G6PD expression, but also maintaining genome instability by regulating Poly [ADP-ribose] polymerase 1 (PARP1) expression. These findings shed light on new molecular mechanisms of CRC development and treatments mediated by m6A modification."
item1166	REG00025	M6ATAR00206	.	.	.	35112553	Dysfunction of Ythdf3 and Mettl3 results in the translational defect of G1/S-specific cyclin-D1 (CCND1). Ythdf3 and Mettl3 regulates HSCs by transmitting m6A RNA methylation on the 5'UTR of Ccnd1.
item1167	REG00007	M6ATAR00490	Down	M6ADIS0061	M6ADRUG0024	33855021	METTL3-mediated m6A modification on Nucleobindin-1 (NUCB1) 5'UTR via the reader YTHDF2 as a mechanism for NUCB1 downregulation in PDAC. This study revealed crucial functions of NUCB1 in suppressing proliferation and enhancing the effects of gemcitabine in pancreatic cancer cells.
item1168	REG00006	M6ATAR00222	Down	M6ADIS0065	M6ADRUG0092	35562334	m6A-hypomethylation regulated FGFR4 phosphorylates GSK-3beta and activates Catenin beta-1 (CTNNB1/Beta-catenin)/TCF4-SLC7A11/FPN1 signaling to drive anti-HER2 resistance. Knockdown of METTL14 significantly increased the expression level of FGFR4 in HER2-positive breast cancer cells. FGFR4 reduced the sensitivity of HER2-positive breast cancer to trastuzumab plus pertuzumab or tucatinib. These results pinpoint a mechanism of anti-HER2 resistance and provide a strategy for overcoming resistance via FGFR4 inhibition in recalcitrant HER2-positive breast cancer.
item1169	REG00005	.	.	M6ADIS0167	.	32583611	"These findings suggested decreased YTHDF2 that was associated with disease activity play an important role in the pathogenesis of SLE, METTL14 and ALKBH5 were concomitantly decreased."
item1170	REG00001	M6ATAR00491	Down	M6ADIS0057	.	33894267	"FTO suppresses Homeobox protein Hox-B13 (HOXB13) methytlation; FTO and HOXB13 expression promotes GC cell proliferation, migration, and invasion. HOXB13 expression intensifies GC invasion through PI3K/AKT/mTOR signaling via IGF-1R."
item1171	REG00001	M6ATAR00343	Down	M6ADIS0059	.	33533172	"GSK3beta inhibited Myeloid zinc finger 1 (MZF1) expression by mediating FTO-regulated m6A modification of MZF1 and then decreased the proto-oncogene c-Myc expression, thus hampering CRC cell proliferation."
item1172	REG00001	M6ATAR00341	Down	M6ADIS0059	.	33533172	"GSK3beta inhibited MZF1 expression by mediating FTO-regulated m6A modification of MZF1 and then decreased the proto-oncogene Myc proto-oncogene protein (MYC) expression, thus hampering CRC cell proliferation."
item1173	REG00007	M6ATAR00492	Up	M6ADIS0006	.	33582561	METTL3/IGF2BP1/Leukocyte surface antigen CD47 (CD47) mediated EMT transition contributes to the incomplete ablation induced metastasis in HCC cells.
item1174	REG00012	M6ATAR00492	Up	M6ADIS0006	.	33582561	METTL3/IGF2BP1/Leukocyte surface antigen CD47 (CD47) mediated EMT transition contributes to the incomplete ablation induced metastasis in HCC cells.
item1175	REG00001	M6ATAR00141	Up	M6ADIS0070	.	33634966	"FTO facilitates the tumorigenesis of bladder cancer through regulating the Metastasis associated lung adenocarcinoma transcript 1 (MALAT1)/miR-384/MAL2 axis in m6A RNA modification manner, which ensures the potential of FTO for serving as a diagnostic or prognostic biomarker in bladder cancer."
item1176	REG00007	.	.	M6ADIS0140	.	34262022	Knockout of Mettl3 leads to a more severe disruption of translational regulation of mRNAs than deletion of Fto and results in altered translation of crucial genes in cortical radial glial cells and intermediate progenitors. Uncover a profound role of Mettl3 in regulating translation of major mRNAs that control proper cortical development.
item1177	REG00031	.	.	M6ADIS0010	.	34923969	EIF3A could serve as a potential biomarker for prognostic and diagnostic stratification of ccRCC and is related to immune cell infiltrates.
item1178	REG00024	M6ATAR00312	Up	M6ADIS0065	.	35319018	"Tumor hypoxia can transcriptionally induce HIF1alpha and post-transcriptionally inhibit the expression of miR-16-5p to promote YTHDF1 expression, which could sequentially enhance tumor glycolysis by upregulating Pyruvate kinase PKM (PKM2/PKM) and eventually increase the tumorigenesis and metastasis potential of breast cancer cells."
item1179	REG00006	M6ATAR00484	Down	M6ADIS0065	M6ADRUG0092	35562334	m6A-hypomethylation regulated FGFR4 phosphorylates GSK-3beta and activates beta-catenin/TCF4-Cystine/glutamate transporter (SLC7A11)/FPN1 signaling to drive anti-HER2 resistance. Knockdown of METTL14 significantly increased the expression level of FGFR4 in HER2-positive breast cancer cells. FGFR4 reduced the sensitivity of HER2-positive breast cancer to trastuzumab plus pertuzumab or tucatinib. These results pinpoint a mechanism of anti-HER2 resistance and provide a strategy for overcoming resistance via FGFR4 inhibition in recalcitrant HER2-positive breast cancer.
item1180	REG00007	M6ATAR00493	.	M6ADIS0006	.	35274813	"NKILA physically interacted with and suppressed hsa-miR-582-3p, which was regulated by METTL3-mediated N6 -methyladenosine (m6A) modification. YAP1 was a target of NKILA via miR-582-3p and NKILA functioned partially via YAP1 in CCA."
item1181	REG00001	.	.	M6ADIS0057	.	35669943	FTO and ALKBH1 SNPs have predictive value in evaluating susceptibility to GC with differing age or Lauren classification.
item1182	REG00008	M6ATAR00494	Up	M6ADIS0006	.	33344502	"YTHDF2 expression was associated positively with Splicing factor 3A subunit 3 (SF3A3) expression, which implied that they cooperate in LIHC progression."
item1183	REG00007	M6ATAR00495	Up	M6ADIS0138	.	34145224	METTL3 acts on the m6A functional site of 1956 bp in hsa_circ_0008542. RNA demethylase ALKBH5 inhibits the binding of circ_0008542 with miRNA-185-5p to correct the bone resorption process.
item1184	REG00005	M6ATAR00495	Down	M6ADIS0138	.	34145224	METTL3 acts on the m6A functional site of 1956 bp in hsa_circ_0008542. RNA demethylase ALKBH5 inhibits the binding of circ_0008542 with miRNA-185-5p to correct the bone resorption process.
item1185	REG00018	.	.	M6ADIS0057	.	34702266	"METTL5 protein was decreased in GCTs compared with AIMTs and ANTs, and it is a potential prognostic biomarker in GC."
item1186	REG00007	M6ATAR00496	Up	M6ADIS0068	.	34185427	"METTL3-mediated m6A modification contributed to Prostate cancer associated transcript 6 (PCAT6) upregulation in an IGF2BP2-dependent manner. Furthermore, PCAT6 upregulated IGF1R expression by enhancing IGF1R mRNA stability through the PCAT6/IGF2BP2/IGF1R RNA-protein three-dimensional complex. The m6 A-induced PCAT6/IGF2BP2/IGF1R axis promotes PCa bone metastasis and tumor growth, suggesting that PCAT6 serves as a promising prognostic marker and therapeutic target against bone-metastatic PCa."
item1187	REG00007	M6ATAR00497	Up	M6ADIS0068	.	34185427	"METTL3-mediated m6A modification contributed to PCAT6 upregulation in an IGF2BP2-dependent manner. Furthermore, PCAT6 upregulated Insulin-like growth factor 1 receptor (IGF1R) expression by enhancing IGF1R mRNA stability through the PCAT6/IGF2BP2/IGF1R RNA-protein three-dimensional complex. The m6 A-induced PCAT6/IGF2BP2/IGF1R axis promotes PCa bone metastasis and tumor growth, suggesting that PCAT6 serves as a promising prognostic marker and therapeutic target against bone-metastatic PCa."
item1188	REG00013	M6ATAR00496	Up	M6ADIS0068	.	34185427	"METTL3-mediated m6A modification contributed to Prostate cancer associated transcript 6 (PCAT6) upregulation in an IGF2BP2-dependent manner. Furthermore, PCAT6 upregulated IGF1R expression by enhancing IGF1R mRNA stability through the PCAT6/IGF2BP2/IGF1R RNA-protein three-dimensional complex. The m6 A-induced PCAT6/IGF2BP2/IGF1R axis promotes PCa bone metastasis and tumor growth, suggesting that PCAT6 serves as a promising prognostic marker and therapeutic target against bone-metastatic PCa."
item1189	REG00013	M6ATAR00497	Up	M6ADIS0068	.	34185427	"METTL3-mediated m6A modification contributed to PCAT6 upregulation in an IGF2BP2-dependent manner. Furthermore, PCAT6 upregulated Insulin-like growth factor 1 receptor (IGF1R) expression by enhancing IGF1R mRNA stability through the PCAT6/IGF2BP2/IGF1R RNA-protein three-dimensional complex. The m6 A-induced PCAT6/IGF2BP2/IGF1R axis promotes PCa bone metastasis and tumor growth, suggesting that PCAT6 serves as a promising prognostic marker and therapeutic target against bone-metastatic PCa."
item1190	REG00006	M6ATAR00498	Down	M6ADIS0065	M6ADRUG0092	35562334	m6A-hypomethylation regulated FGFR4 phosphorylates GSK-3beta and activates beta-catenin/TCF4-SLC7A11/Solute carrier family 40 member 1 (FPN1) signaling to drive anti-HER2 resistance. Knockdown of METTL14 significantly increased the expression level of FGFR4 in HER2-positive breast cancer cells. FGFR4 reduced the sensitivity of HER2-positive breast cancer to trastuzumab plus pertuzumab or tucatinib. These results pinpoint a mechanism of anti-HER2 resistance and provide a strategy for overcoming resistance via FGFR4 inhibition in recalcitrant HER2-positive breast cancer.
item1191	REG00007	M6ATAR00446	Up	M6ADIS0138	.	30696066	"Mettl3 knockdown not only reduced the expression of Vascular endothelial growth factor A (VEGFA) but also decreased the level of its splice variants, vegfa-164 and vegfa-188, in Mettl3-deficient BMSCs. These findings contribute to novel progress in understanding the role of epitranscriptomic regulation in the osteogenic differentiation of BMSCs."
item1192	REG00022	M6ATAR00499	.	M6ADIS0046	.	34255814	"YTHDC1 knockdown has a strong inhibitory effect on proliferation of primary AML cells. YTHDC1 regulates leukemogenesis through DNA replication licensing factor MCM4 (MCM4), which is a critical regulator of DNA replication."
item1193	REG00008	M6ATAR00500	Down	M6ADIS0010	.	35042525	"CircMET enhances mRNA decay of Cyclin-dependent kinase inhibitor 2A (CDKN2A) by direct interaction and recruitment of YTHDF2. CircMET promotes the development of NONO-TFE3 tRCC, and the regulation to both CDKN2A and SMAD3 of circMET was revealed."
item1194	REG00023	.	.	M6ADIS0138	.	34018357	YTHDC2 knockdown can promote the osteogenic differentiation of hBMSCs and inhibit the adipogenic differentiation. YTHDC2 knockdown cause changes in ribosome function.
item1195	REG00007	.	.	M6ADIS0008	.	33059689	CD33+ MDSC expansion is linked to high levels of METTL3 and that METTL3 and CD33+ MDSCs are independent prognostic factors in CC.
item1196	REG00005	M6ATAR00501	Up	M6ADIS0051	.	35303054	"In osteosarcoma, ALKBH5 mediates its protumorigenic function by regulating m6A levels of histone deubiquitinase Ubiquitin carboxyl-terminal hydrolase 22 (USP22) and the ubiquitin ligase RNF40."
item1197	REG00005	M6ATAR00502	Up	M6ADIS0051	.	35303054	"In osteosarcoma, ALKBH5 mediates its protumorigenic function by regulating m6A levels of histone deubiquitinase USP22 and the ubiquitin ligase E3 ubiquitin-protein ligase BRE1B (RNF40)."
item1198	REG00006	M6ATAR00375	Down	M6ADIS0117	.	33414476	METTL14-regulated PI3K/Akt signaling pathway via Mutated in multiple advanced cancers 1 (PTEN) affected HDAC5-mediated EMT of renal tubular cells in diabetic kidney disease.
item1199	REG00020	.	.	M6ADIS0061	.	35223996	Pan-cancer analysis of RBM15 suggested it is served as a prognostic biomarker and immunotherapeutic target for PAAD.
item1200	REG00008	M6ATAR00503	Down	M6ADIS0001	.	33420027	"YTHDF2 facilitates m6A-dependent mRNA decay of Oxysterols receptor LXR-alpha (LXRA) and HIVEP2, which impacts the glioma patient survival. YTHDF2 promotes tumorigenesis of GBM cells, largely through the downregulation of LXRA and HIVEP2."
item1201	REG00008	M6ATAR00504	Down	M6ADIS0001	M6ADRUG0010	35582627	YTHDF2 enhanced TMZ resistance in GBM by activation of the PI3K/Akt and NF-Kappa-B signalling pathways via inhibition of Ephrin type-B receptor 3 (EPHB3) and TNFAIP3.
item1202	REG00008	M6ATAR00505	Down	M6ADIS0001	.	33420027	"YTHDF2 facilitates m6A-dependent mRNA decay of LXRA and Transcription factor HIVEP2 (HIVEP2), which impacts the glioma patient survival. YTHDF2 promotes tumorigenesis of GBM cells, largely through the downregulation of LXRA and HIVEP2."
item1203	REG00006	M6ATAR00506	Down	M6ADIS0056	.	34586732	"METTL14, an m6A RNA methyltransferase downregulated in ESCC, suppresses Tribbles homolog 2 (TRIB2) expression via miR-99a-5p-mediated degradation of TRIB2 mRNA by targeting its 3' untranslated region, whereas TRIB2 induces ubiquitin-mediated proteasomal degradation of METTL14 in a COP1-dependent manner."
item1204	REG00006	M6ATAR00507	Up	M6ADIS0056	.	34586732	"METTL14, an m6A RNA methyltransferase downregulated in ESCC, suppresses TRIB2 expression via hsa-miR-99a-5p-mediated degradation of TRIB2 mRNA by targeting its 3' untranslated region, whereas TRIB2 induces ubiquitin-mediated proteasomal degradation of METTL14 in a COP1-dependent manner."
item1205	REG00013	M6ATAR00508	Up	.	.	34753397	"Insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) is an important N6-methyladenosine (m6A) reader, which is involved in multiple processes, including wound healing. IGF2BP2 knockdown repressed proliferation, migration, and angiogenesis of HaCaT cells by decreasing Heparanase (HPSE) stability."
item1206	REG00013	M6ATAR00509	Up	M6ADIS0061	.	35526050	PTGS2 antisense RNA 1 (PACERR) which bound to IGF2BP2 acts as an m6A-dependent manner to enhance the stability of KLF12 and c-myc in cytoplasm. This study found that LncRNA-PACERR functions as key regulator of TAMs in PDAC microenvironment and revealed the novel mechanisms in cytoplasm and in nucleus.
item1207	REG00013	M6ATAR00510	Up	M6ADIS0061	.	35526050	LncRNA-PACERR which bound to IGF2BP2 acts as an m6A-dependent manner to enhance the stability of Krueppel-like factor 12 (KLF12) and c-myc in cytoplasm. This study found that LncRNA-PACERR functions as key regulator of TAMs in PDAC microenvironment and revealed the novel mechanisms in cytoplasm and in nucleus.
item1208	REG00013	M6ATAR00341	Up	M6ADIS0061	.	35526050	LncRNA-PACERR which bound to IGF2BP2 acts as an m6A-dependent manner to enhance the stability of KLF12 and Myc proto-oncogene protein (MYC) in cytoplasm. This study found that LncRNA-PACERR functions as key regulator of TAMs in PDAC microenvironment and revealed the novel mechanisms in cytoplasm and in nucleus.
item1209	REG00008	M6ATAR00511	Up	M6ADIS0006	.	35526051	PA2G4 plays a pro-metastatic role by increasing Tyrosine-protein kinase Fyn (FYN) expression through binding with YTHDF2 in HCC. PA2G4 becomes a reliable prognostic marker or therapeutic target for HCC patients.
item1210	REG00008	M6ATAR00512	Up	M6ADIS0006	.	35526051	Proliferation-associated protein 2G4 (PA2G4) plays a pro-metastatic role by increasing FYN expression through binding with YTHDF2 in HCC. PA2G4 becomes a reliable prognostic marker or therapeutic target for HCC patients.
item1211	REG00005	M6ATAR00513	Up	M6ADIS0138	.	34105773	ALKBH5 promotes osteogenesis through modulating Runt-related transcription factor 2 (Runx2) mRNA stability.
item1212	REG00008	M6ATAR00514	Down	M6ADIS0001	M6ADRUG0010	35582627	YTHDF2 enhanced TMZ resistance in GBM by activation of the PI3K/Akt and NF-Kappa-B signalling pathways via inhibition of EPHB3 and TNF alpha-induced protein 3 (TNFAIP3).
item1213	REG00025	M6ATAR00258	Up	M6ADIS0149	.	34818872	m6A reader Ythdf3 protects hematopoietic stem cell integrity under stress by promoting the translation of Forkhead box protein M1 (FOXM1) and Asxl1 transcripts.
item1214	REG00025	M6ATAR00515	Up	M6ADIS0149	.	34818872	m6A reader Ythdf3 protects hematopoietic stem cell integrity under stress by promoting the translation of Foxm1 and Polycomb group protein ASXL1 (Asxl1) transcripts.
item1215	REG00020	M6ATAR00516	Up	M6ADIS0010	.	35381326	"RBM15 enhanced the stability of C-X-C motif chemokine 11 (CXCL11) mRNA in an m6A-dependent manner. These findings highlight the function of RBM15 in ccRCC and reveal a novel identified EP300/CBP-RBM15-CXCL11 signaling axis, which promotes ccRCC progression and provides new insight into ccRCC therapy."
item1216	REG00007	M6ATAR00169	Up	M6ADIS0107	.	35192934	Targeting METTL3/14 in vitro increases protein level of ATP-citrate synthase (ACLY) and SCD1 as well as triglyceride and cholesterol production and accumulation of lipid droplets. These findings demonstrate a new NAFLD mouse model that provides a study platform for DM2-related NAFLD and reveals a unique epitranscriptional regulating mechanism for lipid metabolism via m6A-modified protein expression of ACLY and SCD1.
item1217	REG00007	M6ATAR00388	Up	M6ADIS0107	.	35192934	Targeting METTL3/14 in vitro increases protein level of ACLY and Stearoyl-CoA desaturase (SCD) as well as triglyceride and cholesterol production and accumulation of lipid droplets. These findings demonstrate a new NAFLD mouse model that provides a study platform for DM2-related NAFLD and reveals a unique epitranscriptional regulating mechanism for lipid metabolism via m6A-modified protein expression of ACLY and SCD1.
item1218	REG00006	M6ATAR00169	Up	M6ADIS0107	.	35192934	Targeting METTL3/14 in vitro increases protein level of ATP-citrate synthase (ACLY) and SCD1 as well as triglyceride and cholesterol production and accumulation of lipid droplets. These findings demonstrate a new NAFLD mouse model that provides a study platform for DM2-related NAFLD and reveals a unique epitranscriptional regulating mechanism for lipid metabolism via m6A-modified protein expression of ACLY and SCD1.
item1219	REG00006	M6ATAR00388	Up	M6ADIS0107	.	35192934	Targeting METTL3/14 in vitro increases protein level of ACLY and Stearoyl-CoA desaturase (SCD) as well as triglyceride and cholesterol production and accumulation of lipid droplets. These findings demonstrate a new NAFLD mouse model that provides a study platform for DM2-related NAFLD and reveals a unique epitranscriptional regulating mechanism for lipid metabolism via m6A-modified protein expression of ACLY and SCD1.
item1220	REG00015	M6ATAR00517	Down	M6ADIS0006	.	33391541	"Circ_DLC1, a downstream target of KIAA1429, is a promising prognostic marker for HCC patients, and the circDLC1-HuR-MMP1 axis serve as a potential therapeutic target for HCC treatment."
item1221	REG00007	M6ATAR00222	Up	M6ADIS0054	.	32668092	"METTL3 activated the luciferase activity of TOPflash (a reporter for beta-catenin/TCF signaling), and downregulation of METTL3 inhibited the expression of Catenin beta-1 (CTNNB1/Beta-catenin)/TCF target genes vimentin and N-cadherin, which are two regulators of epithelial-mesenchymal transition. METTL3 silencing decreased the m6A methylation and total mRNA levels of Tankyrase, a negative regulator of axin. METTL3 is a therapeutic target for <span class=""dissease"">NPC."
item1222	REG00007	M6ATAR00518	Up	M6ADIS0054	.	32668092	"METTL3 activated the luciferase activity of TOPflash (a reporter for beta-catenin/TCF signaling), and downregulation of METTL3 inhibited the expression of beta-catenin/TCF target genes Vimentin (vimentin) and N-cadherin, which are two regulators of epithelial-mesenchymal transition. METTL3 silencing decreased the m6A methylation and total mRNA levels of Tankyrase, a negative regulator of axin. METTL3 is a therapeutic target for <span class=""dissease"">NPC."
item1223	REG00006	M6ATAR00435	Up	M6ADIS0010	M6ADRUG0093	35538475	"In renal cell carcinoma, overexpression of TNF receptor-associated factor 1 (TRAF1) promotes sunitinib resistance by modulating apoptotic and angiogenic pathways in a METTL14-dependent manner."
item1224	REG00007	M6ATAR00202	Up	M6ADIS0054	.	32668092	"METTL3 activated the luciferase activity of TOPflash (a reporter for beta-catenin/TCF signaling), and downregulation of METTL3 inhibited the expression of beta-catenin/TCF target genes vimentin and Cadherin-2 (CDH2/N-cadherin), which are two regulators of epithelial-mesenchymal transition. METTL3 silencing decreased the m6A methylation and total mRNA levels of Tankyrase, a negative regulator of axin. METTL3 is a therapeutic target for <span class=""dissease"">NPC."
item1225	REG00007	M6ATAR00519	Up	M6ADIS0054	.	32668092	"METTL3 activated the luciferase activity of TOPflash (a reporter for beta-catenin/TCF signaling), and downregulation of METTL3 inhibited the expression of beta-catenin/TCF target genes vimentin and N-cadherin, which are two regulators of epithelial-mesenchymal transition. METTL3 silencing decreased the m6A methylation and total mRNA levels of Poly [ADP-ribose] polymerase tankyrase-1 (Tankyrase), a negative regulator of axin. METTL3 is a therapeutic target for <span class=""dissease"">NPC."
item1226	REG00009	M6ATAR00520	Up	M6ADIS0065	.	34312368	"The stabilization of WTAP further promotes RNA m6A methylation of Alpha-enolase (ENO1), impacting the glycolytic activity of BC cells."
item1227	REG00007	M6ATAR00521	Down	M6ADIS0059	.	32964498	"In colorectal cancer, Mettl3- or Mettl14-deficient tumors increased cytotoxic tumor-infiltrating CD8+ T cells and elevated secretion of Interferon gamma (IFN-gamma), Cxcl9, and Cxcl10 in tumor microenvironment in vivo. Mechanistically, Mettl3 or Mettl14 loss promoted IFN-gamma-Stat1-Irf1 signaling through stabilizing the Stat1 and Irf1 mRNA via Ythdf2."
item1228	REG00007	M6ATAR00522	Down	M6ADIS0059	.	32964498	"In colorectal cancer, Mettl3- or Mettl14-deficient tumors increased cytotoxic tumor-infiltrating CD8+ T cells and elevated secretion of IFN-gamma, C-X-C motif chemokine 9 (Cxcl9), and Cxcl10 in tumor microenvironment in vivo. Mechanistically, Mettl3 or Mettl14 loss promoted IFN-gamma-Stat1-Irf1 signaling through stabilizing the Stat1 and Irf1 mRNA via Ythdf2."
item1229	REG00007	M6ATAR00523	Down	M6ADIS0059	.	32964498	"In colorectal cancer, Mettl3- or Mettl14-deficient tumors increased cytotoxic tumor-infiltrating CD8+ T cells and elevated secretion of IFN-gamma, Cxcl9, and C-X-C motif chemokine 10 (Cxcl10) in tumor microenvironment in vivo. Mechanistically, Mettl3 or Mettl14 loss promoted IFN-gamma-Stat1-Irf1 signaling through stabilizing the Stat1 and Irf1 mRNA via Ythdf2."
item1230	REG00007	M6ATAR00524	Down	M6ADIS0059	.	32964498	"In colorectal cancer, Mettl3- or Mettl14-deficient tumors increased cytotoxic tumor-infiltrating CD8+ T cells and elevated secretion of IFN-gamma, Cxcl9, and Cxcl10 in tumor microenvironment in vivo. Mechanistically, Mettl3 or Mettl14 loss promoted IFN-gamma-Stat1-Irf1 signaling through stabilizing the Transcription factor ISGF-3 components p91/p84 (Stat1) and Irf1 mRNA via Ythdf2."
item1231	REG00007	M6ATAR00525	Down	M6ADIS0059	.	32964498	"In colorectal cancer, Mettl3- or Mettl14-deficient tumors increased cytotoxic tumor-infiltrating CD8+ T cells and elevated secretion of IFN-gamma, Cxcl9, and Cxcl10 in tumor microenvironment in vivo. Mechanistically, Mettl3 or Mettl14 loss promoted IFN-gamma-Stat1-Irf1 signaling through stabilizing the Stat1 and Interferon regulatory factor 1 (Irf1) mRNA via Ythdf2."
item1232	REG00006	M6ATAR00521	Down	M6ADIS0059	.	32964498	"In colorectal cancer, Mettl3- or Mettl14-deficient tumors increased cytotoxic tumor-infiltrating CD8+ T cells and elevated secretion of Interferon gamma (IFN-gamma), Cxcl9, and Cxcl10 in tumor microenvironment in vivo. Mechanistically, Mettl3 or Mettl14 loss promoted IFN-gamma-Stat1-Irf1 signaling through stabilizing the Stat1 and Irf1 mRNA via Ythdf2."
item1233	REG00006	M6ATAR00522	Down	M6ADIS0059	.	32964498	"In colorectal cancer, Mettl3- or Mettl14-deficient tumors increased cytotoxic tumor-infiltrating CD8+ T cells and elevated secretion of IFN-gamma, C-X-C motif chemokine 9 (Cxcl9), and Cxcl10 in tumor microenvironment in vivo. Mechanistically, Mettl3 or Mettl14 loss promoted IFN-gamma-Stat1-Irf1 signaling through stabilizing the Stat1 and Irf1 mRNA via Ythdf2."
item1234	REG00006	M6ATAR00526	Down	M6ADIS0065	M6ADRUG0095	35562334	m6A-hypomethylation regulated Fibroblast growth factor receptor 4 (FGFR4) phosphorylates GSK-3beta and activates beta-catenin/TCF4-SLC7A11/FPN1 signaling to drive anti-HER2 resistance. Knockdown of METTL14 significantly increased the expression level of FGFR4 in HER2-positive breast cancer cells. FGFR4 reduced the sensitivity of HER2-positive breast cancer to trastuzumab plus pertuzumab or tucatinib. These results pinpoint a mechanism of anti-HER2 resistance and provide a strategy for overcoming resistance via FGFR4 inhibition in recalcitrant HER2-positive breast cancer.
item1235	REG00006	M6ATAR00523	Down	M6ADIS0059	.	32964498	"In colorectal cancer, Mettl3- or Mettl14-deficient tumors increased cytotoxic tumor-infiltrating CD8+ T cells and elevated secretion of IFN-gamma, Cxcl9, and C-X-C motif chemokine 10 (Cxcl10) in tumor microenvironment in vivo. Mechanistically, Mettl3 or Mettl14 loss promoted IFN-gamma-Stat1-Irf1 signaling through stabilizing the Stat1 and Irf1 mRNA via Ythdf2."
item1236	REG00006	M6ATAR00524	Down	M6ADIS0059	.	32964498	"In colorectal cancer, Mettl3- or Mettl14-deficient tumors increased cytotoxic tumor-infiltrating CD8+ T cells and elevated secretion of IFN-gamma, Cxcl9, and Cxcl10 in tumor microenvironment in vivo. Mechanistically, Mettl3 or Mettl14 loss promoted IFN-gamma-Stat1-Irf1 signaling through stabilizing the Transcription factor ISGF-3 components p91/p84 (Stat1) and Irf1 mRNA via Ythdf2."
item1237	REG00006	M6ATAR00525	Down	M6ADIS0059	.	32964498	"In colorectal cancer, Mettl3- or Mettl14-deficient tumors increased cytotoxic tumor-infiltrating CD8+ T cells and elevated secretion of IFN-gamma, Cxcl9, and Cxcl10 in tumor microenvironment in vivo. Mechanistically, Mettl3 or Mettl14 loss promoted IFN-gamma-Stat1-Irf1 signaling through stabilizing the Stat1 and Interferon regulatory factor 1 (Irf1) mRNA via Ythdf2."
item1238	REG00008	M6ATAR00524	Down	M6ADIS0059	.	32964498	"In colorectal cancer, Mettl3- or Mettl14-deficient tumors increased cytotoxic tumor-infiltrating CD8+ T cells and elevated secretion of IFN-gamma, Cxcl9, and Cxcl10 in tumor microenvironment in vivo. Mechanistically, Mettl3 or Mettl14 loss promoted IFN-gamma-Stat1-Irf1 signaling through stabilizing the Transcription factor ISGF-3 components p91/p84 (Stat1) and Irf1 mRNA via Ythdf2."
item1239	REG00008	M6ATAR00525	Down	M6ADIS0059	.	32964498	"In colorectal cancer, Mettl3- or Mettl14-deficient tumors increased cytotoxic tumor-infiltrating CD8+ T cells and elevated secretion of IFN-gamma, Cxcl9, and Cxcl10 in tumor microenvironment in vivo. Mechanistically, Mettl3 or Mettl14 loss promoted IFN-gamma-Stat1-Irf1 signaling through stabilizing the Stat1 and Interferon regulatory factor 1 (Irf1) mRNA via Ythdf2."
item1240	REG00006	M6ATAR00527	Up	M6ADIS0059	.	34916487	"Knockdown of METTL14 significantly enhanced Arrestin domain-containing protein 4 (ARRDC4) mRNA stability relying on the ""reader"" protein YHTDF2 dependent manner in colorectal cancer."
item1241	REG00008	M6ATAR00527	Up	M6ADIS0059	.	34916487	"Knockdown of METTL14 significantly enhanced Arrestin domain-containing protein 4 (ARRDC4) mRNA stability relying on the ""reader"" protein YTHDF2 dependent manner in colorectal cancer."
item1242	REG00007	M6ATAR00528	Up	M6ADIS0007	.	34416901	"In non-small-cell lung carcinoma, METTL3 mediates the N6-methyladenosine (m6A) modification of Circ_IGF2BP3 and promotes its circularization in a manner dependent on the m6A reader protein YTHDC1."
item1243	REG00022	M6ATAR00528	Up	M6ADIS0007	.	34416901	"In non-small-cell lung carcinoma, METTL3 mediates the N6-methyladenosine (m6A) modification of Circ_IGF2BP3 and promotes its circularization in a manner dependent on the m6A reader protein YTHDC1."
item1244	REG00007	.	.	M6ADIS0055	.	34689367	METTL3 and METTL14 are overexpressed in OSCC tissues and in the HN6 OSCC cell line that promotes cell proliferation. Overexpressed METTL3 or METTL14 is found to be an independent prognostic factor for short overall survival in patients with OSCC.
item1245	REG00006	M6ATAR00268	Down	M6ADIS0065	M6ADRUG0095	35562334	m6A-hypomethylation regulated FGFR4 phosphorylates Glycogen synthase kinase-3 beta (GSK3Beta/GSK3B) and activates beta-catenin/TCF4-SLC7A11/FPN1 signaling to drive anti-HER2 resistance. Knockdown of METTL14 significantly increased the expression level of FGFR4 in HER2-positive breast cancer cells. FGFR4 reduced the sensitivity of HER2-positive breast cancer to trastuzumab plus pertuzumab or tucatinib. These results pinpoint a mechanism of anti-HER2 resistance and provide a strategy for overcoming resistance via FGFR4 inhibition in recalcitrant HER2-positive breast cancer.
item1246	REG00006	.	.	M6ADIS0055	.	34689367	METTL3 and METTL14 are overexpressed in OSCC tissues and in the HN6 OSCC cell line that promotes cell proliferation. Overexpressed METTL3 or METTL14 is found to be an independent prognostic factor for short overall survival in patients with OSCC.
item1247	REG00007	M6ATAR00529	Up	M6ADIS0112	.	34295905	"METTL3 knockdown suppressed Interleukin-6 (IL-6), matrix metalloproteinase (MMP)-3, and MMP-9 levels in human RA-FLSs and rat AIA-FLSs."
item1248	REG00007	M6ATAR00530	Up	M6ADIS0112	.	34295905	"METTL3 knockdown suppressed interleukin (IL)-6, matrix metalloproteinase Stromelysin-1 (MMP-3), and MMP-9 levels in human RA-FLSs and rat AIA-FLSs."
item1249	REG00007	M6ATAR00335	Up	M6ADIS0112	.	34295905	"METTL3 knockdown suppressed interleukin (IL)-6, matrix metalloproteinase (MMP)-3, and Matrix metalloproteinase-9 (MMP9) levels in human RA-FLSs and rat AIA-FLSs."
item1250	REG00008	M6ATAR00531	Down	M6ADIS0007	.	35186724	"YTHDF2 inhibits the migration and invasion of lung adenocarcinoma cells by regulating the Protein FAM83D (FAM83D)-TGFbeta1-pSMAD2/3 pathway, which will play an important role in lung cancer metastasis."
item1251	REG00008	M6ATAR00488	Down	M6ADIS0007	.	35186724	"YTHDF2 inhibits the migration and invasion of lung adenocarcinoma cells by regulating the FAM83D-Transforming growth factor beta-1 proprotein (TGFB1)-pSMAD2/3 pathway, which will play an important role in lung cancer metastasis."
item1252	REG00008	M6ATAR00532	Down	M6ADIS0007	.	35186724	"YTHDF2 inhibits the migration and invasion of lung adenocarcinoma cells by regulating the FAM83D-TGFbeta1-Mothers against decapentaplegic homolog 2 (SMAD2) pathway, which will play an important role in lung cancer metastasis."
item1253	REG00008	M6ATAR00396	Down	M6ADIS0007	.	35186724	"YTHDF2 inhibits the migration and invasion of lung adenocarcinoma cells by regulating the FAM83D-TGFbeta1-Mothers against decapentaplegic homolog 3 (SMAD3) pathway, which will play an important role in lung cancer metastasis."
item1254	REG00005	.	.	M6ADIS0001	.	33375621	ALKBH5 contributes to the aggressiveness of GBM by favoring the invasion of GBMSCs.
item1255	REG00007	M6ATAR00533	Up	M6ADIS0008	.	35255776	"METTL3 interacts with IGF2BP3 to promote the mRNA stability of Apoptotic chromatin condensation inducer in the nucleus (ACIN1), the overexpression of which induces the aggressiveness of CC cells."
item1256	REG00006	M6ATAR00222	Down	M6ADIS0065	M6ADRUG0095	35562334	m6A-hypomethylation regulated FGFR4 phosphorylates GSK-3beta and activates Catenin beta-1 (CTNNB1/Beta-catenin)/TCF4-SLC7A11/FPN1 signaling to drive anti-HER2 resistance. Knockdown of METTL14 significantly increased the expression level of FGFR4 in HER2-positive breast cancer cells. FGFR4 reduced the sensitivity of HER2-positive breast cancer to trastuzumab plus pertuzumab or tucatinib. These results pinpoint a mechanism of anti-HER2 resistance and provide a strategy for overcoming resistance via FGFR4 inhibition in recalcitrant HER2-positive breast cancer.
item1257	REG00014	M6ATAR00533	Up	M6ADIS0008	.	35255776	"METTL3 interacts with IGF2BP3 to promote the mRNA stability of Apoptotic chromatin condensation inducer in the nucleus (ACIN1), the overexpression of which induces the aggressiveness of CC cells."
item1258	REG00006	M6ATAR00534	Up	M6ADIS0007	.	34586620	METTL14 was remarkably downregulated in LC tissues and cell lines. METTL14 mediated the maturation of hsa-miR-30c-1-3p.
item1259	REG00006	M6ATAR00486	Down	M6ADIS0068	.	35354789	"In prostate cancer, METTL14 downregulated Thrombospondin-1 (THBS1) expression in an m6A-dependent manner, which resulted in the recruitment of YTHDF2 to recognize and degrade Thrombospondin 1 (THBS1) mRNA."
item1260	REG00008	M6ATAR00486	Down	M6ADIS0068	.	35354789	"In prostate cancer, METTL14 downregulated Thrombospondin-1 (THBS1) expression in an m6A-dependent manner, which resulted in the recruitment of YTHDF2 to recognize and degrade Thrombospondin 1 (THBS1) mRNA."
item1261	REG00007	.	.	M6ADIS0163	.	33759344	"METTL3 is involved in the PVR process, and METTL3 overexpression inhibits the EMT of ARPE-19 cells in vitro and suppresses the PVR process in vivo."
item1262	REG00003	M6ATAR00290	Down	M6ADIS0088	.	34966539	"Overexpression of HNRNPC can promote the proliferation of PC12 cells, inhibit their apoptosis, and inhibit the expression of inflammatory factors Interferon beta (IFNB1), IL-6, and TNF-Alpha, suggesting that HNRNPC can cause PD by inhibiting the proliferation of dopaminergic nerve cells, promoting their apoptosis, and causing immune inflammation."
item1263	REG00007	.	.	M6ADIS0059	.	35541914	The results revealed a negative functional regulation of the LINC01559/miR-106b-5p/PTEN axis in CRC progression and explored a new mechanism of METTL3-mediated m6A modification on LINC01559.
item1264	REG00001	.	.	M6ADIS0002	.	35121941	"Identify FTO as a key regulator, across epithelial cancers, of Wnt-triggered EMT and tumor progression."
item1265	REG00001	M6ATAR00535	Up	M6ADIS0070	.	33461172	FTO decreased N6-methyladenosine methylation level in P5C reductase 1 (PYCR1) through its demethylase enzymatic activity and stabilized PYCR1 transcript to promote bladder cancer initiation and progression.
item1266	REG00007	M6ATAR00536	Up	M6ADIS0001	.	33509238	"METTL3, upregulated in glioblastoma, methylates Interferon-inducible protein 4 (ADAR1) mRNA and increases its protein level leading to a pro-tumorigenic mechanism connecting METTL3, YTHDF1, and ADAR1."
item1267	REG00006	M6ATAR00484	Down	M6ADIS0065	M6ADRUG0095	35562334	m6A-hypomethylation regulated FGFR4 phosphorylates GSK-3beta and activates beta-catenin/TCF4-Cystine/glutamate transporter (SLC7A11)/FPN1 signaling to drive anti-HER2 resistance. Knockdown of METTL14 significantly increased the expression level of FGFR4 in HER2-positive breast cancer cells. FGFR4 reduced the sensitivity of HER2-positive breast cancer to trastuzumab plus pertuzumab or tucatinib. These results pinpoint a mechanism of anti-HER2 resistance and provide a strategy for overcoming resistance via FGFR4 inhibition in recalcitrant HER2-positive breast cancer.
item1268	REG00008	M6ATAR00298	Down	M6ADIS0015	.	34098071	KAT1 triggers YTHDF2-mediated Integrin beta-1 (ITGB1) mRNA instability to alleviate the progression of DR.
item1269	REG00008	M6ATAR00537	Down	M6ADIS0125	.	30875984	"YTHDF2 knockdown increases mRNA expression levels of MAP kinase kinase 4 (MAP2K4) and MAP4K4 via stabilizing the mRNA transcripts, which activate MAPK and NF-Kappa-B signaling pathways, which promote the expression of proinflammatory cytokines and aggravate the inflammatory response in LPS-stimulated RAW 264.7 cells."
item1270	REG00008	M6ATAR00538	Down	M6ADIS0125	.	30875984	"YTHDF2 knockdown increases mRNA expression levels of MAP2K4 and HPK/GCK-like kinase HGK (MAP4K4) via stabilizing the mRNA transcripts, which activate MAPK and NF-Kappa-B signaling pathways, which promote the expression of proinflammatory cytokines and aggravate the inflammatory response in LPS-stimulated RAW 264.7 cells."
item1271	REG00001	M6ATAR00539	Up	M6ADIS0065	.	32805088	FTO up-regulated ADP-ribosylation factor-like protein 5B (ARL5B) by inhibiting miR-181b-3p. The carcinogenic activity of FTO in promoting the invasion and migration of breast cancer cells via the FTO/miR-181b-3p/ARL5B signaling pathway.
item1272	REG00001	M6ATAR00540	Down	M6ADIS0065	.	32805088	FTO up-regulated ARL5B by inhibiting hsa-miR-181b-3p. The carcinogenic activity of FTO in promoting the invasion and migration of breast cancer cells via the FTO/miR-181b-3p/ARL5B signaling pathway.
item1273	REG00006	M6ATAR00541	Down	M6ADIS0010	.	33664855	"METTL14 deficiency promoted RCC metastasis in vitro and in vivo. Mechanistically, METTL14-mediated m6A modification negatively regulated the mRNA stability of Nucleosome-remodeling factor subunit BPTF (BPTF) and depended on BPTF to drive lung metastasis."
item1274	REG00001	M6ATAR00542	Down	M6ADIS0059	.	34218271	"FTO inhibited CRC metastasis both in vitro and in vivo. FTO exerted a tumor suppressive role by inhibiting Metastasis-associated protein MTA1 (MTA1) expression in an m6A-dependent manner. Methylated MTA1 transcripts were recognized by an m6A ""reader"", insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2), which then stabilized its mRNA."
item1275	REG00013	M6ATAR00542	Up	M6ADIS0059	.	34218271	"FTO inhibited CRC metastasis both in vitro and in vivo. FTO exerted a tumor suppressive role by inhibiting Metastasis-associated protein MTA1 (MTA1) expression in an m6A-dependent manner. Methylated MTA1 transcripts were recognized by an m6A ""reader"", insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2), which then stabilized its mRNA."
item1276	.	.	.	M6ADIS0061	.	34362795	m6A-mediated increases in WTAPP1 expression promote PDAC progression.
item1277	REG00008	.	.	M6ADIS0007	.	34996459	"High-YTHDF2 expression predicted a worse prognosis of LUSC, while hypoxia-mediated YTHDF2 overexpression promotes lung squamous cell carcinoma progression by activation of the mTOR/AKT signaling pathway."
item1278	REG00008	M6ATAR00490	Down	M6ADIS0061	M6ADRUG0024	33855021	METTL3-mediated m6A modification on Nucleobindin-1 (NUCB1) 5'UTR via the reader YTHDF2 as a mechanism for NUCB1 downregulation in PDAC. This study revealed crucial functions of NUCB1 in suppressing proliferation and enhancing the effects of gemcitabine in pancreatic cancer cells.
item1279	REG00006	M6ATAR00498	Down	M6ADIS0065	M6ADRUG0095	35562334	m6A-hypomethylation regulated FGFR4 phosphorylates GSK-3beta and activates beta-catenin/TCF4-SLC7A11/Solute carrier family 40 member 1 (FPN1) signaling to drive anti-HER2 resistance. Knockdown of METTL14 significantly increased the expression level of FGFR4 in HER2-positive breast cancer cells. FGFR4 reduced the sensitivity of HER2-positive breast cancer to trastuzumab plus pertuzumab or tucatinib. These results pinpoint a mechanism of anti-HER2 resistance and provide a strategy for overcoming resistance via FGFR4 inhibition in recalcitrant HER2-positive breast cancer.
item1280	REG00007	M6ATAR00010	Up	M6ADIS0134	.	35656115	The knockout of methyltransferase 3 (N6-adenosine-methyltransferase complex catalytic subunit) removed the m6A modification of hsa-miR-29a-3p and reduced miR-29a-3p expression. These findings suggest that miR-29a-3p is a potential target that can be manipulated for ALI/ARDS.
item1281	REG00006	M6ATAR00544	Up	M6ADIS0136	.	34508078	"TNF-alpha leads to increased expression of ELMO1 in AS-MSC, which is mediated by a METTL14 dependent m6A modification in Engulfment and cell motility protein 1 (ELMO1) 3'UTR. Higher ELMO1 expression of AS-MSC is found in vivo in AS patients."
item1282	REG00007	M6ATAR00545	Down	M6ADIS0138	.	35461899	"METTL3 knockdown enhanced Endoplasmic reticulum chaperone BiP (Grp78) expression through YTHDF2-mediated RNA degradation, which elicited ER stress, thereby promoting osteoblast apoptosis and inhibiting cell proliferation and differentiation under LPS-induced inflammatory condition."
item1283	REG00008	M6ATAR00545	Down	M6ADIS0138	.	35461899	"METTL3 knockdown enhanced Endoplasmic reticulum chaperone BiP (Grp78) expression through YTHDF2-mediated RNA degradation, which elicited ER stress, thereby promoting osteoblast apoptosis and inhibiting cell proliferation and differentiation under LPS-induced inflammatory condition."
item1284	REG00007	M6ATAR00546	Down	M6ADIS0057	.	35574388	METTL3 facilitates GC progression through the A disintegrin and metalloproteinase with thrombospondin motifs 9 (ADAMTS9)-mediated PI3K/AKT pathway.
item1285	.	M6ATAR00547	Up	M6ADIS0081	.	33705986	"In T2D, IMP2 directly binds to In Pancreas/duodenum homeobox protein 1 (Pdx1) mRNA and stimulates its translation in an m6A dependent manner."
item1286	REG00012	M6ATAR00548	Up	M6ADIS0070	.	33853613	IGF2BP1 was predominantly binded with Circ_PTPRA in the cytoplasm in BC cells.
item1287	REG00006	M6ATAR00549	Down	M6ADIS0010	.	31159832	"In RCC, METTL14 implicated m6A modification in RCC and down-regulated P2X purinoceptor 6 (P2RX6) protein translation."
item1288	REG00007	M6ATAR00269	Up	M6ADIS0059	.	33217448	"METTL3 induced Glucose transporter type 1 (SLC2A1) translation in an m6A-dependent manner, which subsequently promoted glucose uptake and lactate production, leading to the activation of mTORC1 signaling and CRC development."
item1289	REG00007	M6ATAR00550	Down	M6ADIS0051	.	32853985	E3 ubiquitin-protein ligase TRIM7 (TRIM7) mRNA stability was regulated by the METTL3/14-YTHDF2-mRNA in a decay-dependent manner. TRIM7 plays a key role in regulating metastasis and chemoresistance in osteosarcoma through ubiquitination of BRMS1.
item1290	REG00007	M6ATAR00551	Up	M6ADIS0057	M6ADRUG0048	35179655	m6A methyltransferase METTL3 facilitates oxaliplatin resistance in CD133+ gastric cancer stem cells by Promoting Poly [ADP-ribose] polymerase 1 (PARP1) mRNA stability which increases base excision repair pathway activity. METTTL3 enhances the stability of PARP1 by recruiting YTHDF1 to target the 3'-untranslated Region (3'-UTR) of PARP1 mRNA.
item1291	REG00006	M6ATAR00550	Down	M6ADIS0051	.	32853985	E3 ubiquitin-protein ligase TRIM7 (TRIM7) mRNA stability was regulated by the METTL3/14-YTHDF2-mRNA in a decay-dependent manner. TRIM7 plays a key role in regulating metastasis and chemoresistance in osteosarcoma through ubiquitination of BRMS1.
item1292	REG00008	M6ATAR00550	Down	M6ADIS0051	.	32853985	E3 ubiquitin-protein ligase TRIM7 (TRIM7) mRNA stability was regulated by the METTL3/14-YTHDF2-mRNA in a decay-dependent manner. TRIM7 plays a key role in regulating metastasis and chemoresistance in osteosarcoma through ubiquitination of BRMS1.
item1293	REG00007	M6ATAR00552	Up	M6ADIS0057	M6ADRUG0105	33037176	"In gastric cancer, m6A facilitated processing of pri-miR-17-92 into the miR-17-92 cluster through an m6A/DGCR8-dependent mechanism. METTL3-high tumors showed preferred sensitivity to an mTOR inhibitor, everolimus."
item1294	REG00007	M6ATAR00553	Down	M6ADIS0007	.	33510938	METTL3-mediated m6A modification of Zinc finger and BTB domain-containing protein 4 (ZBTB4) via EZH2 is involved in the CS-induced EMT and in lung cancer.
item1295	REG00009	M6ATAR00554	Up	M6ADIS0061	M6ADRUG0024	30851419	WTAP could promote migration/invasion and suppress chemo-sensitivity to gemcitabine in PC. Further mechanical investigation revealed that WTAP could bind to and stabilize Focal adhesion kinase 1 (Fak) mRNA which in turn activated the Fak-PI3K-AKT and Fak-Src-GRB2-Erk1/2 signaling pathways.
item1296	REG00007	M6ATAR00555	Up	M6ADIS0002	.	32444598	m6A regulates glycolysis of cancer cells through Pyruvate dehydrogenase kinase isoform 4 (PDK4). Knockdown of Mettl3 significantly attenuated m6A antibody enriched PDK4 mRNA in Huh7 cells. It reveals that m6A regulates glycolysis of cancer cells through PDK4.
item1297	REG00007	M6ATAR00451	Up	M6ADIS0006	.	32920668	m6A methylation plays a key role in VM formation in HCC. METTL3 and Transcriptional coactivator YAP1 (YAP1) could be potential therapeutic targets via impairing VM formation in anti-metastatic strategies.
item1298	REG00024	M6ATAR00237	Up	M6ADIS0006	.	33638162	"Sublethal heat treatment increases epidermal factor growth receptor (EGFR) m6A modification in the vicinity of the 5' untranslated region and promotes its binding with YTHDF1, which enhances the translation of Epidermal growth factor receptor (EGFR) mRNA. Combination of YTHDF1 silencing and EGFR inhibition suppressed the malignancies of HCC cells synergically."
item1299	REG00008	M6ATAR00556	Down	M6ADIS0066	.	33658012	FBW7 suppresses tumor growth and progression via antagonizing YTHDF2-mediated Bcl-2-modifying factor (BMF) mRNA decay in ovarian cancer.
item1300	REG00017	M6ATAR00356	.	M6ADIS0006	.	33133142	Deletion of METTL16 or ALKBH5 predicted poor OS and DFS of hepatocellular carcinoma (HCC) patients. And this study found significant associations between the genetic alterations and clinicopathological features as well as Cellular tumor antigen p53 (TP53/p53) alteration.
item1301	REG00024	M6ATAR00551	Up	M6ADIS0057	M6ADRUG0048	35179655	m6A methyltransferase METTL3 facilitates oxaliplatin resistance in CD133+ gastric cancer stem cells by Promoting PARP1 mRNA stability which increases base excision repair pathway activity. METTTL3 enhances the stability of PARP1 by recruiting Poly [ADP-ribose] polymerase 1 (PARP1) to target the 3'-untranslated Region (3'-UTR) of PARP1 mRNA.
item1302	REG00005	M6ATAR00356	.	M6ADIS0006	.	33133142	Deletion of METTL16 or ALKBH5 predicted poor OS and DFS of hepatocellular carcinoma (HCC) patients. And this study found significant associations between the genetic alterations and clinicopathological features as well as Cellular tumor antigen p53 (TP53/p53) alteration.
item1303	REG00007	M6ATAR00279	Up	M6ADIS0162	.	32983644	Findings show that METTL3 and METTL14 were up-regulated in preeclampsia(PE). Heat shock 70 kDa protein 1A (HSPA1A) is involved in the pathophysiology of PE as its mRNA and protein expression is regulated by m6A modification.
item1304	REG00006	M6ATAR00279	Up	M6ADIS0162	.	32983644	Findings show that METTL3 and METTL14 were up-regulated in preeclampsia(PE). Heat shock 70 kDa protein 1A (HSPA1A) is involved in the pathophysiology of PE as its mRNA and protein expression is regulated by m6A modification.
item1305	REG00004	.	.	M6ADIS0068	.	34899855	"Knockdown of HNRNPA2B1 or FTO prominently inhibited prostate cancer cells migration and invasion in vitro experiment. Determined CBLL1, FTO, YTHDC1, HNRNPA2B1 as crucial m6A regulators of prostate cancer."
item1306	REG00032	.	.	M6ADIS0068	.	34899855	"Knockdown of HNRNPA2B1 or FTO prominently inhibited prostate cancer cells migration and invasion in vitro experiment. Determined CBLL1, FTO, YTHDC1, HNRNPA2B1 as crucial m6A regulators of prostate cancer."
item1307	REG00001	.	.	M6ADIS0068	.	34899855	"Knockdown of HNRNPA2B1 or FTO prominently inhibited prostate cancer cells migration and invasion in vitro experiment. Determined CBLL1, FTO, YTHDC1, HNRNPA2B1 as crucial m6A regulators of prostate cancer."
item1308	REG00022	.	.	M6ADIS0068	.	34899855	"Knockdown of HNRNPA2B1 or FTO prominently inhibited prostate cancer cells migration and invasion in vitro experiment. Determined CBLL1, FTO, YTHDC1, HNRNPA2B1 as crucial m6A regulators of prostate cancer."
item1309	.	M6ATAR00557	.	M6ADIS0148	.	33667648	Down-regulation of m6A both in the 3'-UTR and CDS near stop codons of placental mRNAs is involved in gestational diabetes mellitus(GDM) development in Han Chinese women. MazF-qPCR verified that the m6A levels of the Non-metastatic gene A protein (BAMBI) 3'-UTR and CDS were significantly decreased in GDM. m6A levels of GDM related genes (INSR and IRS1) were significantly reduced in GDM.
item1310	.	M6ATAR00558	.	M6ADIS0148	.	33667648	Down-regulation of m6A both in the 3'-UTR and CDS near stop codons of placental mRNAs is involved in gestational diabetes mellitus(GDM) development in Han Chinese women. MazF-qPCR verified that the m6A levels of the BAMBI 3'-UTR and CDS were significantly decreased in GDM. m6A levels of GDM related genes (Insulin receptor (INSR) and IRS1) were significantly reduced in GDM.
item1311	.	M6ATAR00559	.	M6ADIS0148	.	33667648	Down-regulation of m6A both in the 3'-UTR and CDS near stop codons of placental mRNAs is involved in gestational diabetes mellitus(GDM) development in Han Chinese women. MazF-qPCR verified that the m6A levels of the BAMBI 3'-UTR and CDS were significantly decreased in GDM. m6A levels of GDM related genes (INSR and Insulin receptor substrate 1 (IRS1)) were significantly reduced in GDM.
item1312	REG00024	M6ATAR00560	Up	M6ADIS0065	M6ADRUG0097	35279688	"In breast cancer, accordingly YTHDF1 knockdown sensitizes breast cancer cells to Adriamycin and Cisplatin as well as Olaparib, a PARP inhibitor. Transcription factor E2F8 (E2F8) is a target molecule by YTHDF1 which modulates E2F8 mRNA stability and DNA damage repair in a METTL14-dependent manner."
item1313	REG00025	.	.	M6ADIS0164	.	34647423	"m6A(YTHDF3 and YTHDC1) modification plays a key role in severe asthma, and is able to guide the future strategy of immunotherapy."
item1314	REG00022	.	.	M6ADIS0164	.	34647423	"m6A(YTHDF3 and YTHDC1) modification plays a key role in severe asthma, and is able to guide the future strategy of immunotherapy."
item1315	REG00025	.	.	M6ADIS0102	.	32042813	"YTHDF3 represented an even greater risk of rupture. Regarding the cellular location, METTL14 seemed to be associated with inflammatory infiltrates and neovascularization. Furthermore, a strong correlation was seen between FTO and aneurysmal smooth muscle cells (SMCs), YTHDF3, and macrophage infiltrate. The results also reveal the important roles of m6A modulators, including YTHDF3, FTO, and METTL14, in the pathogenesis of human human abdominal aortic aneurysm(AAA) and provide a new view on m6A modification in AAA."
item1316	REG00006	.	.	M6ADIS0102	.	32042813	"YTHDF3 represented an even greater risk of rupture. Regarding the cellular location, METTL14 seemed to be associated with inflammatory infiltrates and neovascularization. Furthermore, a strong correlation was seen between FTO and aneurysmal smooth muscle cells (SMCs), YTHDF3, and macrophage infiltrate. The results also reveal the important roles of m6A modulators, including YTHDF3, FTO, and METTL14, in the pathogenesis of human human abdominal aortic aneurysm(AAA) and provide a new view on m6A modification in AAA."
item1317	REG00001	.	.	M6ADIS0102	.	32042813	"YTHDF3 represented an even greater risk of rupture. Regarding the cellular location, METTL14 seemed to be associated with inflammatory infiltrates and neovascularization. Furthermore, a strong correlation was seen between FTO and aneurysmal smooth muscle cells (SMCs), YTHDF3, and macrophage infiltrate. The results also reveal the important roles of m6A modulators, including YTHDF3, FTO, and METTL14, in the pathogenesis of human human abdominal aortic aneurysm(AAA) and provide a new view on m6A modification in AAA."
item1318	.	M6ATAR00368	.	M6ADIS0147	.	32863943	"m6A regulators were mostly upregulated in Gastrointestinal cancer and their differential expression significantly influenced the overall survival of patients with GI cancer. The PI3-kinase subunit alpha (PI3k/PIK3CA)/Akt and mammalian target of rapamycin (mTOR) signaling pathways were found to be potentially affected by m6A modification in most human cancers, including GI cancer, which was further verified by m6A-Seq and phospho-MAPK array."
item1319	.	M6ATAR00175	.	M6ADIS0147	.	32863943	"m6A regulators were mostly upregulated in Gastrointestinal cancer and their differential expression significantly influenced the overall survival of patients with GI cancer. The phosphatidylinositol-3-kinase (PI3K)/RAC-alpha serine/threonine-protein kinase (AKT1) and mammalian target of rapamycin (mTOR) signaling pathways were found to be potentially affected by m6A modification in most human cancers, including GI cancer, which was further verified by m6A-Seq and phospho-MAPK array."
item1320	.	M6ATAR00339	.	M6ADIS0147	.	32863943	"m6A regulators were mostly upregulated in Gastrointestinal cancer and their differential expression significantly influenced the overall survival of patients with GI cancer. The phosphatidylinositol-3-kinase (PI3K)/Akt and mammalian target of rapamycin Serine/threonine-protein kinase mTOR (MTOR) signaling pathways were found to be potentially affected by m6A modification in most human cancers, including GI cancer, which was further verified by m6A-Seq and phospho-MAPK array."
item1321	REG00024	M6ATAR00561	Up	M6ADIS0016	.	34111558	Lowering m6A levels through silencing METTL3 suppresses the FMT process in vitro and in vivo. m6A modification regulates EMT by modulating the translation of Potassium voltage-gated channel subfamily H member 6 (KCNH6) mRNA in a YTHDF1-dependent manner. Manipulation of m6A modification through targeting METTL3 becomes a promising strategy for the treatment of idiopathic pulmonary fibrosis.
item1322	REG00007	M6ATAR00561	Up	M6ADIS0016	.	34111558	Lowering m6A levels through silencing METTL3 suppresses the FMT process in vitro and in vivo. m6A modification regulates EMT by modulating the translation of Potassium voltage-gated channel subfamily H member 6 (KCNH6) mRNA in a YTHDF1-dependent manner. Manipulation of m6A modification through targeting METTL3 becomes a promising strategy for the treatment of idiopathic pulmonary fibrosis.
item1323	REG00006	M6ATAR00560	Up	M6ADIS0065	M6ADRUG0097	35279688	"In breast cancer, accordingly YTHDF1 knockdown sensitizes breast cancer cells to Adriamycin and Cisplatin as well as Olaparib, a PARP inhibitor. Transcription factor E2F8 (E2F8) is a target molecule by YTHDF1 which modulates E2F8 mRNA stability and DNA damage repair in a METTL14-dependent manner."
item1324	REG00007	M6ATAR00054	Up	M6ADIS0107	.	33992834	"Nuclear factor NF-kappa-B p105 subunit (NF-Kappa-B/NFKB1) acts as transcription factor to transactivate METTL3/METTL14 genes upon LPS challenge, leading to global RNA m6A hypermethylation. m6A modification in TGF-beta1 upregulation, which helps to shed light on the molecular mechanism of nonalcoholic steatohepatitis(NASH) progression."
item1325	REG00006	M6ATAR00054	Up	M6ADIS0107	.	33992834	"Nuclear factor NF-kappa-B p105 subunit (NF-Kappa-B/NFKB1) acts as transcription factor to transactivate METTL3/METTL14 genes upon LPS challenge, leading to global RNA m6A hypermethylation. m6A modification in TGF-beta1 upregulation, which helps to shed light on the molecular mechanism of nonalcoholic steatohepatitis(NASH) progression."
item1326	REG00007	M6ATAR00199	Up	M6ADIS0086	.	30428350	"PPaRalpha to mediate its mRNA stability to regulate lipid metabolism. Hepatic deletion of Brain and muscle ARNT-like 1 (Bmal1/ARNTL) increases m6A mRNA methylation, particularly of PPaRalpha. Inhibition of m6A methylation via knockdown of m6A methyltransferase METTL3 decreases PPaR-Alpha m6A abundance and increases PPaRalpha mRNA lifetime and expression, reducing lipid accumulation in cells in vitro. YTHDF2 binds to PPaRalpha to mediate its mRNA stability to regulate lipid metabolism. Transcriptional regulation of circadian rhythms is essential for lipid metabolic homeostasis, disruptions of which can lead to metabolic diseases."
item1327	REG00007	M6ATAR00475	Down	M6ADIS0086	.	30428350	"PPaRalpha to mediate its mRNA stability to regulate lipid metabolism. Hepatic deletion of Bmal1 increases m6A mRNA methylation, particularly of Peroxisome proliferator-activated receptor alpha (PPARalpha/PPARA). Inhibition of m6A methylation via knockdown of m6A methyltransferase METTL3 decreases PPaR-Alpha m6A abundance and increases PPaRalpha mRNA lifetime and expression, reducing lipid accumulation in cells in vitro. YTHDF2 binds to PPaRalpha to mediate its mRNA stability to regulate lipid metabolism. Transcriptional regulation of circadian rhythms is essential for lipid metabolic homeostasis, disruptions of which can lead to metabolic diseases."
item1328	REG00008	M6ATAR00199	Down	M6ADIS0086	.	30428350	"PPaRalpha to mediate its mRNA stability to regulate lipid metabolism. Hepatic deletion of Brain and muscle ARNT-like 1 (Bmal1/ARNTL) increases m6A mRNA methylation, particularly of PPaRalpha. Inhibition of m6A methylation via knockdown of m6A methyltransferase METTL3 decreases PPaR-Alpha m6A abundance and increases PPaRalpha mRNA lifetime and expression, reducing lipid accumulation in cells in vitro. YTHDF2 binds to PPaRalpha to mediate its mRNA stability to regulate lipid metabolism. Transcriptional regulation of circadian rhythms is essential for lipid metabolic homeostasis, disruptions of which can lead to metabolic diseases."
item1329	REG00008	M6ATAR00475	Down	M6ADIS0086	.	30428350	"PPaRalpha to mediate its mRNA stability to regulate lipid metabolism. Hepatic deletion of Bmal1 increases m6A mRNA methylation, particularly of Peroxisome proliferator-activated receptor alpha (PPARalpha/PPARA). Inhibition of m6A methylation via knockdown of m6A methyltransferase METTL3 decreases PPaR-Alpha m6A abundance and increases PPaRalpha mRNA lifetime and expression, reducing lipid accumulation in cells in vitro. YTHDF2 binds to PPaRalpha to mediate its mRNA stability to regulate lipid metabolism. Transcriptional regulation of circadian rhythms is essential for lipid metabolic homeostasis, disruptions of which can lead to metabolic diseases."
item1330	REG00004	M6ATAR00169	Up	M6ADIS0056	.	33134163	"The levels of m6A and its regulator HNRNPA2B1 were significantly increased in cancerous tissues of esophageal cancer(ESCA), and overexpression of HNRNPA2B1 promotes ESCA progression via up-regulation of de novo fatty acid synthetic enzymes ATP-citrate synthase (ACLY) and ACC1."
item1331	REG00004	M6ATAR00168	Up	M6ADIS0056	.	33134163	"The levels of m6A and its regulator HNRNPA2B1 were significantly increased in cancerous tissues of esophageal cancer(ESCA), and overexpression of HNRNPA2B1 promotes ESCA progression via up-regulation of de novo fatty acid synthetic enzymes ACLY and Acetyl-CoA carboxylase 1 (ACC1/ACACA)."
item1332	REG00007	.	.	M6ADIS0152	.	34671602	"m6A is the most abundant internal modification described in eukaryotic mRNA and several viral RNA including human respiratory syncytial virus (HRSV) infection. METTL3/METTL14 m6A writer complex plays a negative role in HRSV infections protein synthesis and viral titers, while m6A erasers FTO and ALKBH5 had the opposite effect."
item1333	REG00006	.	.	M6ADIS0152	.	34671602	"m6A is the most abundant internal modification described in eukaryotic mRNA and several viral RNA including human respiratory syncytial virus (HRSV) infection. METTL3/METTL14 m6A writer complex plays a negative role in HRSV infections protein synthesis and viral titers, while m6A erasers FTO and ALKBH5 had the opposite effect."
item1334	REG00007	M6ATAR00063	Up	M6ADIS0070	M6ADRUG0098	35278613	"METTL3 acts as a fate determinant that controls the sensitivity of bladder cancer cells to melittin treatment. Moreover, METTL3/hsa-miR-146a-5p/NUMB/NOTCH2 axis plays an oncogenic role in bladder cancer pathogenesis and could be a potential therapeutic target for recurrent bladder cancer treatment."
item1335	REG00001	.	.	M6ADIS0152	.	34671602	"m6A is the most abundant internal modification described in eukaryotic mRNA and several viral RNA including human respiratory syncytial virus (HRSV) infection. METTL3/METTL14 m6A writer complex plays a negative role in HRSV infections protein synthesis and viral titers, while m6A erasers FTO and ALKBH5 had the opposite effect."
item1336	REG00005	.	.	M6ADIS0152	.	34671602	"m6A is the most abundant internal modification described in eukaryotic mRNA and several viral RNA including human respiratory syncytial virus (HRSV) infection. METTL3/METTL14 m6A writer complex plays a negative role in HRSV infections protein synthesis and viral titers, while m6A erasers FTO and ALKBH5 had the opposite effect."
item1337	REG00008	M6ATAR00559	Down	M6ADIS0067	.	34093789	"YTHDF2 inhibited the proliferation and invasion of endometrial cancer(EC) via inhibiting Insulin receptor substrate 1 (IRS1) expression in m6A epigenetic way, which suggests a potential therapeutic target for EC."
item1338	.	M6ATAR00019	.	M6ADIS0135	.	34681673	"Translocated in LipoSarcoma/Fused in Sarcoma (TLS/FUS) is a nuclear RNA binding protein whose mutations cause amyotrophic lateral sclerosis. The binding specificity of TLS/FUS to short RNA fragments derived from PncRNA-D, both wild type and ALS-related TLS/FUS mutants demonstrated stronger binding to m6A-modified RNA fragments."
item1339	REG00007	M6ATAR00399	Up	M6ADIS0059	.	34457066	"METTL3 acts as a critical m6A methyltransferase capable of facilitating colorectal cancer(CRC) progression, and revealed a novel mechanism by which METTL3 promotes CRC cell proliferation and invasion via stabilizing Zinc finger protein SNAI1 (SNAI1) mRNA in an m6A-dependent manner."
item1340	REG00004	M6ATAR00562	Up	M6ADIS0055	.	34631545	"HNRNPA2B1, as an m6A reader, is critical in OSCC development. Its expression is significantly associated with the prognosis of Oral Squamous Cell Carcinoma(OSCC). m6A acts as a proto-oncogene that promotes the OSCC proliferation, migration, and invasion through the EMT progression via the LINE-1 (LINE-1)/TGF-beta1/Snail/Smad2 signaling pathway."
item1341	REG00004	M6ATAR00488	Up	M6ADIS0055	.	34631545	"HNRNPA2B1, as an m6A reader, is critical in OSCC development. Its expression is significantly associated with the prognosis of Oral Squamous Cell Carcinoma(OSCC). m6A acts as a proto-oncogene that promotes the OSCC proliferation, migration, and invasion through the EMT progression via the LINE-1/Transforming growth factor beta-1 proprotein (TGFB1)/Snail/Smad2 signaling pathway."
item1342	REG00004	M6ATAR00399	Up	M6ADIS0055	.	34631545	"HNRNPA2B1, as an m6A reader, is critical in OSCC development. Its expression is significantly associated with the prognosis of Oral Squamous Cell Carcinoma(OSCC). m6A acts as a proto-oncogene that promotes the OSCC proliferation, migration, and invasion through the EMT progression via the LINE-1/TGF-beta1/Zinc finger protein SNAI1 (SNAI1)/Smad2 signaling pathway."
item1343	REG00004	M6ATAR00532	Up	M6ADIS0055	.	34631545	"HNRNPA2B1, as an m6A reader, is critical in OSCC development. Its expression is significantly associated with the prognosis of Oral Squamous Cell Carcinoma(OSCC). m6A acts as a proto-oncogene that promotes the OSCC proliferation, migration, and invasion through the EMT progression via the LINE-1/TGF-beta1/Snail/Mothers against decapentaplegic homolog 2 (SMAD2) signaling pathway."
item1344	REG00007	M6ATAR00563	Down	M6ADIS0070	M6ADRUG0098	35278613	"METTL3 acts as a fate determinant that controls the sensitivity of bladder cancer cells to melittin treatment. Moreover, METTL3/miR-146a-5p/Protein numb homolog (NUMB)/NOTCH2 axis plays an oncogenic role in bladder cancer pathogenesis and could be a potential therapeutic target for recurrent bladder cancer treatment."
item1345	REG00001	.	.	M6ADIS0142	.	34368154	Overexpression of FTO in diabetic cardiomyopathy(DCM) model mice improved cardiac function by reducing myocardial fibrosis and myocyte hypertrophy.
item1346	REG00024	M6ATAR00356	Down	M6ADIS0002	M6ADRUG0067	31931413	"METTL3 significantly decreased m6A level, restoring Cellular tumor antigen p53 (TP53/p53) activation and inhibiting cellular transformation phenotypes in the arsenite-transformed cells. m6A downregulated the expression of the positive p53 regulator, PRDM2, through the YTHDF2-promoted decay of PRDM2 mRNAs. m6A upregulated the expression of the negative p53 regulator, YY1 and MDM2 through YTHDF1-stimulated translation of YY1 and MDM2 mRNA. This study further sheds light on the mechanisms of arsenic carcinogenesis via RNA epigenetics."
item1347	REG00024	M6ATAR00564	Down	M6ADIS0002	M6ADRUG0067	31931413	"METTL3 significantly decreased m6A level, restoring p53 activation and inhibiting cellular transformation phenotypes in the arsenite-transformed cells. m6A downregulated the expression of the positive p53 regulator, PR domain zinc finger protein 2 (PRDM2), through the YTHDF2-promoted decay of PRDM2 mRNAs. m6A upregulated the expression of the negative p53 regulator, YY1 and MDM2 through YTHDF1-stimulated translation of YY1 and MDM2 mRNA. This study further sheds light on the mechanisms of arsenic carcinogenesis via RNA epigenetics."
item1348	REG00007	M6ATAR00356	Up	M6ADIS0002	M6ADRUG0067	31931413	"METTL3 significantly decreased m6A level, restoring Cellular tumor antigen p53 (TP53/p53) activation and inhibiting cellular transformation phenotypes in the arsenite-transformed cells. m6A downregulated the expression of the positive p53 regulator, PRDM2, through the YTHDF2-promoted decay of PRDM2 mRNAs. m6A upregulated the expression of the negative p53 regulator, YY1 and MDM2 through YTHDF1-stimulated translation of YY1 and MDM2 mRNA. This study further sheds light on the mechanisms of arsenic carcinogenesis via RNA epigenetics."
item1349	REG00007	M6ATAR00564	Up	M6ADIS0002	M6ADRUG0067	31931413	"METTL3 significantly decreased m6A level, restoring p53 activation and inhibiting cellular transformation phenotypes in the arsenite-transformed cells. m6A downregulated the expression of the positive p53 regulator, PR domain zinc finger protein 2 (PRDM2), through the YTHDF2-promoted decay of PRDM2 mRNAs. m6A upregulated the expression of the negative p53 regulator, YY1 and MDM2 through YTHDF1-stimulated translation of YY1 and MDM2 mRNA. This study further sheds light on the mechanisms of arsenic carcinogenesis via RNA epigenetics."
item1350	REG00007	M6ATAR00565	Up	M6ADIS0092	.	34660602	"m6A writers METTL3/METTL14 and the m6A reader YTHDF1 orchestrate MAP kinase signal-integrating kinase 2 (MNK2) expression posttranscriptionally and thus control ERK signaling, which is required for the maintenance of muscle myogenesis and contributes to regeneration."
item1351	REG00007	M6ATAR00244	Up	M6ADIS0092	.	34660602	"m6A writers METTL3/METTL14 and the m6A reader YTHDF1 orchestrate MNK2 expression posttranscriptionally and thus control Ephrin type-B receptor 2 (ERK/EPHB2) signaling, which is required for the maintenance of muscle myogenesis and contributes to regeneration."
item1352	REG00006	M6ATAR00565	Up	M6ADIS0092	.	34660602	"m6A writers METTL3/METTL14 and the m6A reader YTHDF1 orchestrate MAP kinase signal-integrating kinase 2 (MNK2) expression posttranscriptionally and thus control ERK signaling, which is required for the maintenance of muscle myogenesis and contributes to regeneration."
item1353	REG00006	M6ATAR00244	Up	M6ADIS0092	.	34660602	"m6A writers METTL3/METTL14 and the m6A reader YTHDF1 orchestrate MNK2 expression posttranscriptionally and thus control Ephrin type-B receptor 2 (ERK/EPHB2) signaling, which is required for the maintenance of muscle myogenesis and contributes to regeneration."
item1354	REG00024	M6ATAR00565	Up	M6ADIS0092	.	34660602	"m6A writers METTL3/METTL14 and the m6A reader YTHDF1 orchestrate MAP kinase signal-integrating kinase 2 (MNK2) expression posttranscriptionally and thus control ERK signaling, which is required for the maintenance of muscle myogenesis contributes to regeneration."
item1355	REG00007	M6ATAR00566	Down	M6ADIS0070	M6ADRUG0098	35278613	"METTL3 acts as a fate determinant that controls the sensitivity of bladder cancer cells to melittin treatment. Moreover, METTL3/miR-146a-5p/NUMB/Neurogenic locus notch homolog protein 2 (NOTCH2) axis plays an oncogenic role in bladder cancer pathogenesis and could be a potential therapeutic target for recurrent bladder cancer treatment."
item1356	REG00024	M6ATAR00244	Up	M6ADIS0092	.	34660602	"m6A writers METTL3/METTL14 and the m6A reader YTHDF1 orchestrate MNK2 expression posttranscriptionally and thus control Ephrin type-B receptor 2 (ERK/EPHB2) signaling, which is required for the maintenance of muscle myogenesis and contribute to regeneration."
item1357	REG00001	.	.	M6ADIS0068	.	33571513	FTO m6A demethylase inhibits prostate cancer cell invasion and migration by regulating total m6A levels.
item1358	REG00007	M6ATAR00567	Down	M6ADIS0178	.	32719095	"<span class=""regualtor"">METTL3 and METTL14 leads to an increase in viral RNA recognition by RIG-I-like receptor 1 (RIG-I), thereby stimulating type I interferon production. The obvious advantage is that m6A deficiency in HBV and HCV induces a higher IFN synthesis and in turn enhance adaptive immunity."
item1359	REG00006	M6ATAR00567	Down	M6ADIS0178	.	32719095	"METTL3 and <span class=""regualtor"">METTL14 leads to an increase in viral RNA recognition by RIG-I-like receptor 1 (RIG-I), thereby stimulating type I interferon production. The obvious advantage is that m6A deficiency in HBV and HCV induces a higher IFN synthesis and in turn enhance adaptive immunity."
item1360	REG00007	M6ATAR00567	Down	M6ADIS0178	.	32719095	"<span class=""regualtor"">METTL3 and METTL14 leads to an increase in viral RNA recognition by RIG-I-like receptor 1 (RIG-I), thereby stimulating type I interferon production. The obvious advantage is that m6A deficiency in HBV and HCV induces a higher IFN synthesis and in turn enhance adaptive immunity."
item1361	REG00006	M6ATAR00567	Down	M6ADIS0178	.	32719095	"METTL3 and <span class=""regualtor"">METTL14 leads to an increase in viral RNA recognition by RIG-I-like receptor 1 (RIG-I), thereby stimulating type I interferon production. The obvious advantage is that m6A deficiency in HBV and HCV induces a higher IFN synthesis and in turn enhance adaptive immunity."
item1362	REG00007	M6ATAR00568	Up	M6ADIS0110	.	35501316	"m6A-mediated Long intergenic non-protein coding RNA 680 (LINC00680) regulates the proliferation and ECM degradation of chondrocytes through LINC00680/m6A/SIRT1 mRNA axis. METTL3-mediated LINC00680 accelerates osteoarthritis(OA) progression, which provides novel understanding of the role of m6A and lncRNA in OA."
item1363	REG00007	M6ATAR00393	Up	M6ADIS0110	.	35501316	"m6A-mediated LINC00680 regulates the proliferation and ECM degradation of chondrocytes through LINC00680/m6A/NAD-dependent protein deacetylase sirtuin-1 (SIRT1) mRNA axis. METTL3-mediated LINC00680 accelerates osteoarthritis(OA) progression, which provides novel understanding of the role of m6A and lncRNA in OA."
item1364	REG00007	M6ATAR00356	Up	M6ADIS0006	M6ADRUG0094	35503144	Cellular tumor antigen p53 (TP53/p53) n6-methyladenosine (m6A) played a decisive role in regulating Hepatocellular carcinoma(HCC) sensitivity to chemotherapy via the p53 activator RG7112 and the vascular endothelial growth factor receptor inhibitor apatinib. p53 mRNA m6A modification blockage induced by S-adenosyl homocysteine or siRNA-mediated METTL3 inhibition enhanced HCC sensitivity to chemotherapy.
item1365	REG00007	M6ATAR00356	Up	M6ADIS0006	M6ADRUG0104	35503144	Cellular tumor antigen p53 (TP53/p53) n6-methyladenosine (m6A) played a decisive role in regulating Hepatocellular carcinoma(HCC) sensitivity to chemotherapy via the p53 activator RG7112 and the vascular endothelial growth factor receptor inhibitor apatinib. p53 mRNA m6A modification blockage induced by S-adenosyl homocysteine or siRNA-mediated METTL3 inhibition enhanced HCC sensitivity to chemotherapy.
item1366	.	M6ATAR00416	.	M6ADIS0061	M6ADRUG0024	35545048	Serine/arginine-rich splicing factor 3 (SRSF3) promotes gemcitabine resistance by regulating ANRIL's splicing and ANRIL-208 (one of the ANRIL spliceosomes) can enhance DNA homologous recombination repair (HR) capacity by forming a complex with Ring1b and EZH2. Demonstrates that abnormal alternative splicing and m6A modification are closely related to chemotherapy resistance in pancreatic cancer.
item1367	REG00007	M6ATAR00569	Up	M6ADIS0070	.	30796352	m6A methyltransferase METTL3 and demethylases ALKBH5 mediate the m6A modification in 3'-UTR of CDCP1 mRNA. METTL3 and CUB domain-containing protein 1 (CDCP1) are upregulated in the bladder cancer patient samples and the expression of METTL3 and CDCP1 is correlated with the progression status of the bladder cancers.
item1368	REG00005	M6ATAR00569	Down	M6ADIS0070	.	30796352	m6A methyltransferase METTL3 and demethylases ALKBH5 mediate the m6A modification in 3'-UTR of CDCP1 mRNA. METTL3 and CUB domain-containing protein 1 (CDCP1) are upregulated in the bladder cancer patient samples and the expression of METTL3 and CDCP1 is correlated with the progression status of the bladder cancers.
item1369	REG00005	M6ATAR00514	Down	M6ADIS0015	.	35300330	"Lower expression TNF alpha-induced protein 3 (TNFAIP3) resulted in the enhanced M1 polarization of retinal microglia in diabetic retinopathy, which was caused by <span class=""regualtor"">ALKBH5 mediated m6A modification."
item1370	REG00022	M6ATAR00416	Up	M6ADIS0157	.	28592530	"Kaposi's sarcoma-associated herpesvirus(KSHV) productive lytic replication plays a pivotal role in the initiation and progression of Kaposi's sarcoma tumors. m6A sites in RTA pre-mRNA crucial for splicing through interactions with <span class=""regualtor"">YTHDC1, Serine/arginine-rich splicing factor 3 (SRSF3) and SRSF10. m6A in regulating RTA pre-mRNA splicing but also suggest that KSHV has evolved a mechanism to manipulate the host m6A machinery to its advantage in promoting lytic replication."
item1371	REG00022	M6ATAR00570	Up	M6ADIS0157	.	28592530	"Kaposi's sarcoma-associated herpesvirus(KSHV) productive lytic replication plays a pivotal role in the initiation and progression of Kaposi's sarcoma tumors. m6A sites in RTA pre-mRNA crucial for splicing through interactions with <span class=""regualtor"">YTHDC1, SRSF3 and Serine/arginine-rich splicing factor 10 (SRSF10). m6A in regulating RTA pre-mRNA splicing but also suggest that KSHV has evolved a mechanism to manipulate the host m6A machinery to its advantage in promoting lytic replication."
item1372	REG00001	M6ATAR00571	Up	M6ADIS0046	.	35211409	"<span class=""regualtor"">FTO depended on its m6A RNA demethylase activity to activate Platelet-derived growth factor receptor beta (PDGFRB)/ERK signaling axis. FTO-mediated m6A demethylation plays an oncogenic role in NPM1-mutated Acute myeloid leukemia(AML)."
item1373	REG00001	M6ATAR00244	Up	M6ADIS0046	.	35211409	"<span class=""regualtor"">FTO depended on its m6A RNA demethylase activity to activate PDGFRB/Ephrin type-B receptor 2 (ERK/EPHB2) signaling axis. FTO-mediated m6A demethylation plays an oncogenic role in NPM1-mutated Acute myeloid leukemia(AML)."
item1374	REG00001	M6ATAR00572	Up	M6ADIS0046	.	35211409	"<span class=""regualtor"">FTO depended on its m6A RNA demethylase activity to activate PDGFRB/ERK signaling axis. FTO-mediated m6A demethylation plays an oncogenic role in Nucleophosmin (NPM1)-mutated Acute myeloid leukemia(AML)."
item1375	REG00004	M6ATAR00573	.	M6ADIS0001	.	35558067	"HNRNPA2B1 and HNRNPC were extensively expressed in the Glioblastoma multiforme(GBM) microenvironment.m6A regulators promoted the stemness state in GBM cancer cells. Cell communication analysis identified genes in the GALECTIN signaling network in GBM samples, and expression of these genes (Galectin-9 (LGALS9), CD44, CD45, and HAVCR2) correlated with that of m6A regulators."
item1376	REG00004	M6ATAR00574	.	M6ADIS0001	.	35558067	"HNRNPA2B1 and HNRNPC were extensively expressed in the Glioblastoma multiforme(GBM) microenvironment.m6A regulators promoted the stemness state in GBM cancer cells. Cell communication analysis identified genes in the GALECTIN signaling network in GBM samples, and expression of these genes (LGALS9, CD44 antigen (CD44), CD45, and HAVCR2) correlated with that of m6A regulators."
item1377	REG00008	M6ATAR00575	Down	M6ADIS0007	M6ADRUG0030	34389432	Increased YTHDF2-mediated endoribonucleolytic cleavage of m6A-modified Circ_ASK1 accounts for its downregulation in gefitinib-resistant cells. Either METTL3 silencing or YTHDF2 silencing suppressed the decay of circASK1 in HCC827-GR cells. This study provides a novel therapeutic target to overcome gefitinib resistance in LUAD patients.
item1378	REG00004	M6ATAR00576	.	M6ADIS0001	.	35558067	"HNRNPA2B1 and HNRNPC were extensively expressed in the Glioblastoma multiforme(GBM) microenvironment.m6A regulators promoted the stemness state in GBM cancer cells. Cell communication analysis identified genes in the GALECTIN signaling network in GBM samples, and expression of these genes (LGALS9, CD44, Receptor-type tyrosine-protein phosphatase C (CD45), and HAVCR2) correlated with that of m6A regulators."
item1379	REG00004	M6ATAR00577	.	M6ADIS0001	.	35558067	"HNRNPA2B1 and HNRNPC were extensively expressed in the Glioblastoma multiforme(GBM) microenvironment.m6A regulators promoted the stemness state in GBM cancer cells. Cell communication analysis identified genes in the GALECTIN signaling network in GBM samples, and expression of these genes (LGALS9, CD44, CD45, and Hepatitis A virus cellular receptor 2 (HAVCR2)) correlated with that of m6A regulators."
item1380	REG00003	M6ATAR00573	.	M6ADIS0001	.	35558067	"HNRNPA2B1 and HNRNPC were extensively expressed in the Glioblastoma multiforme(GBM) microenvironment. m6A regulators promoted the stemness state in GBM cancer cells. Cell communication analysis identified genes in the GALECTIN signaling network in GBM samples, and expression of these genes (Galectin-9 (LGALS9), CD44, CD45, and HAVCR2) correlated with that of m6A regulators."
item1381	REG00003	M6ATAR00574	.	M6ADIS0001	.	35558067	"HNRNPA2B1 and HNRNPC were extensively expressed in the Glioblastoma multiforme(GBM) microenvironment. m6A regulators promoted the stemness state in GBM cancer cells. Cell communication analysis identified genes in the GALECTIN signaling network in GBM samples, and expression of these genes (LGALS9, CD44 antigen (CD44), CD45, and HAVCR2) correlated with that of m6A regulators."
item1382	REG00003	M6ATAR00576	.	M6ADIS0001	.	35558067	"HNRNPA2B1 and HNRNPC were extensively expressed in the Glioblastoma multiforme(GBM) microenvironment. m6A regulators promoted the stemness state in GBM cancer cells. Cell communication analysis identified genes in the GALECTIN signaling network in GBM samples, and expression of these genes (LGALS9, CD44, Receptor-type tyrosine-protein phosphatase C (CD45), and HAVCR2) correlated with that of m6A regulators."
item1383	REG00003	M6ATAR00577	.	M6ADIS0001	.	35558067	"HNRNPA2B1 and HNRNPC were extensively expressed in the Glioblastoma multiforme(GBM) microenvironment. m6A regulators promoted the stemness state in GBM cancer cells. Cell communication analysis identified genes in the GALECTIN signaling network in GBM samples, and expression of these genes (LGALS9, CD44, CD45, and Hepatitis A virus cellular receptor 2 (HAVCR2)) correlated with that of m6A regulators."
item1384	REG00007	M6ATAR00578	Up	M6ADIS0029	.	35117988	"<span class=""regualtor"">METTL3 regulates certain m6A-methylated transcripts, Thioredoxin domain-containing protein 5 (TXNDC5), targeting the m6A dependent-METTL3 signaling pathway serves as a promising therapeutic strategy for management of patients of acral melanomas."
item1385	REG00005	.	.	M6ADIS0096	.	35530959	"The downregulated <span class=""regualtor"">ALKBH5 contributes to myocardial ischemia/reperfusion injury(MIRI) process by increasing the m6A modification of Trio mRNA and downregulating Trio."
item1386	REG00007	M6ATAR00579	Up	M6ADIS0046	.	35154467	"<span class=""regualtor"">METTL3 and METTL14 play an oncogenic role in acute myeloid leukemia(AML) by targeting E3 ubiquitin-protein ligase Mdm2 (Mdm2)/p53 signal pathway. The knockdown of METTL3 and METTL14 in K562 cell line leads to several changes in the expression of p53 signal pathway, including the upregulation of p53, cyclin dependent kinase inhibitor 1A (CDKN1A/p21), and downregulation of mdm2."
item1387	REG00007	M6ATAR00356	Down	M6ADIS0046	.	35154467	"<span class=""regualtor"">METTL3 and METTL14 play an oncogenic role in acute myeloid leukemia(AML) by targeting mdm2/Cellular tumor antigen p53 (TP53/p53) signal pathway. The knockdown of METTL3 and METTL14 in K562 cell line leads to several changes in the expression of p53 signal pathway, including the upregulation of p53, cyclin dependent kinase inhibitor 1A (CDKN1A/p21), and downregulation of mdm2."
item1388	REG00006	M6ATAR00526	Down	M6ADIS0065	M6ADRUG0091	35562334	m6A-hypomethylation regulated Fibroblast growth factor receptor 4 (FGFR4) phosphorylates GSK-3beta and activates beta-catenin/TCF4-SLC7A11/FPN1 signaling to drive anti-HER2 resistance. Knockdown of METTL14 significantly increased the expression level of FGFR4 in HER2-positive breast cancer cells. FGFR4 reduced the sensitivity of HER2-positive breast cancer to trastuzumab plus pertuzumab or tucatinib. These results pinpoint a mechanism of anti-HER2 resistance and provide a strategy for overcoming resistance via FGFR4 inhibition in recalcitrant HER2-positive breast cancer.
item1389	REG00007	M6ATAR00575	Up	M6ADIS0007	M6ADRUG0030	34389432	Increased YTHDF2-mediated endoribonucleolytic cleavage of m6A-modified Circ_ASK1 accounts for its downregulation in gefitinib-resistant cells. Either METTL3 silencing or YTHDF2 silencing suppressed the decay of circASK1 in HCC827-GR cells. This study provides a novel therapeutic target to overcome gefitinib resistance in LUAD patients.
item1390	REG00007	M6ATAR00213	Up	M6ADIS0046	.	35154467	"<span class=""regualtor"">METTL3 and METTL14 play an oncogenic role in acute myeloid leukemia(AML) by targeting mdm2/p53 signal pathway. The knockdown of METTL3 and METTL14 in K562 cell line leads to several changes in the expression of p53 signal pathway, including the upregulation of p53, cyclin dependent kinase inhibitor 1A (CDKN1A/Cyclin-dependent kinase inhibitor 1 (CDKN1A)), and downregulation of mdm2."
item1391	REG00006	M6ATAR00579	Up	M6ADIS0046	.	35154467	"METTL3 and <span class=""regualtor"">METTL14 play an oncogenic role in acute myeloid leukemia(AML) by targeting E3 ubiquitin-protein ligase Mdm2 (Mdm2)/p53 signal pathway. The knockdown of METTL3 and METTL14 in K562 cell line leads to several changes in the expression of p53 signal pathway, including the upregulation of p53, cyclin dependent kinase inhibitor 1A (CDKN1A/p21), and downregulation of mdm2."
item1392	REG00006	M6ATAR00356	Down	M6ADIS0046	.	35154467	"METTL3 and <span class=""regualtor"">METTL14 play an oncogenic role in acute myeloid leukemia(AML) by targeting mdm2/Cellular tumor antigen p53 (TP53/p53) signal pathway. The knockdown of METTL3 and METTL14 in K562 cell line leads to several changes in the expression of p53 signal pathway, including the upregulation of p53, cyclin dependent kinase inhibitor 1A (CDKN1A/p21), and downregulation of mdm2."
item1393	REG00006	M6ATAR00213	Up	M6ADIS0046	.	35154467	"METTL3 and <span class=""regualtor"">METTL14 play an oncogenic role in acute myeloid leukemia(AML) by targeting mdm2/p53 signal pathway. The knockdown of METTL3 and METTL14 in K562 cell line leads to several changes in the expression of p53 signal pathway, including the upregulation of p53, cyclin dependent kinase inhibitor 1A (CDKN1A/Cyclin-dependent kinase inhibitor 1 (CDKN1A)), and downregulation of mdm2."
item1394	REG00005	M6ATAR00356	Up	M6ADIS0007	.	35530319	"Knockdown of Cellular tumor antigen p53 (TP53/p53) or inhibition of p53's transcriptional activity by addition of its specific inhibitor PFT-Alpha decreased expression of ALKBH5 and Cancer stem cells' malignancies, the pivotal role of <span class=""regualtor"">ALKBH5 in Cancer stem cells derived from nonsmall-cell lung cancer and highlight the regulatory function of the p53/ALKBH5 axis in modulating CSC progression. p53 transcriptionally regulates PRRX1, which is consistent with our previous report."
item1395	REG00005	M6ATAR00580	Up	M6ADIS0007	.	35530319	"Knockdown of p53 or inhibition of p53's transcriptional activity by addition of its specific inhibitor PFT-Alpha decreased expression of ALKBH5 and Cancer stem cells' malignancies, the pivotal role of <span class=""regualtor"">ALKBH5 in Cancer stem cells derived from nonsmall-cell lung cancer and highlight the regulatory function of the p53/ALKBH5 axis in modulating CSC progression. p53 transcriptionally regulates Paired mesoderm homeobox protein 1 (PRRX1), which is consistent with our previous report."
item1396	REG00001	M6ATAR00581	Down	M6ADIS0081	.	34882999	FTO knockdown elevated Transgelin (SM22alpha) expression and m6A-binding protein IGF2BP2 enhanced SM22alpha mRNA stability by recognizing and binding to m6A methylation modified mRNA. m6A methylation-mediated elevation of SM22alpha restrained VSMC proliferation and migration and ameliorated intimal hyperplasia in T2DM.
item1397	REG00007	M6ATAR00520	Up	M6ADIS0007	.	35078505	"Alpha-enolase (ENO1) positively correlated with <span class=""regualtor"">METTL3 and global m6A levels, and negatively correlated with ALKBH5 in human Lung adenocarcinoma(LUAD). In addition, m6A-dependent elevation of ENO1 was associated with LUAD progression."
item1398	REG00005	M6ATAR00520	Down	M6ADIS0007	.	35078505	"Alpha-enolase (ENO1) positively correlated with METTL3 and global m6A levels, and negatively correlated with <span class=""regualtor"">ALKBH5 in human Lung adenocarcinoma(LUAD). In addition, m6A-dependent elevation of ENO1 was associated with LUAD progression."
item1399	REG00001	M6ATAR00582	Down	M6ADIS0073	.	35090515	FTO acts as a tumor suppressor to inhibit tumor glycolysis in Papillary thyroid cancer(PTC). FTO/Apolipoprotein E (APOE) axis inhibits PTC glycolysis by modulating IL-6/JAK2/STAT3 signaling pathway.
item1400	REG00001	M6ATAR00418	.	M6ADIS0065	M6ADRUG0022	34076564	"Decreased doxorubicin resistance by Signal transducer and activator of transcription 3 (STAT3) knockdown was abolished by FTO overexpression and decreased doxorubicin sensitivity by STAT3 overexpression was reversed by FTO knockdown, indicating that FTO was implicated in STAT3-mediated doxorubicin resistance and impairment of doxorubicin sensitivity of BC cells."
item1401	REG00005	M6ATAR00583	Up	M6ADIS0061	.	34733841	"<span class=""regualtor"">ALKBH5 overexpression incurred a significant reduction in iron-regulatory protein IRP2 and the modulator of epithelial-mesenchymal transition (EMT) SNAI1. Owing to F-box/LRR-repeat protein 5 (FBXL5)-mediated degradation, ALKBH5 overexpression incurred a significant reduction in iron-regulatory protein IRP2 and the modulator of epithelial-mesenchymal transition (EMT) SNAI1. ALKBH5 in protecting against PDAC through modulating regulators of iron metabolism and underscore the multifaceted role of m6A in pancreatic cancer."
item1402	REG00005	M6ATAR00584	Down	M6ADIS0061	.	34733841	"<span class=""regualtor"">ALKBH5 overexpression incurred a significant reduction in iron-regulatory protein Iron-responsive element-binding protein 2 (IRP2) and the modulator of epithelial-mesenchymal transition (EMT) SNAI1. Owing to FBXL5-mediated degradation, ALKBH5 overexpression incurred a significant reduction in iron-regulatory protein IRP2 and the modulator of epithelial-mesenchymal transition (EMT) SNAI1. ALKBH5 in protecting against PDAC through modulating regulators of iron metabolism and underscore the multifaceted role of m6A in pancreatic cancer."
item1403	REG00005	M6ATAR00399	Down	M6ADIS0061	.	34733841	"<span class=""regualtor"">ALKBH5 overexpression incurred a significant reduction in iron-regulatory protein IRP2 and the modulator of epithelial-mesenchymal transition (EMT) Zinc finger protein SNAI1 (SNAI1). Owing to FBXL5-mediated degradation, ALKBH5 overexpression incurred a significant reduction in iron-regulatory protein IRP2 and the modulator of epithelial-mesenchymal transition (EMT) SNAI1. ALKBH5 in protecting against PDAC through modulating regulators of iron metabolism and underscore the multifaceted role of m6A in pancreatic cancer."
item1404	REG00012	M6ATAR00341	Up	M6ADIS0057	.	35489385	"<span class=""regualtor"">IGF2BP1 upregulated in GC tissue and acted as a predictor of poor prognosis for GC patients. IGF2BP1 directly interacted with Myc proto-oncogene protein (MYC) mRNA via m6A-dependent manner to by stabilize its stability."
item1405	REG00007	M6ATAR00585	Up	M6ADIS0068	.	35413135	"<span class=""regualtor"">METTL3 promoted cell proliferation, migration, invasion and tumorigenesis in PCa. METTL3 upregulating the level of m6A, and interacted with DGCR8 to recognize the m6A modification of pre-miR-182 to regulate its splicing and maturation and promote the high expression of miRNA."
item1406	REG00007	M6ATAR00228	Up	M6ADIS0068	.	35413135	"<span class=""regualtor"">METTL3 promoted cell proliferation, migration, invasion and tumorigenesis in PCa. METTL3 upregulating the level of m6A, and interacted with Microprocessor complex subunit DGCR8 (DGCR8) to recognize the m6A modification of pre-miR-182 to regulate its splicing and maturation and promote the high expression of miRNA."
item1407	REG00009	M6ATAR00283	Up	M6ADIS0057	.	33378974	"Oncogenic role of WTAP and its m6A-mediated regulation on gastric cancer Warburg effect, providing a novel approach and therapeutic target in gastric cancer. WTAP enhanced the stability of Hexokinase-2 (HK2) mRNA through binding with the 3'-UTR m6A site."
item1408	REG00006	M6ATAR00425	Up	M6ADIS0099	.	35543357	"Knocking down METTL14 could inhibit the development of atherosclerosis in high-fat diet-treated APOE mice. After transfection with si-METTL14, the bcl-2 expression level and the viability of ox-LDL-incubated cells increased, whereas the apoptosis rate and the expressions of Bax and cleaved caspase-3 decreased. However, the effect of METTL14 knockdown was reversed by Transcription factor p65 (RELA) overexpression."
item1409	REG00006	M6ATAR00196	Down	M6ADIS0099	.	35543357	"Knocking down METTL14 could inhibit the development of atherosclerosis in high-fat diet-treated APOE mice. After transfection with si-METTL14, the Apoptosis regulator Bcl-2 (BCL2) expression level and the viability of ox-LDL-incubated cells increased, whereas the apoptosis rate and the expressions of Bax and cleaved caspase-3 decreased. However, the effect of METTL14 knockdown was reversed by p65 overexpression."
item1410	REG00001	.	.	M6ADIS0018	.	31316467	CTX is associated with reproductive failure and premature ovarian insufficiency (POI) or premature ovarian aging. CTX significantly inhibited the expression levels of RNA demethylase FTO in a time- and concentration-dependent manner.
item1411	REG00012	M6ATAR00586	Up	M6ADIS0006	M6ADRUG0047	35366894	"Driven by m6A modification, Circ_MAP3K4 encoded circMAP3K4-455aa, protected HCC cells from cisplatin exposure, and predicted worse prognosis of HCC patients. IGF2BP1 facilitates circMAP3K4 peptide translation, then the circMAP3K4 peptide inhibits AIF cleavage and nuclear distribution."
item1412	REG00023	M6ATAR00497	Up	M6ADIS0054	.	32850334	YTHDC2 promotes radiotherapy resistance of NPC cells by activating the Insulin-like growth factor 1 receptor (IGF1R)/ATK/S6 signaling axis and serves as a potential therapeutic target in radiosensitization of NPC cells.
item1413	REG00023	M6ATAR00175	Up	M6ADIS0054	.	32850334	YTHDC2 promotes radiotherapy resistance of NPC cells by activating the IGF1R/RAC-alpha serine/threonine-protein kinase (AKT1)/S6 signaling axis and serves as a potential therapeutic target in radiosensitization of NPC cells.
item1414	REG00023	M6ATAR00587	Up	M6ADIS0054	.	32850334	YTHDC2 promotes radiotherapy resistance of NPC cells by activating the IGF1R/ATK/40S ribosomal protein S6 (S6) signaling axis and serves as a potential therapeutic target in radiosensitization of NPC cells.
item1415	REG00009	M6ATAR00094	Up	M6ADIS0051	.	35356854	"A remarkable m6A-modified site was found on the 3'-UTR of FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1), and m6A methyltransferase WTAP promoted the methylation modification, thus enhancing the stability of FOXD2-AS1 transcripts. m6A-modified FOXD2-AS1 accelerates the osteosarcoma progression through m6A manner, which provides new concepts for osteosarcoma tumorigenesis. FOXD2-AS1 interacted with downstream target FOXM1 mRNA through m6A sites, forming a FOXD2-AS1/m6A/FOXM1 complex to heighten FOXM1 mRNA stability."
item1416	REG00009	M6ATAR00258	Up	M6ADIS0051	.	35356854	"A remarkable m6A-modified site was found on the 3'-UTR of FOXD2-AS1, and m6A methyltransferase WTAP promoted the methylation modification, thus enhancing the stability of FOXD2-AS1 transcripts. m6A-modified FOXD2-AS1 accelerates the osteosarcoma progression through m6A manner, which provides new concepts for osteosarcoma tumorigenesis. FOXD2-AS1 interacted with downstream target FOXM1 mRNA through m6A sites, forming a FOXD2-AS1/m6A/Forkhead box protein M1 (FOXM1) complex to heighten FOXM1 mRNA stability."
item1417	REG00001	.	.	M6ADIS0004	.	30297871	Developing resistant phenotypes during tyrosine kinase inhibitor (TKI) therapy depends on m6A reduction resulting from FTO overexpression in leukemia cells.
item1418	REG00007	M6ATAR00213	Down	M6ADIS0056	.	34624569	METTL3 modulates the cell cycle of Esophageal squamous cell carcinoma(ESCC) cells through a Cyclin-dependent kinase inhibitor 1 (CDKN1A)-dependent pattern. METTL3-guided m6A modification contributes to the progression of ESCC via the p21-axis.
item1419	.	M6ATAR00400	.	M6ADIS0157	.	31647415	Staphylococcal nuclease domain-containing protein 1 (SND1) depletion leads to inhibition of KSHV early gene expression showing that SND1 is essential for Kaposi's sarcoma associated herpesvirus(KSHV) lytic replication.
item1420	REG00006	M6ATAR00588	Up	M6ADIS0010	.	35036065	"The expression of METTL14 was negatively correlated to the prognosis, stage, and ccRCC tumor grade. Lnc-LSG1 could be regulated by METTL14. Lnc_LSG1 can directly bind to ESRP2 protein and promote ESRP2 degradation via facilitating ESRP2 ubiquitination."
item1421	REG00006	M6ATAR00589	Up	M6ADIS0010	.	35036065	"The expression of METTL14 was negatively correlated to the prognosis, stage, and ccRCC tumor grade. Lnc-LSG1 could be regulated by METTL14. Lnc-LSG1 can directly bind to Epithelial splicing regulatory protein 2 (ESRP2) protein and promote ESRP2 degradation via facilitating ESRP2 ubiquitination."
item1422	REG00024	M6ATAR00560	Up	M6ADIS0065	M6ADRUG0047	35279688	"In breast cancer, accordingly YTHDF1 knockdown sensitizes breast cancer cells to Adriamycin and Cisplatin as well as Olaparib, a PARP inhibitor. Transcription factor E2F8 (E2F8) is a target molecule by YTHDF1 which modulates E2F8 mRNA stability and DNA damage repair in a METTL14-dependent manner."
item1423	REG00020	M6ATAR00084	Up	M6ADIS0066	.	34951345	"IGF2BP1 was identified as the m6A reader protein of UBA6 divergent transcript (UBA6-DT/UBA6-AS1)-RBM15-mediated m6A modification of UBA6 mRNA, which enhanced the stability of UBA6 mRNA. UBA6-AS1 suppressed the proliferation, migration and invasion of OC cells via UBA6."
item1424	REG00020	M6ATAR00590	Up	M6ADIS0066	.	34951345	"IGF2BP1 was identified as the m6A reader protein of UBA6-AS1-RBM15-mediated m6A modification of Ubiquitin-like modifier-activating enzyme 6 (UBA6) mRNA, which enhanced the stability of UBA6 mRNA. UBA6-AS1 suppressed the proliferation, migration and invasion of OC cells via UBA6."
item1425	REG00012	M6ATAR00084	Up	M6ADIS0066	.	34951345	"IGF2BP1 was identified as the m6A reader protein of UBA6 divergent transcript (UBA6-DT/UBA6-AS1)-RBM15-mediated m6A modification of UBA6 mRNA, which enhanced the stability of UBA6 mRNA. UBA6-AS1 suppressed the proliferation, migration and invasion of OC cells via UBA6."
item1426	REG00012	M6ATAR00590	Up	M6ADIS0066	.	34951345	"IGF2BP1 was identified as the m6A reader protein of UBA6-AS1-RBM15-mediated m6A modification of Ubiquitin-like modifier-activating enzyme 6 (UBA6) mRNA, which enhanced the stability of UBA6 mRNA. UBA6-AS1 suppressed the proliferation, migration and invasion of OC cells via UBA6."
item1427	REG00007	M6ATAR00163	Down	M6ADIS0099	.	35359726	"m6A driven machinery in virus-induced vascular endothelium damage and highlight the significance of vitamin D3 in the intervention of HCMV-induced atherosclerosis. METTL3 methylates mitochondrial calcium uniporter (MCU), the main contributor to HCMV-induced apoptosis of vascular endothelial cells, at three m6A residues in the 3'-UTR. Vitamin D3 downregulated the METTL3 by inhibiting the activation of AMPK subunit alpha-1 (AMPK/PRKAA1), thereby inhibiting the m6A modification of MCU and cell apoptosis."
item1428	REG00023	M6ATAR00591	.	M6ADIS0157	.	35177478	This modification recruits the m6A reader YTHDC2 and found that YTHDC2 is necessary for the escape of the IL-6 transcript. m6A modification is essential to confer SOX (SOX) resistance to the IL-6 mRNA. These results shed light on how the host cell has evolved to use RNA modifications to circumvent viral manipulation of RNA fate during KSHV infection Kaposi's sarcoma.
item1429	REG00023	M6ATAR00529	.	M6ADIS0157	.	35177478	This modification recruits the m6A reader YTHDC2 and found that YTHDC2 is necessary for the escape of the IL-6 transcript. m6A modification is essential to confer SOX resistance to the Interleukin-6 (IL-6) mRNA. These results shed light on how the host cell has evolved to use RNA modifications to circumvent viral manipulation of RNA fate during KSHV infection Kaposi's sarcoma.
item1430	REG00026	M6ATAR00489	.	M6ADIS0002	.	34764728	Ginsenoside Rh2 reduces m6A RNA methylation via downregulating KIF26B expression in some cancer cells. KIF26B elevates m6A RNA methylation via enhancing ZC3H13/CBLL1 nuclear localization. KIF26B-SRF forms a positive feedback loop facilitating tumor growth.
item1431	REG00032	M6ATAR00489	.	M6ADIS0002	.	34764728	Ginsenoside Rh2 reduces m6A RNA methylation via downregulating KIF26B expression in some cancer cells. KIF26B elevates m6A RNA methylation via enhancing ZC3H13/CBLL1 nuclear localization. KIF26B-SRF forms a positive feedback loop facilitating tumor growth.
item1432	REG00007	M6ATAR00484	Up	M6ADIS0007	.	34996469	"METTL3-mediated m-6A modification could stabilize Cystine/glutamate transporter (SLC7A11) mRNA and promote its translation, thus promoting LUAD cell proliferation and inhibiting cell ferroptosis, a novel form of programmed cell death."
item1433	REG00006	M6ATAR00560	Up	M6ADIS0065	M6ADRUG0047	35279688	"In breast cancer, accordingly YTHDF1 knockdown sensitizes breast cancer cells to Adriamycin and Cisplatin as well as Olaparib, a PARP inhibitor. Transcription factor E2F8 (E2F8) is a target molecule by YTHDF1 which modulates E2F8 mRNA stability and DNA damage repair in a METTL14-dependent manner."
item1434	REG00001	M6ATAR00592	Down	M6ADIS0115	.	34462564	Both depletion of FTO and application of the FTO inhibitor FB23 or FB23-2 impaired osteogenic differentiation of human MSCs. Knockdown of Peroxisome proliferator-activated receptor gamma (PPARG) promoted FTO-induced expression of the osteoblast biomarkers ALPL and OPN during osteogenic differentiation. This study demonstrates the functional significance of the FTO-PPARG axis in promoting the osteogenesis of human MSCs and sheds light on the role of m6A modification in mediating osteoporosis and osteonecrosis.
item1435	REG00007	M6ATAR00488	Up	M6ADIS0002	.	31991845	"The expression of Transforming growth factor beta-1 proprotein (TGFB1) was up-regulated, while self-stimulated expression of TGFbeta1 was suppressed in METTL3Mut/- cells. m6A performed multi-functional roles in TGFbeta1 expression and EMT modulation, suggesting the critical roles of m6A in cancer progression regulation. Snail, which was down-regulated in Mettl3Mut/- cells, was a key factor responding to TGF-Beta-1-induced EMT."
item1436	REG00007	M6ATAR00399	Up	M6ADIS0002	.	31991845	"The expression of TGFbeta1 was up-regulated, while self-stimulated expression of TGFbeta1 was suppressed in METTL3Mut/- cells. m6A performed multi-functional roles in TGFbeta1 expression and EMT modulation, suggesting the critical roles of m6A in cancer progression regulation. Zinc finger protein SNAI1 (SNAI1), which was down-regulated in Mettl3Mut/- cells, was a key factor responding to TGF-Beta-1-induced EMT."
item1437	REG00015	M6ATAR00283	Up	M6ADIS0059	.	35546050	"KIAA1429 has the potential to promote CRC carcinogenesis by targeting Hexokinase-2 (HK2) via m6A-independent manner, providing insight into the critical roles of m6A in CRC."
item1438	REG00001	M6ATAR00593	Up	M6ADIS0048	M6ADRUG0102	34915192	"FTO significantly promotes MM cell proliferation, migration, and invasion by targeting Heat shock factor protein 1 (HSF1)/HSPs in a YTHDF2-dependent manner. FTO inhibition, especially when combined with bortezomib (BTZ) treatment, synergistically inhibited myeloma bone tumor formation and extramedullary spread in NCG mice."
item1439	REG00006	M6ATAR00260	Up	M6ADIS0162	.	35597169	"Global RNA m6A methylation and METTL14 expression were significantly increased in placental tissues obtained from patients with preeclampsia. Forkhead box protein O3 (FOXO3) inhibition effectively prevented the impairment of trophoblast proliferation and invasion, and diminished the induction of trophoblast autophagy and apoptosis in METTL14-overexpressing HTR-8/SVneo cells."
item1440	REG00001	.	.	M6ADIS0104	M6ADRUG0093	35402566	"The RNA demethylase FTO was downregulated, whereas METTL14 and WTAP were upregulated. Furthermore, gain- and loss-of-function studies substantiated that FTO is cardioprotective in TKI(Sunitinib)."
item1441	REG00006	.	.	M6ADIS0104	M6ADRUG0093	35402566	"The RNA demethylase FTO was downregulated, whereas METTL14 and WTAP were upregulated. Furthermore, gain- and loss-of-function studies substantiated that FTO is cardioprotective in TKI(Sunitinib)."
item1442	REG00009	.	.	M6ADIS0104	M6ADRUG0093	35402566	"The RNA demethylase FTO was downregulated, whereas METTL14 and WTAP were upregulated. Furthermore, gain- and loss-of-function studies substantiated that FTO is cardioprotective in TKI(Sunitinib)."
item1443	REG00005	M6ATAR00497	Up	M6ADIS0067	.	32913456	ALKBH5 promoted proliferation and invasion of endometrial cancer via erasing Insulin-like growth factor 1 receptor (IGF1R) m6A-modifications.
item1444	REG00008	M6ATAR00594	Up	M6ADIS0008	M6ADRUG0047	35489084	YTHDF2 interference could suppress the EMT of cervical cancer cells and enhance cisplatin chemosensitivity by regulating Axin-1 (AXIN1).
item1445	REG00006	M6ATAR00595	Down	M6ADIS0066	.	35251990	METTL14 overexpression decreased ovarian cancer proliferation by inhibition of Tastin (TROAP) expression via an m6A RNA methylation-dependent mechanism.
item1446	REG00007	M6ATAR00596	Up	M6ADIS0051	.	35145841	"METTL3 is highly expressed in OS and enhances TNF receptor-associated factor 6 (TRAF6) expression through m6A modification, thereby promoting the metastases of OS cells."
item1447	REG00007	M6ATAR00283	Up	M6ADIS0008	.	33099572	"METTL3 enhanced the Hexokinase-2 (HK2) stability through YTHDF1-mediated m6A modification, thereby promoting the Warburg effect of CC, which promotes a novel insight for the CC treatment."
item1448	REG00024	M6ATAR00283	Up	M6ADIS0008	.	33099572	"METTL3 enhanced the Hexokinase-2 (HK2) stability through YTHDF1-mediated m6A modification, thereby promoting the Warburg effect of CC, which promotes a novel insight for the CC treatment."
item1449	REG00007	M6ATAR00597	Down	M6ADIS0065	.	32766145	"METTL3 could down-regulate the expression of Collagen alpha-1 (III) chain (COL3A1) by increasing its m6A methylation, ultimately inhibiting the metastasis of TNBC cells."
item1450	REG00005	M6ATAR00598	Up	M6ADIS0151	.	35190939	"Overexpression of the ALKBH5 promoted production of intron retention on the human papillomavirus type 16 (HPV16) Protein E6 (E6) mRNAs thereby promoting E6 mRNA production. METLL3 induced production of intron-containing HPV16 E1 mRNAs over spliced E2 mRNAs and altered HPV16 L1 mRNA splicing in a manner opposite to ALKBH5. Overexpression of YTHDC1, enhanced retention of the E6-encoding intron and promoted E6 mRNA production. HPV16 mRNAs are m6A-methylated in tonsillar cancer cells."
item1451	REG00022	M6ATAR00598	Up	M6ADIS0151	.	35190939	"Overexpression of the ALKBH5 promoted production of intron retention on the human papillomavirus type 16 (HPV16) E6 mRNAs thereby promoting Protein E6 (E6) mRNA production. METLL3 induced production of intron-containing HPV16 E1 mRNAs over spliced E2 mRNAs and altered HPV16 L1 mRNA splicing in a manner opposite to ALKBH5. Overexpression of YTHDC1, enhanced retention of the E6-encoding intron and promoted E6 mRNA production. HPV16 mRNAs are m6A-methylated in tonsillar cancer cells."
item1452	REG00007	M6ATAR00598	Up	M6ADIS0151	.	35190939	"Overexpression of the ALKBH5 promoted production of intron retention on the human papillomavirus type 16 (HPV16) E6 mRNAs thereby promoting Protein E6 (E6) mRNA production.METLL3 induced production of intron-containing HPV16 E1 mRNAs over spliced E2 mRNAs and altered HPV16 L1 mRNA splicing in a manner opposite to ALKBH5. Overexpression of YTHDC1, enhanced retention of the E6-encoding intron and promoted E6 mRNA production. HPV16 mRNAs are m6A-methylated in tonsillar cancer cells."
item1453	REG00007	M6ATAR00599	Up	M6ADIS0008	.	34178650	METTL3 modulates miR-193b mature process in an m6A-dependent manner. Reintroduction of hsa-miR-193b profoundly inhibits tumorigenesis of cervical cancer cells both in vivo and in vitro through CCND1 targeting.
item1454	REG00007	M6ATAR00206	Down	M6ADIS0008	.	34178650	METTL3 modulates miR-193b mature process in an m6A-dependent manner. Reintroduction of miR-193b profoundly inhibits tumorigenesis of cervical cancer cells both in vivo and in vitro through G1/S-specific cyclin-D1 (CCND1) targeting.
item1455	REG00004	M6ATAR00600	Up	M6ADIS0059	M6ADRUG0101	35279145	Mir-100-let-7a-2-mir-125b-1 cluster host gene (MIR100HG) and hnRNPA2B1 interact to control the transcriptional activity of Wnt signaling in CRC via regulation of TCF7L2 mRNA stability. These findings identified MIR100HG as a potent EMT inducer in CRC that will contribute to cetuximab resistance and metastasis by activation of a MIR100HG/hnRNPA2B1/TCF7L2 feedback loop.
item1456	.	M6ATAR00601	.	M6ADIS0088	.	35453019	"Paraquat (PQ) is a ubiquitously applied herbicide. Long-term PQ exposure with low dose has been reported to induce abnormal expression of long non-coding RNAs (lncRNAs) in brain nerve cells, which could further lead to Parkinson's disease (PD). Tow specific m6A modified lncRNAs were identified: Lnc_CDC5L and lncRNA STAT3, which could influence downstream autophagy related biological function."
item1457	.	M6ATAR00602	.	M6ADIS0088	.	35453019	"Paraquat (PQ) is a ubiquitously applied herbicide. Long-term PQ exposure with low dose has been reported to induce abnormal expression of long non-coding RNAs (lncRNAs) in brain nerve cells, which could further lead to Parkinson's disease (PD). Tow specific m6A modified lncRNAs were identified: lncRNA CDC5L and Lnc_STAT3, which could influence downstream autophagy related biological function."
item1458	REG00007	M6ATAR00137	Up	M6ADIS0144	.	34382070	"The METTL3/m6A/miR126 pathway, whose inhibition contributes to endometriosis development by enhancing cellular migration and invasion."
item1459	REG00015	M6ATAR00603	Up	M6ADIS0007	M6ADRUG0030	34001850	"m6A methyltransferase KIAA1429 was highly expressed in gefitinib-resistant NSCLC cells (PC9-GR), tissues, and closely related to unfavorable survival. KIAA1429 plays essential oncogenic roles in NSCLC gefitinib resistance, which provided a feasible therapeutic target for NSCLC."
item1460	REG00007	M6ATAR00375	Down	M6ADIS0007	.	35069732	Bete-elemene exerted the restrictive impacts on the cell growth of lung cancer in vivo and in vitro through targeting METTL3. Bete-elemene contributed to the augmented PTEN expression via suppressing its m6A modification.
item1461	REG00007	M6ATAR00604	Down	M6ADIS0143	.	33869171	"The NRIP1 mRNA increased in fetal brain tissues of DS, whereas the m6A modification of the NRIP1 mRNA significantly decreased. METTL3 knockdown reduced the m6A modification of NRIP1 mRNA and increased its expression, and an increase in NRIP1 m6A modification and a decrease in its expression were observed in METTL3-overexpressed cells."
item1462	REG00007	M6ATAR00605	Down	M6ADIS0117	.	34335245	"TFA could ameliorate HG-induced pyroptosis and injury in podocytes by targeting METTL3-dependent m6A modification via the regulation of NACHT, LRR and PYD domains-containing protein 3 (NLRP3)-inflammasome activation and PTEN/PI3K/Akt signaling. This study provides a better understanding of how TFA can protect podocytes in diabetic kidney disease (DKD)."
item1463	REG00013	.	Up	M6ADIS0006	.	34347395	"The combination of m6A writers, IGF2BP2, and CTNNB1 distinguished CCA tissues from normal tissues."
item1464	REG00007	M6ATAR00606	Up	M6ADIS0089	.	35547627	"METTL3 rescues the A-Bete-induced reduction of Nucleolar protein 3 (ARC) expression via YTHDF1-Dependent m6A modification, which suggests an important mechanism of epigenetic alteration in AD."
item1465	REG00024	M6ATAR00606	Up	M6ADIS0089	.	35547627	"METTL3 rescues the A-Bete-induced reduction of Nucleolar protein 3 (ARC) expression via YTHDF1-Dependent m6A modification, which suggests an important mechanism of epigenetic alteration in AD."
item1466	REG00004	M6ATAR00607	Up	M6ADIS0059	M6ADRUG0101	35279145	MIR100HG and hnRNPA2B1 interact to control the transcriptional activity of Wnt signaling in CRC via regulation of Transcription factor 7-like 2 (TCF7L2) mRNA stability. These findings identified MIR100HG as a potent EMT inducer in CRC that contribute to cetuximab resistance and metastasis by activation of a MIR100HG/hnRNPA2B1/TCF7L2 feedback loop.
item1467	REG00007	M6ATAR00175	Up	M6ADIS0007	.	35284536	"METTL3 contributes to the progression and chemoresistance of NSCLC by promoting RAC-alpha serine/threonine-protein kinase (AKT1) protein expression through regulating AKT1 mRNA m6A levels, and provides an efficient therapeutic intervention target for overcoming chemoresistance in NSCLC."
item1468	REG00007	M6ATAR00608	Up	M6ADIS0177	.	33061938	Overexpressed Pigment epithelium-derived factor (PEDF) abrogates the inhibition of cell proliferation in DLBCL cells that is caused by METTL3 silence.
item1469	REG00007	M6ATAR00609	Up	M6ADIS0029	.	34430596	"m6A-METTL3 axis induced abnormal Uridine-cytidine kinase 2 (UCK2) expression plays a role in melanoma metastasis by enhancing the Wnt/Bete-catenin pathway, which provided new clues for melanoma metastasis. It also provides a potential target for the prevention and treatment of melanoma."
item1470	REG00008	M6ATAR00341	Up	M6ADIS0001	M6ADRUG0099	33023892	"The IGF1/IGF1R inhibitor, linsitinib for further investigation based upon the role of the IGF pathway member, IGFBP3, as a downstream effector of YTHDF2-Myc proto-oncogene protein (MYC) axis in GSCs. Inhibiting glioblastoma stem cells viability without affecting NSCs and impairing in vivo glioblastoma growth."
item1471	REG00007	M6ATAR00351	Up	M6ADIS0056	.	34513313	"METTL3-catalyzed m6A modification promotes Neurogenic locus notch homolog protein 1 (NOTCH1) expression and the activation of the Notch signaling pathway. Forced activation of Notch signaling pathway successfully rescues the growth, migration, and invasion capacities of METTL3-depleted ESCC cells."
item1472	REG00007	M6ATAR00500	Up	M6ADIS0003	.	35446451	"The decline in METTL3 levels was responsible for CTCL cell proliferation and migration,Cyclin-dependent kinase inhibitor 2A (CDKN2A) was a key regulator during this process in vitro and in vivo, and insufficient methylation modification blocked the interaction between CDKN2A and m6A reader IGF2BP2, resulting in mRNA degradation."
item1473	REG00013	M6ATAR00500	Up	M6ADIS0003	.	35446451	"The decline in METTL3 levels was responsible for CTCL cell proliferation and migration,Cyclin-dependent kinase inhibitor 2A (CDKN2A) was a key regulator during this process in vitro and in vivo, and insufficient methylation modification blocked the interaction between CDKN2A and m6A reader IGF2BP2, resulting in mRNA degradation."
item1474	REG00007	M6ATAR00360	Up	M6ADIS0065	.	35197058	Programmed cell death 1 ligand 1 (CD274/PD-L1) was a downstream target of METTL3-mediated m6A modification in breast cancer cells. METTL3-mediated PD-L1 mRNA activation was m6A-IGF2BP3-dependent. PD-L1 expression was also positively correlated with METTL3 and IGF2BP3 expression in breast cancer tissues.
item1475	REG00014	M6ATAR00360	Up	M6ADIS0065	.	35197058	Programmed cell death 1 ligand 1 (CD274/PD-L1) was a downstream target of METTL3-mediated m6A modification in breast cancer cells. METTL3-mediated PD-L1 mRNA activation was m6A-IGF2BP3-dependent. PD-L1 expression was also positively correlated with METTL3 and IGF2BP3 expression in breast cancer tissues.
item1476	REG00005	M6ATAR00221	Down	M6ADIS0070	M6ADRUG0047	33376625	"Knockdown of ALKBH5 promoted bladder cancer cell proliferation, migration, invasion, and decreased cisplatin chemosensitivity, ALKBH5 inhibited the progression and sensitized bladder cancer cells to cisplatin through a Casein kinase II subunit alpha' (CSNK2A2)-mediated glycolysis pathway in an m6A-dependent manner."
item1477	REG00024	M6ATAR00560	Up	M6ADIS0065	M6ADRUG0022	35279688	"In breast cancer, accordingly YTHDF1 knockdown sensitizes breast cancer cells to Adriamycin and Cisplatin as well as Olaparib, a PARP inhibitor. Transcription factor E2F8 (E2F8) is a target molecule by YTHDF1 which modulates E2F8 mRNA stability and DNA damage repair in a METTL14-dependent manner."
item1478	REG00005	M6ATAR00418	Down	M6ADIS0051	.	35490460	"ALKBH5 inactivated Signal transducer and activator of transcription 3 (STAT3) pathway by increasing SOCS3 expression via an m6A-YTHDF2-dependent manner. Reducing m6A mRNA levels in human osteosarcoma cells through ALKBH5 up-regulation lead to cell proliferation inhibition, cell apoptosis and cycle arrest."
item1479	REG00008	M6ATAR00418	Down	M6ADIS0051	.	35490460	"ALKBH5 inactivated Signal transducer and activator of transcription 3 (STAT3) pathway by increasing SOCS3 expression via an m6A-YTHDF2-dependent manner. Reducing m6A mRNA levels in human osteosarcoma cells through ALKBH5 up-regulation lead to cell proliferation inhibition, cell apoptosis and cycle arrest."
item1480	REG00005	M6ATAR00610	Down	M6ADIS0051	.	35490460	"ALKBH5 inactivated STAT3 pathway by increasing Suppressor of cytokine signaling 3 (SOCS3) expression via an m6A-YTHDF2-dependent manner. Reducing m6A mRNA levels in human osteosarcoma cells through ALKBH5 up-regulation lead to cell proliferation inhibition, cell apoptosis and cycle arrest."
item1481	REG00008	M6ATAR00610	Down	M6ADIS0051	.	35490460	"ALKBH5 inactivated STAT3 pathway by increasing Suppressor of cytokine signaling 3 (SOCS3) expression via an m6A-YTHDF2-dependent manner.Reducing m6A mRNA levels in human osteosarcoma cells through ALKBH5 up-regulation lead to cell proliferation inhibition, cell apoptosis and cycle arrest."
item1482	REG00024	M6ATAR00427	Up	M6ADIS0005	.	33204330	YTHDF1 enhanced Transferrin receptor protein 1 (TFRC) expression in HPSCC through an m6A-dependent mechanism.
item1483	REG00006	M6ATAR00611	Down	M6ADIS0163	.	35139773	"The expression of METTL14 is significantly reduced in patients with retinitis pigmentosa (RP). METTL14 regulates the expression of Microtubule-associated protein 2 (MAP2) via the modification of m6A, resulting in the dysregulation of NEUROD1 and pathologic changes in RPE cells."
item1484	REG00006	M6ATAR00612	Down	M6ADIS0163	.	35139773	"The expression of METTL14 is significantly reduced in patients with retinitis pigmentosa (RP). METTL14 regulates the expression of MAP2 via the modification of m6A, resulting in the dysregulation of Neurogenic differentiation factor 1 (NEUROD1) and pathologic changes in RPE cells."
item1485	REG00007	M6ATAR00517	Up	M6ADIS0001	.	35474040	"METTL3-mediated m6A modification upregulated Circ_DLC1 expression, and circDLC1 promoted CTNNBIP1 transcription by sponging miR-671-5p, thus repressing the malignant proliferation of glioma."
item1486	REG00007	M6ATAR00613	Up	M6ADIS0001	.	35474040	"METTL3-mediated m6A modification upregulated circDLC1 expression, and circDLC1 promoted CTNNBIP1 transcription by sponging hsa-miR-671-5p, thus repressing the malignant proliferation of glioma."
item1487	REG00007	M6ATAR00614	Up	M6ADIS0001	.	35474040	"METTL3-mediated m6A modification upregulated circDLC1 expression, and circDLC1 promoted Beta-catenin-interacting protein 1 (CTNNBIP1) transcription by sponging miR-671-5p, thus repressing the malignant proliferation of glioma."
item1488	REG00006	M6ATAR00560	Up	M6ADIS0065	M6ADRUG0022	35279688	"In breast cancer, accordingly YTHDF1 knockdown sensitizes breast cancer cells to Adriamycin and Cisplatin as well as Olaparib, a PARP inhibitor. Transcription factor E2F8 (E2F8) is a target molecule by YTHDF1 which modulates E2F8 mRNA stability and DNA damage repair in a METTL14-dependent manner."
item1489	REG00001	M6ATAR00615	Down	M6ADIS0061	.	35404184	"Knockdown of FTO increases m6A methylation of Tissue factor pathway inhibitor 2 (TFPI-2) mRNA in PC cells, thereby increasing mRNA stability via the m6A reader YTHDF1."
item1490	REG00024	M6ATAR00615	Up	M6ADIS0061	.	35404184	"Knockdown of FTO increases m6A methylation of Tissue factor pathway inhibitor 2 (TFPI-2) mRNA in PC cells, thereby increasing mRNA stability via the m6A reader YTHDF1."
item1491	REG00006	M6ATAR00616	Down	M6ADIS0057	.	35164771	METTL14-mediated m6A modification of Circ_ORC5 suppresses gastric cancer progression by regulating miR-30c-2-3p/AKT1S1 axis. METTL14 was downregulated in GC tissue samples and its low expression acted as a prognostic factor of poor survival in patients with GC.
item1492	REG00006	M6ATAR00617	Up	M6ADIS0057	.	35164771	METTL14-mediated m6A modification of circORC5 suppresses gastric cancer progression by regulating hsa-miR-30c-2-3p/AKT1S1 axis.METTL14 was downregulated in GC tissue samples and its low expression acted as a prognostic factor of poor survival in patients with GC.
item1493	REG00006	M6ATAR00618	Down	M6ADIS0057	.	35164771	METTL14-mediated m6A modification of circORC5 suppresses gastric cancer progression by regulating miR-30c-2-3p/Proline-rich AKT1 substrate 1 (AKT1S1) axis. METTL14 was downregulated in GC tissue samples and its low expression acted as a prognostic factor of poor survival in patients with GC.
item1494	REG00005	M6ATAR00374	Up	M6ADIS0017	.	35318034	"ALKBH5 mediated Protein patched homolog 1 (PTCH1) activation via a m6A-dependent manner,ALKBH5 ameliorated liver fibrosis and suppressed HSCs activation via triggering PTCH1 activation in a m6A dependent manner."
item1495	REG00007	M6ATAR00619	Down	M6ADIS0158	.	34987645	"Specific depletion of METTL3 in pericytes suppressed diabetes-induced pericyte dysfunction and Microvascular complication in vivo. METTL3 overexpression impaired pericyte function by repressing PKC-Eta, Protocadherin Fat 4 (FAT4), and PDGFRA expression, which was mediated by YTHDF2-dependent mRNA decay."
item1496	REG00007	M6ATAR00620	Down	M6ADIS0158	.	34987645	"Specific depletion of METTL3 in pericytes suppressed diabetes-induced pericyte dysfunction and Microvascular complication in vivo. METTL3 overexpression impaired pericyte function by repressing PKC-Eta, FAT4, and Platelet-derived growth factor receptor alpha (PDGFRA) expression, which was mediated by YTHDF2-dependent mRNA decay."
item1497	REG00007	M6ATAR00621	Down	M6ADIS0158	.	34987645	"Specific depletion of METTL3 in pericytes suppressed diabetes-induced pericyte dysfunction and Microvascular complication in vivo. METTL3 overexpression impaired pericyte function by repressing Protein kinase C eta type (PKC-eta), FAT4, and PDGFRA expression, which was mediated by YTHDF2-dependent mRNA decay."
item1498	REG00007	M6ATAR00622	Down	M6ADIS0007	.	34298122	"Cigarette smoking induced aberrant N6-methyladenosine modification of Death-associated protein kinase 2 (DAPK2), which resulted in decreased DAPK2 mRNA stability and expression of its mRNA and protein. This modification was mediated by the m6A ""writer"" METTL3 and the m6A ""reader"" YTHDF2. BAY 11-7085, a NF-Kappa-B signaling selective inhibitor, was shown to efficiently suppressed downregulation of DAPK2-induced oncogenic phenotypes of NSCLC cells."
item1499	REG00006	M6ATAR00268	Down	M6ADIS0065	M6ADRUG0091	35562334	m6A-hypomethylation regulated FGFR4 phosphorylates Glycogen synthase kinase-3 beta (GSK3Beta/GSK3B) and activates beta-catenin/TCF4-SLC7A11/FPN1 signaling to drive anti-HER2 resistance. Knockdown of METTL14 significantly increased the expression level of FGFR4 in HER2-positive breast cancer cells. FGFR4 reduced the sensitivity of HER2-positive breast cancer to trastuzumab plus pertuzumab or tucatinib. These results pinpoint a mechanism of anti-HER2 resistance and provide a strategy for overcoming resistance via FGFR4 inhibition in recalcitrant HER2-positive breast cancer.
item1500	REG00007	M6ATAR00344	Up	M6ADIS0065	.	35121826	"In breast cancer, ZNF217 could upregulate Homeobox protein NANOG (NANOG) by reducing N6-methyladenosine levels via methyltransferase-like 13 (METTL3)."
item1501	REG00008	M6ATAR00622	Down	M6ADIS0007	.	34298122	"Cigarette smoking induced aberrant N6-methyladenosine modification of Death-associated protein kinase 2 (DAPK2), which resulted in decreased DAPK2 mRNA stability and expression of its mRNA and protein. This modification was mediated by the m6A ""writer"" METTL3 and the m6A ""reader"" YTHDF2. BAY 11-7085, a NF-Kappa-B signaling selective inhibitor, was shown to efficiently suppressed downregulation of DAPK2-induced oncogenic phenotypes of NSCLC cells."
item1502	REG00006	M6ATAR00259	Up	M6ADIS0145	.	32802173	METTL14 promotes Forkhead box protein O1 (FOXO1) expression by enhancing its m6A modification and inducing endothelial cell inflammatory response as well as atherosclerotic plaque formation.
item1503	REG00006	M6ATAR00259	Up	M6ADIS0099	.	32802173	METTL14 promotes Forkhead box protein O1 (FOXO1) expression by enhancing its m6A modification and inducing endothelial cell inflammatory response as well as atherosclerotic plaque formation.
item1504	REG00007	M6ATAR00623	Down	M6ADIS0097	.	34428587	METTL3 deficiency contributes to heart regeneration after MI via METTL3-pri-miR-143-(miR-143)-Yap/Ctnnd1 axis.
item1505	REG00008	M6ATAR00175	Up	M6ADIS0068	.	33121495	Knock-down of YTHDF2 or METTL3 significantly induced the expression of LHPP and NKX3-1 at both mRNA and protein level with inhibited phosphorylated RAC-alpha serine/threonine-protein kinase (AKT1). YTHDF2 mediates the mRNA degradation of the tumor suppressors LHPP and NKX3-1 in m6A-dependent way to regulate AKT phosphorylation-induced tumor progression in prostate cancer.
item1506	REG00008	M6ATAR00624	Down	M6ADIS0068	.	33121495	Knock-down of YTHDF2 or METTL3 significantly induced the expression of Phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP) and NKX3-1 at both mRNA and protein level with inhibited phosphorylated AKT. YTHDF2 mediates the mRNA degradation of the tumor suppressors LHPP and NKX3-1 in m6A-dependent way to regulate AKT phosphorylation-induced tumor progression in prostate cancer.
item1507	REG00008	M6ATAR00625	Down	M6ADIS0068	.	33121495	Knock-down of YTHDF2 or METTL3 significantly induced the expression of LHPP and Homeobox protein Nkx-3.1 (NKX3-1) at both mRNA and protein level with inhibited phosphorylated AKT. YTHDF2 mediates the mRNA degradation of the tumor suppressors LHPP and NKX3-1 in m6A-dependent way to regulate AKT phosphorylation-induced tumor progression in prostate cancer.
item1508	REG00007	M6ATAR00175	Up	M6ADIS0068	.	33121495	Knock-down of YTHDF2 or METTL3 significantly induced the expression of LHPP and NKX3-1 at both mRNA and protein level with inhibited phosphorylated RAC-alpha serine/threonine-protein kinase (AKT1). YTHDF2 mediates the mRNA degradation of the tumor suppressors LHPP and NKX3-1 in m6A-dependent way to regulate AKT phosphorylation-induced tumor progression in prostate cancer.
item1509	REG00007	M6ATAR00624	Down	M6ADIS0068	.	33121495	Knock-down of YTHDF2 or METTL3 significantly induced the expression of Phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP) and NKX3-1 at both mRNA and protein level with inhibited phosphorylated AKT. YTHDF2 mediates the mRNA degradation of the tumor suppressors LHPP and NKX3-1 in m6A-dependent way to regulate AKT phosphorylation-induced tumor progression in prostate cancer.
item1510	REG00007	M6ATAR00625	Down	M6ADIS0068	.	33121495	Knock-down of YTHDF2 or METTL3 significantly induced the expression of LHPP and Homeobox protein Nkx-3.1 (NKX3-1) at both mRNA and protein level with inhibited phosphorylated AKT. YTHDF2 mediates the mRNA degradation of the tumor suppressors LHPP and NKX3-1 in m6A-dependent way to regulate AKT phosphorylation-induced tumor progression in prostate cancer.
item1511	.	M6ATAR00626	.	M6ADIS0013	.	35227296	Correlation analysis indicated that Mimecan (OGN) function is closely related to m6A and ferroptosis. The hub gene OGN represent a significant gene involved in OC and PCOS progression by regulating the hormonal response.
item1512	REG00009	M6ATAR00627	Up	M6ADIS0054	.	34999731	"WTAP-mediated m6A modification of DIAPH1 antisense RNA 1 (DIAPH1-AS1) enhanced its stability relying on the m6A reader IGF2BP2-dependent pathway. Furthermore, DIAPH1-AS1 acted as a molecular adaptor that promoted MTDH-LASP1 complex formation and upregulated LASP1 expression, ultimately facilitating NPC growth and metastasis."
item1513	REG00009	M6ATAR00628	Up	M6ADIS0054	.	34999731	"WTAP-mediated m6A modification of LIM and SH3 domain protein 1 (LASP1) enhanced its stability relying on the m6A reader IGF2BP2-dependent pathway. Furthermore, DIAPH1-AS1 acted as a molecular adaptor that promoted MTDH-LASP1 complex formation and upregulated LASP1 expression, ultimately facilitating NPC growth and metastasis."
item1514	REG00013	M6ATAR00627	Up	M6ADIS0054	.	34999731	"WTAP-mediated m6A modification of DIAPH1 antisense RNA 1 (DIAPH1-AS1) enhanced its stability relying on the m6A reader IGF2BP2-dependent pathway. Furthermore, DIAPH1-AS1 acted as a molecular adaptor that promoted MTDH-LASP1 complex formation and upregulated LASP1 expression, ultimately facilitating NPC growth and metastasis."
item1515	REG00013	M6ATAR00628	Up	M6ADIS0054	.	34999731	"WTAP-mediated m6A modification of LIM and SH3 domain protein 1 (LASP1) enhanced its stability relying on the m6A reader IGF2BP2-dependent pathway. Furthermore, DIAPH1-AS1 acted as a molecular adaptor that promoted MTDH-LASP1 complex formation and upregulated LASP1 expression, ultimately facilitating NPC growth and metastasis."
item1516	REG00007	.	.	M6ADIS0141	.	34168039	"Replication of SARS-CoV-2, the agent responsible for the COVID-19 pandemic, and a seasonal human Bete-coronavirus HCoV-OC43, can be suppressed by depletion of METTL3 or cytoplasmic m6A reader proteins YTHDF1 and YTHDF3 and by a highly specific small molecule METTL3 inhibitor."
item1517	REG00005	M6ATAR00629	Up	M6ADIS0104	.	35127873	The study aimed to find the role of m6A RNA demethylase alkB homolog 5 (ALKBH5) in ECs angiogenesis during ischemic injury. ALKBH5 helps in the maintenance of angiogenesis in endothelial cells following acute ischemic stress via reduced SPHK1 m6A methylation and downstream eNOS-AKT signaling.
item1518	REG00017	M6ATAR00630	Down	M6ADIS0180	.	35259473	METTL16 regulates Extracellular sulfatase Sulf-2 (Sulf2) expression via m6A modification and thereby contribute to PM2.5-induced pulmonary microvascular injury.
item1519	REG00009	M6ATAR00631	Down	M6ADIS0051	.	32814762	"Homeobox-containing protein 1 (HMBOX1) was identified as the target gene of WTAP, WTAP/HMBOX1 regulated osteosarcoma growth and metastasis via PI3K/AKT pathway."
item1520	REG00001	M6ATAR00408	Down	M6ADIS0001	.	35317283	"FTO inhibited growth, migration and invasion of GBM cells in vitro and in vivo.decreased FTO expression could induce the downregulation of MTMR3 expression by modulating the processing of pri-miR-10a in an m6A/HNRNPA2B1-dependent manner in GBM cells. Furthermore, the transcriptional activity of FTO was inhibited by the transcription factor Transcription factor PU.1 (SPI1)."
item1521	REG00001	M6ATAR00632	Up	M6ADIS0001	.	35317283	"FTO inhibited growth, migration and invasion of GBM cells in vitro and in vivo.decreased FTO expression could induce the downregulation of MTMR3 expression by modulating the processing of pri-miR-10a in an m6A/HNRNPA2B1-dependent manner in GBM cells. Furthermore, the transcriptional activity of FTO was inhibited by the transcription factor SPI1."
item1522	.	M6ATAR00626	.	M6ADIS0066	.	35227296	Correlation analysis indicated that Mimecan (OGN) function is closely related to m6A and ferroptosis. The hub gene OGN represent a significant gene involved in OC and PCOS progression by regulating the hormonal response.
item1523	REG00014	M6ATAR00633	Up	M6ADIS0046	.	35217832	"IGF2BP3 is required for maintaining AML cell survival in an m6A-dependent manner, and knockdown of IGF2BP3 dramatically suppresses the apoptosis, reduces the proliferation, and impairs the leukemic capacity of AML cells in vitro and in vivo.IGF2BP3 interacts with Protein RCC2 (RCC2) mRNA and stabilizes the expression of m6A-modified RNA."
item1524	REG00007	M6ATAR00634	Up	M6ADIS0139	.	34721590	"METTL3 knockout in the limbal stem cells promotes the in vivo cell proliferation and migration, leading to the fast repair of corneal injury. In addition, m6A modification profiling identified stem cell regulatory factors Neuroblast differentiation-associated protein AHNAK (AHNAK) and DDIT4 as m6A targets."
item1525	REG00007	M6ATAR00225	Up	M6ADIS0139	.	34721590	"METTL3 knockout in the limbal stem cells promotes the in vivo cell proliferation and migration, leading to the fast repair of corneal injury. In addition, m6A modification profiling identified stem cell regulatory factors AHNAK and DNA damage-inducible transcript 4 protein (DDIT4) as m6A targets."
item1526	REG00007	M6ATAR00635	Up	M6ADIS0048	.	35038059	"METTL3 affected the growth, apoptosis, and stemness of MM cells through accelerating the stability of Transcriptional repressor protein YY1 (YY1) mRNA and the maturation of primary-miR-27a-3p in vitro and in vivo."
item1527	REG00007	M6ATAR00636	Down	M6ADIS0048	.	35038059	"METTL3 affected the growth, apoptosis, and stemness of MM cells through accelerating the stability of YY1 mRNA and the maturation of pri-miR-27 in vitro and in vivo."
item1528	REG00001	M6ATAR00206	.	M6ADIS0083	.	35481401	"Metformin could inhibit adipogenesis and combat obesity, metformin could inhibit protein expression of FTO, leading to increased m6A methylation levels of G1/S-specific cyclin-D1 (CCND1) and Cdk2(two crucial regulators in cell cycle). Ccnd1 and Cdk2 with increased m6A levels were recognised by YTHDF2, causing an YTHDF2-dependent decay and decreased protein expressions."
item1529	REG00008	M6ATAR00210	.	M6ADIS0083	.	35481401	"Metformin could inhibit adipogenesis and combat obesity, metformin could inhibit protein expression of FTO, leading to increased m6A methylation levels of Ccnd1 and Cyclin-dependent kinase 2 (CDK2)(two crucial regulators in cell cycle). Ccnd1 and Cdk2 with increased m6A levels were recognised by YTHDF2, causing an YTHDF2-dependent decay and decreased protein expressions."
item1530	REG00001	M6ATAR00210	.	M6ADIS0083	.	35481401	"Metformin could inhibit adipogenesis and combat obesity, metformin could inhibit protein expression of FTO, leading to increased m6A methylation levels of Ccnd1 and Cyclin-dependent kinase 2 (CDK2)(two crucial regulators in cell cycle). Ccnd1 and Cdk2 with increased m6A levels were recognised by YTHDF2, causing an YTHDF2-dependent decay and decreased protein expressions."
item1531	REG00008	M6ATAR00206	.	M6ADIS0083	.	35481401	"Metformin could inhibit adipogenesis and combat obesity, metformin could inhibit protein expression of FTO, leading to increased m6A methylation levels of G1/S-specific cyclin-D1 (CCND1) and Cdk2(two crucial regulators in cell cycle). Ccnd1 and Cdk2 with increased m6A levels were recognised by YTHDF2, causing an YTHDF2-dependent decay and decreased protein expressions."
item1532	REG00007	M6ATAR00637	Down	M6ADIS0024	.	34130310	Downregulated spinal cord METTL3 coordinating with YTHDF2 contributes to the modulation of inflammatory pain through stabilizing upregulation of Methylcytosine dioxygenase TET1 (TET1) in spinal neurons.
item1533	REG00024	M6ATAR00638	Up	.	.	34821414	"YTHDF1 recruits Protein argonaute-2 (AGO2) through the YTH domain. YTHDF1 degrades targeting mRNAs by promoting P-body formation through LLPS. The deletion of YTHDF1 causes the P-body to change from liquid droplets to gel/solid droplets, and form AGO2/RNA patches, resulting in a degradation delay of mRNAs."
item1534	REG00008	M6ATAR00637	Down	M6ADIS0024	.	34130310	Downregulated spinal cord METTL3 coordinating with YTHDF2 contributes to the modulation of inflammatory pain through stabilizing upregulation of Methylcytosine dioxygenase TET1 (TET1) in spinal neurons.
item1535	REG00006	M6ATAR00368	Down	M6ADIS0057	.	33314339	"The m6A modification level was decreased in GC and METTL14 was a key regulator resulting in m6A disorder in GC. METTL14 overexpression suppressed GC cell proliferation and aggression by deactivating the PI3-kinase subunit alpha (PI3k/PIK3CA)/AKT/mTOR pathway and the EMT pathway, respectively."
item1536	REG00006	M6ATAR00175	Down	M6ADIS0057	.	33314339	"The m6A modification level was decreased in GC and METTL14 was a key regulator resulting in m6A disorder in GC. METTL14 overexpression suppressed GC cell proliferation and aggression by deactivating the PI3K/RAC-alpha serine/threonine-protein kinase (AKT1)/mTOR pathway and the EMT pathway, respectively."
item1537	REG00006	M6ATAR00339	Down	M6ADIS0057	.	33314339	"The m6A modification level was decreased in GC and METTL14 was a key regulator resulting in m6A disorder in GC. METTL14 overexpression suppressed GC cell proliferation and aggression by deactivating the PI3K/AKT/Serine/threonine-protein kinase mTOR (MTOR) pathway and the EMT pathway, respectively."
item1538	REG00006	M6ATAR00639	Up	M6ADIS0181	.	34910686	"Imbalanced osteogenic/adipogenic differentiation of bone marrow mesenchymal stem cells BMSCs is considered the core pathological characteristic of SONFH. METTL14 regulated Tyrosine-protein phosphatase non-receptor type 6 (PTPN6) expression by increasing PTPN6 mRNA stability in an m6A-dependent manner. Moreover, PTPN6 knockdown abrogated the beneficial effects of METTL14 overexpression on BMSCs."
item1539	REG00006	M6ATAR00054	Up	M6ADIS0099	.	35598196	"Mettl14 gene knockout significantly reduced the inflammatory response of macrophages and the development of atherosclerotic plaques, Mettl14 plays a vital role in macrophage inflammation in atherosclerosis via the Nuclear factor NF-kappa-B p105 subunit (NF-Kappa-B/NFKB1)/IL-6 signaling pathway."
item1540	REG00006	M6ATAR00529	Up	M6ADIS0099	.	35598196	"Mettl14 gene knockout significantly reduced the inflammatory response of macrophages and the development of atherosclerotic plaques, Mettl14 plays a vital role in macrophage inflammation in atherosclerosis via the NF-Kappa-B/Interleukin-6 (IL-6) signaling pathway."
item1541	REG00001	M6ATAR00298	Up	M6ADIS0057	.	34277426	FTO was an independent risk factor for overall survival (OS) of GC patients and FTO could promote GC metastasis by upregulating the expression of Integrin beta-1 (ITGB1) via decreasing its m6A level.
item1542	REG00007	M6ATAR00360	Up	M6ADIS0070	.	35502544	"METTL3 was essential for bladder cancer cells to resist the cytotoxicity of CD8+ T cells by regulating Programmed cell death 1 ligand 1 (CD274/PD-L1) expression. Additionally, JNK signaling contributed to tumor immune escape in a METTL3-dependent manner both in vitro and in vivo."
item1543	REG00023	M6ATAR00640	Up	M6ADIS0007	.	34326699	"Smoking-related downregulation of YTHDC2 was associated with enhanced proliferation and migration in lung cancer cells, YTHDC2 functions as a tumor suppressor through the Ubiquitin carboxyl-terminal hydrolase CYLD (CYLD)/NF-Kappa-B signaling pathway, which is mediated by m6A modification."
item1544	REG00007	M6ATAR00641	Down	M6ADIS0007	.	34774019	hsa-miR-1915-3p expression was regulated by METTL3/YTHDF2 m6A axis through transcription factor KLF4. miR-1915-3p function as a tumor suppressor by targeting SET and has an anti-metastatic therapeutic potential for lung cancer treatment.
item1545	REG00007	M6ATAR00249	Up	M6ADIS0065	.	35392146	"METTL3 is upregulated in Breast Cancer. It could regulate the protein level of Histone-lysine N-methyltransferase EZH2 (EZH2) through m6A modification to promote EMT and metastasis in BCa cells, thereafter aggravating the progression of BCa."
item1546	REG00001	M6ATAR00642	Down	M6ADIS0053	M6ADRUG0096	30967398	"Downregulation of m6A demethylases FTO and ALKBH5 was sufficient to increase Frizzled-10 (FZD10) mRNA m6A modification and reduce PARPi sensitivity, the finding elucidates a novel regulatory mechanism of PARPi resistance in EOC by showing that m6A modification of FZD10 mRNA contributes to PARPi resistance in BRCA-deficient EOC cells via upregulation of Wnt/Bete-catenin pathway."
item1547	REG00005	M6ATAR00642	Down	M6ADIS0053	M6ADRUG0096	30967398	"Downregulation of m6A demethylases FTO and ALKBH5 was sufficient to increase Frizzled-10 (FZD10) mRNA m6A modification and reduce PARPi sensitivity, the finding elucidates a novel regulatory mechanism of PARPi resistance in EOC by showing that m6A modification of FZD10 mRNA contributes to PARPi resistance in BRCA-deficient EOC cells via upregulation of Wnt/Bete-catenin pathway."
item1548	REG00006	M6ATAR00643	Down	M6ADIS0166	.	33706799	Mettl14-mediated m6A modification inhibited Dexamethasone-induced Ras-related protein 1 (RASD1) and induced the apoptosis of spinal cord neurons in SCI by promoting the transformation of pri-miR-375 to mature miR-375.
item1549	REG00006	M6ATAR00118	Up	M6ADIS0166	.	33706799	Mettl14-mediated m6A modification inhibited RASD1 and induced the apoptosis of spinal cord neurons in SCI by promoting the transformation of pri-miR-375 to mature microRNA 375 (MIR375).
item1550	REG00026	M6ATAR00312	Down	M6ADIS0006	M6ADRUG0047	35003256	"ZC3H13 overexpression sensitized to cisplatin and weakened metabolism reprogramming of HCC cells, ZC3H13-induced m6A modified patterns substantially abolished Pyruvate kinase PKM (PKM2/PKM) mRNA stability."
item1551	REG00007	M6ATAR00446	Up	M6ADIS0070	.	33681207	"Deletion of Mettl3 leads to the suppression of TEK and Vascular endothelial growth factor A (VEGFA),ablation of Mettl3 in bladder urothelial attenuates the oncogenesis and tumor angiogenesis of bladder cancer."
item1552	REG00007	M6ATAR00644	Up	M6ADIS0070	.	33681207	"Deletion of Mettl3 leads to the suppression of Angiopoietin-1 receptor (TEK) and VEGF-A,ablation of Mettl3 in bladder urothelial attenuates the oncogenesis and tumor angiogenesis of bladder cancer."
item1553	REG00023	M6ATAR00451	Up	M6ADIS0057	.	34911015	"High YTHDC2 was strongly positively correlated with high Transcriptional coactivator YAP1 (YAP1) in clinical GC tissues, YTHDC2 is a novel oncogene in GC, which provides the theoretical basis for the strategy of targeting YTHDC2 for GC patients."
item1554	REG00004	M6ATAR00645	Down	M6ADIS0007	.	35364458	HNRNPA2B1 inhibits Secreted frizzled-related protein 2 (SFRP2) and activates Wnt-Beta/catenin via m6A-mediated maturing of miR-106b-5p to aggravate stemness and LUAD progression.
item1555	REG00007	M6ATAR00310	Down	M6ADIS0007	.	34774019	MiR-1915-3p expression was regulated by METTL3/YTHDF2 m6A axis through transcription factor Krueppel-like factor 4 (KLF4). miR-1915-3p function as a tumor suppressor by targeting SET and has an anti-metastatic therapeutic potential for lung cancer treatment.
item1556	REG00006	M6ATAR00646	Down	M6ADIS0061	.	32843065	"The upregulation of METTL14 leads to the decrease of p53 apoptosis effector related to PMP-22 (PERP) levels via m6A modification, promoting the growth and metastasis of pancreatic cancer; therefore METTL14 is a potential therapeutic target for its treatment."
item1557	REG00024	M6ATAR00647	Up	M6ADIS0059	.	34968454	"YTHDF1 promotes cell growth in CRC cell lines and primary organoids and lung and liver metastasis in vivo. YTHDF1 binds to m6A sites of Rho guanine nucleotide exchange factor 2 (ARHGEF2) messenger RNA, resulting in enhanced translation of ARHGEF2."
item1558	REG00007	M6ATAR00648	Up	M6ADIS0117	.	34995800	METTL3 modulated Notch signaling via the m6A modification of Metalloproteinase inhibitor 2 (TIMP2) in IGF2BP2-dependent manner and exerted pro-inflammatory and pro-apoptotic effects. This study suggested that METTL3-mediated m6A modification is an important mechanism of podocyte injury in DN.
item1559	REG00013	M6ATAR00649	Up	M6ADIS0006	.	33224879	"IGF2BP2 overexpression promoted HCC proliferation in vitro and in vivo, IGF2BP2 directly recognized and bound to the m6A site on FEN1 mRNA and enhanced Flap endonuclease 1 (FEN1) mRNA stability."
item1560	REG00006	M6ATAR00650	Down	M6ADIS0010	.	35305660	"Knockdown of METTL14 promoted ccRCC cell migration, invasiveness and metastasis as well as stimulating the EMT process and the PI3K/AKT signal by overexpressing Integrin beta-4 (ITGB4)."
item1561	REG00007	M6ATAR00213	Down	M6ADIS0065	.	33431790	METTL3 is able to promote breast cancer cell proliferation by regulating the Cyclin-dependent kinase inhibitor 1 (CDKN1A) expression by an m6A-dependent manner. Metformin can take p21 as the main target to inhibit such effect.
item1562	REG00007	M6ATAR00651	Up	M6ADIS0102	.	32650237	METTL3/m6A-mediated hsa-miR-34a maturation in AAA formation and provide a novel therapeutic target and diagnostic biomarker for AAA treatment.
item1563	REG00024	M6ATAR00652	Up	M6ADIS0051	.	35156522	"YTHDF1 could recognize the m6A sites of CCR4-NOT transcription complex subunit 7 (CNOT7) and promote its expression in an m6A manner. Inhibition of YTHDF1 could suppress the proliferation, migration and invasion of the OS cells."
item1564	REG00007	M6ATAR00141	Up	M6ADIS0065	.	34419065	"Silencing METTL3 down-regulate Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) and HMGA2 by sponging miR-26b, and finally inhibit EMT, migration and invasion in BC, providing a theoretical basis for clinical treatment of BC."
item1565	REG00007	M6ATAR00276	Up	M6ADIS0065	.	34419065	"Silencing METTL3 down-regulate MALAT1 and High mobility group protein HMGI-C (HMGA2) by sponging miR-26b, and finally inhibit EMT, migration and invasion in BC, providing a theoretical basis for clinical treatment of BC."
item1566	REG00008	M6ATAR00641	Down	M6ADIS0007	.	34774019	hsa-miR-1915-3p expression was regulated by METTL3/YTHDF2 m6A axis through transcription factor KLF4. miR-1915-3p function as a tumor suppressor by targeting SET and has an anti-metastatic therapeutic potential for lung cancer treatment.
item1567	REG00007	M6ATAR00653	Down	M6ADIS0065	.	34419065	"Silencing METTL3 down-regulate MALAT1 and HMGA2 by sponging hsa-miR-26b, and finally inhibit EMT, migration and invasion in BC, providing a theoretical basis for clinical treatment of BC."
item1568	REG00015	M6ATAR00393	Up	M6ADIS0059	.	35217651	"KIAA1429 increased the expression of NAD-dependent protein deacetylase sirtuin-1 (SIRT1) via regulating its mRNA stability in an m6A-dependent manner. More importantly, in vivo experiment showed that depletion of KIAA1429 significantly inhibited colorectal tumor growth."
item1569	REG00018	.	.	M6ADIS0156	.	35005123	"Mettl5 knockout in mESCs leads to the abnormal craniofacial and nervous development. Moreover, using Mettl5 knockout mouse model, we further demonstrated that Mettl5 knockout mice exhibit intellectual disability, recapitulating the human phenotype."
item1570	REG00008	M6ATAR00654	Up	M6ADIS0101	.	34266473	"Pathological cardiac hypertrophy is a major contributor of heart failure (HF), the m6A Reader YTHDF2 suppresses cardiac hypertrophy via Myosin-7 (Myh7) mRNA decoy in an m6A-dependent manner."
item1571	REG00005	M6ATAR00655	Up	M6ADIS0048	.	35414790	"Inhibiting ALKBH5 in Multiple Myeloma cells increased Protein salvador homolog 1 (SAV1) m6A levels, decreased SAV1 mRNA stability and expression, suppressed the stem cell related HIPPO-pathway signalling and ultimately activates the downstream effector YAP, exerting an anti-myeloma effect."
item1572	REG00021	M6ATAR00656	Up	M6ADIS0006	M6ADRUG0032	35494016	Overexpression of RBM15B promotes HCC cell proliferation and invasion and induces sorafenib resistance in HCC cells. RBM15B is transcriptionally activated by YY1 and regulates the stability of Translocating chain-associated membrane protein 2 (TRAM2) mRNA in an m6A-dependent manner.
item1573	REG00007	M6ATAR00368	Up	M6ADIS0007	.	35434840	METTL3-mediated m6 A methylation promotes lung cancer progression via activating PI3-kinase subunit alpha (PI3k/PIK3CA)/AKT/mTOR pathway.
item1574	REG00007	M6ATAR00175	Up	M6ADIS0007	.	35434840	METTL3-mediated m6 A methylation promotes lung cancer progression via activating PI3K/RAC-alpha serine/threonine-protein kinase (AKT1)/mTOR pathway.
item1575	REG00007	M6ATAR00339	Up	M6ADIS0007	.	35434840	METTL3-mediated m6 A methylation promotes lung cancer progression via activating PI3K/AKT/Serine/threonine-protein kinase mTOR (MTOR) pathway.
item1576	REG00005	M6ATAR00657	Up	M6ADIS0168	.	35340126	"Theses findings reveal an epigenetic interplay mechanism in NPC senescence and IVD degeneration, presenting a critical pro-senescence role of ALKBH5 and m6A hypomethylation, highlighting the therapeutic potential of targeting the m6A/DNMT3B/Transcription factor E4F1 (E4F1) axis for treating IVD degeneration."
item1577	REG00008	M6ATAR00310	Down	M6ADIS0007	.	34774019	MiR-1915-3p expression was regulated by METTL3/YTHDF2 m6A axis through transcription factor Krueppel-like factor 4 (KLF4). miR-1915-3p function as a tumor suppressor by targeting SET and has an anti-metastatic therapeutic potential for lung cancer treatment.
item1578	REG00005	M6ATAR00658	Down	M6ADIS0168	.	35340126	"Theses findings reveal an epigenetic interplay mechanism in NPC senescence and IVD degeneration, presenting a critical pro-senescence role of ALKBH5 and m6A hypomethylation, highlighting the therapeutic potential of targeting the m6A/DNA (cytosine-5)-methyltransferase 3B (DNMT3B)/E4F1 axis for treating IVD degeneration."
item1579	REG00007	M6ATAR00659	Down	M6ADIS0006	M6ADRUG0032	35037556	"Long intergenic non-protein coding RNA 1273 (LINC01273) was modified with m6A, METTL3 increased LINC01273 m6A modification, followed by LINC01273 decay in the presence of YTHDF2, a m6A 'reader'. And LINC01273 plays a key role in sorafenib resistant HCC cells."
item1580	REG00008	M6ATAR00659	Down	M6ADIS0006	M6ADRUG0032	35037556	"Long intergenic non-protein coding RNA 1273 (LINC01273) was modified with m6A, METTL3 increased LINC01273 m6A modification, followed by LINC01273 decay in the presence of YTHDF2, a m6A 'reader'. And LINC01273 plays a key role in sorafenib resistant HCC cells."
item1581	REG00007	M6ATAR00141	Up	M6ADIS0065	M6ADRUG0022	34964205	"METTL3 can regulate the expression of Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) through m6A, mediate the E2F1/AGR2 axis, and promote the adriamycin resistance of breast cancer."
item1582	REG00007	M6ATAR00234	Up	M6ADIS0065	M6ADRUG0022	34964205	"METTL3 can regulate the expression of MALAT1 through m6A, mediate the Transcription factor E2F1 (E2F1)/AGR2 axis, and promote the adriamycin resistance of breast cancer."
item1583	REG00007	M6ATAR00660	Up	M6ADIS0065	M6ADRUG0022	34964205	"METTL3 can regulate the expression of MALAT1 through m6A, mediate the E2F1/Anterior gradient protein 2 homolog (AGR2) axis, and promote the adriamycin resistance of breast cancer."
item1584	REG00012	M6ATAR00661	Up	M6ADIS0067	.	33391523	"IGF2BP1 expression increased in EC, and high expression of this protein correlated with poor prognosis. IGF2BP1 can recognize m6A sites in the 3'UTR of PEG10 mRNA and recruits PABPC1 to enhance Retrotransposon-derived protein PEG10 (PEG10) mRNA stability, which consequently promotes PEG10 protein expression."
item1585	REG00007	M6ATAR00224	Up	M6ADIS0051	.	35096816	"METTL3 contributes to OS progression by increasing Putative uncharacterized protein DANCR (DANCR) mRNA stability via m6A modification, meaning that METTL3 is a promising therapeutic target for OS treatment."
item1586	REG00007	M6ATAR00299	Up	M6ADIS0099	.	34950654	METTL3 knockdown prevented Atherosclerosis progression by inhibiting Tyrosine-protein kinase JAK2 (JAK2)/STAT3 pathway via IGF2BP1.
item1587	REG00007	M6ATAR00418	Up	M6ADIS0099	.	34950654	METTL3 knockdown prevented Atherosclerosis progression by inhibiting JAK2/Signal transducer and activator of transcription 3 (STAT3) pathway via IGF2BP1.
item1588	REG00007	M6ATAR00662	Down	M6ADIS0007	.	34774019	MiR-1915-3p expression was regulated by METTL3/YTHDF2 m6A axis through transcription factor KLF4. miR-1915-3p function as a tumor suppressor by targeting Protein SET (SET) and has an anti-metastatic therapeutic potential for lung cancer treatment.
item1589	REG00012	M6ATAR00299	Up	M6ADIS0099	.	34950654	METTL3 knockdown prevented Atherosclerosis progression by inhibiting Tyrosine-protein kinase JAK2 (JAK2)/STAT3 pathway via IGF2BP1.
item1590	REG00012	M6ATAR00418	Up	M6ADIS0099	.	34950654	METTL3 knockdown prevented Atherosclerosis progression by inhibiting JAK2/Signal transducer and activator of transcription 3 (STAT3) pathway via IGF2BP1.
item1591	REG00007	M6ATAR00663	Up	M6ADIS0059	.	35567945	"METTL3 upregulated Urokinase-type plasminogen activator (PLAU) mRNA in an m6A-dependent manner, and then participated in MAPK/ERK pathway to promote angiogenesis and metastasis in CRC."
item1592	REG00001	M6ATAR00451	Up	M6ADIS0096	.	35176940	"FTO down-expressed in myocardial IRI mice and hypoxia/reoxygenation (H/R)-induced cardiomyocytes. Moreover, FTO uninstalled the methylation of Transcriptional coactivator YAP1 (YAP1) mRNA, and enforced the stability of Yap1 mRNA.The study reveals the role of FTO in H/R-induced myocardial cell injury via m6A-dependent manner, which provided a new approach to improve myocardial IRI."
item1593	REG00007	M6ATAR00664	Up	M6ADIS0055	.	32621798	METTL3 promotes Polycomb complex protein BMI-1 (BMI1) translation in OSCC under the cooperation with m6A reader IGF2BP1. And the study revealed that METTL3 promotes OSCC proliferation and metastasis through BMI1 m6A methylation.
item1594	REG00012	M6ATAR00664	Up	M6ADIS0055	.	32621798	METTL3 promotes Polycomb complex protein BMI-1 (BMI1) translation in OSCC under the cooperation with m6A reader IGF2BP1. And the study revealed that METTL3 promotes OSCC proliferation and metastasis through BMI1 m6A methylation.
item1595	REG00015	M6ATAR00088	Up	M6ADIS0057	.	34409730	"Long intergenic non-protein coding RNA 958 (LINC00958) accelerated the aerobic glycolysis of GC cells. Mechanistically, KIAA1429 interacted with the m6A modification site and promoted the enrichment of LINC00958, and LINC00958 subsequently cooperated with GLUT1 mRNA to enhance its mRNA stability."
item1596	REG00001	M6ATAR00665	Up	M6ADIS0061	.	35422475	"FTO downregulation leads to increased m6A modifications in the 3' UTR of Platelet-derived growth factor C (PDGFC) and then modulates the degradation of its transcriptional level in an m6A-YTHDF2-dependent manner, highlighting a potential therapeutic target for PDAC treatment and prognostic prediction."
item1597	REG00008	M6ATAR00665	Down	M6ADIS0061	.	35422475	"FTO downregulation leads to increased m6A modifications in the 3' UTR of Platelet-derived growth factor C (PDGFC) and then modulates the degradation of its transcriptional level in an m6A-YTHDF2-dependent manner, highlighting a potential therapeutic target for PDAC treatment and prognostic prediction."
item1598	REG00007	M6ATAR00666	Up	M6ADIS0059	M6ADRUG0005	35014676	"METTL3 dependent m6A methylation was upregulated in CRC to promote the processing of miR 181d 5p by DGCR8. This led to increased hsa-miR-181d-5p expression, which inhibited the 5 FU sensitivity of CRC cells by targeting NCALD."
item1599	REG00008	M6ATAR00662	Down	M6ADIS0007	.	34774019	MiR-1915-3p expression was regulated by METTL3/YTHDF2 m6A axis through transcription factor KLF4. miR-1915-3p function as a tumor suppressor by targeting Protein SET (SET) and has an anti-metastatic therapeutic potential for lung cancer treatment.
item1600	REG00007	M6ATAR00667	Down	M6ADIS0059	M6ADRUG0005	35014676	"METTL3 dependent m6A methylation was upregulated in CRC to promote the processing of miR 181d 5p by DGCR8. This led to increased miR 181d 5p expression, which inhibited the 5 FU sensitivity of CRC cells by targeting Neurocalcin-delta (NCALD)."
item1601	REG00007	M6ATAR00668	Down	M6ADIS0068	.	34335955	"m6A modification levels were markedly upregulated in human PCa tissues due to increased expression of METTL3. METTL3 mediates m6A modification of Ubiquitin carboxyl-terminal hydrolase 4 (USP4) mRNA at A2696, and m6A reader protein YTHDF2 binds to and induces degradation of USP4 mRNA by recruiting RNA-binding protein HNRNPD to the mRNA. Decrease of USP4 fails to remove the ubiquitin group from ELAVL1 protein, resulting in a reduction of ELAVL1 protein. Lastly, downregulation of ELAVL1 in turn increases ARHGDIA expression, promoting migration and invasion of PCa cells."
item1602	REG00007	M6ATAR00241	Down	M6ADIS0068	.	34335955	"m6A modification levels were markedly upregulated in human PCa tissues due to increased expression of METTL3. METTL3 mediates m6A modification of USP4 mRNA at A2696, and m6A reader protein YTHDF2 binds to and induces degradation of USP4 mRNA by recruiting RNA-binding protein HNRNPD to the mRNA. Decrease of USP4 fails to remove the ubiquitin group from ELAVL1 protein, resulting in a reduction of ELAVL1 protein. Lastly, downregulation of ELAV-like protein 1 (HuR/ELAVL1) in turn increases ARHGDIA expression, promoting migration and invasion of PCa cells."
item1603	REG00008	M6ATAR00668	Down	M6ADIS0068	.	34335955	"m6A modification levels were markedly upregulated in human PCa tissues due to increased expression of METTL3. METTL3 mediates m6A modification of Ubiquitin carboxyl-terminal hydrolase 4 (USP4) mRNA at A2696, and m6A reader protein YTHDF2 binds to and induces degradation of USP4 mRNA by recruiting RNA-binding protein HNRNPD to the mRNA. Decrease of USP4 fails to remove the ubiquitin group from ELAVL1 protein, resulting in a reduction of ELAVL1 protein. Lastly, downregulation of ELAVL1 in turn increases ARHGDIA expression, promoting migration and invasion of PCa cells."
item1604	REG00008	M6ATAR00241	Down	M6ADIS0068	.	34335955	"m6A modification levels were markedly upregulated in human PCa tissues due to increased expression of METTL3. METTL3 mediates m6A modification of USP4 mRNA at A2696, and m6A reader protein YTHDF2 binds to and induces degradation of USP4 mRNA by recruiting RNA-binding protein HNRNPD to the mRNA. Decrease of USP4 fails to remove the ubiquitin group from ELAV-like protein 1 (HuR/ELAVL1) protein, resulting in a reduction of ELAVL1 protein. Lastly, downregulation of ELAVL1 in turn increases ARHGDIA expression, promoting migration and invasion of PCa cells."
item1605	REG00001	M6ATAR00669	Up	M6ADIS0161	.	32670741	"FTO contributes to neuropathic pain through stabilizing nerve injury-induced upregulation of Histone-lysine N-methyltransferase EHMT2 (G9a), a neuropathic pain initiator, in primary sensory neurons."
item1606	REG00005	M6ATAR00670	Down	M6ADIS0104	.	34047466	ALKBH5 is a negative regulator of post-ischemic angiogenesis via post-transcriptional modulation and destabilization of Protein Wnt-5a (WNT5A) mRNA in an m6A-dependent manner.
item1607	REG00007	M6ATAR00671	Down	M6ADIS0059	M6ADRUG0048	33555197	"2-polarized tumor-associated macrophages enabled the oxaliplatin resistance via the elevation of METTL3-mediated m6A modification in Colorectal Cancer cells. Furthermore, they found that TNF receptor-associated factor 5 (TRAF5) contributes to the METTL3-triggered OX resistance in CRC cells."
item1608	REG00006	M6ATAR00222	Down	M6ADIS0065	M6ADRUG0091	35562334	m6A-hypomethylation regulated FGFR4 phosphorylates GSK-3beta and activates Catenin beta-1 (CTNNB1/Beta-catenin)/TCF4-SLC7A11/FPN1 signaling to drive anti-HER2 resistance. Knockdown of METTL14 significantly increased the expression level of FGFR4 in HER2-positive breast cancer cells. FGFR4 reduced the sensitivity of HER2-positive breast cancer to trastuzumab plus pertuzumab or tucatinib. These results pinpoint a mechanism of anti-HER2 resistance and provide a strategy for overcoming resistance via FGFR4 inhibition in recalcitrant HER2-positive breast cancer.
item1609	REG00007	.	.	M6ADIS0115	.	35470497	"Overexpression of Mettl3 could partially rescue the decreased bone formation ability of OP-BMSCs by the canonical Wnt signalling pathway. Therefore, Mettl3 can be a key targeted gene for bone generation and therapy of bone defects in OP patients."
item1610	REG00005	M6ATAR00672	Down	M6ADIS0016	.	35279083	ALKBH5 promotes silica-induced lung fibrosis via the hsa-miR-320a-3p/FOXM1 axis or targeting FOXM1 directly.
item1611	REG00005	M6ATAR00258	Up	M6ADIS0016	.	35279083	ALKBH5 promotes silica-induced lung fibrosis via the miR-320a-3p/FOXM1 axis or targeting Forkhead box protein M1 (FOXM1) directly.
item1612	REG00023	M6ATAR00484	Down	M6ADIS0007	.	33232910	YTHDC2 destabilized Cystine/glutamate transporter (SLC7A11) mRNA in an m6A-dependent manner because YTHDC2 preferentially bound to m6A-modified SLC7A11 mRNA and thereafter promoted its decay. the promotion of cystine uptake via the suppression of YTHDC2 is critical for LUAD tumorigenesis.
item1613	REG00005	M6ATAR00360	Up	M6ADIS0006	.	34301762	ALKBH5 as an important m6A demethylase that orchestrates Programmed cell death 1 ligand 1 (CD274/PD-L1) expression in intrahepatic cholangiocarcinoma (ICC).
item1614	REG00007	M6ATAR00569	Up	M6ADIS0070	.	33267838	The RCas9-METTL3 system mediates efficient sitespecific m6A installation on CUB domain-containing protein 1 (CDCP1) mRNA and promotes bladder cancer development.
item1615	REG00007	M6ATAR00673	Up	M6ADIS0007	.	35068325	"The reduction in cell proliferation induced by SVIL antisense RNA 1 (SVIL-AS1) overexpression could be rescued by E2F1 overexpression or METTL3 knockdown. In conclusion, METTL3-induced SVIL-AS1 in LUAD, which connects m6A and lncRNA in lung cancer carcinogenesis."
item1616	REG00005	M6ATAR00674	Up	M6ADIS0083	.	33880847	m6A-dependent TNF receptor-associated factor 4 (TRAF4) expression upregulation by ALKBH5 and YTHDF1 contributes to curcumin-induced obesity prevention.
item1617	REG00024	M6ATAR00674	Up	M6ADIS0083	.	33880847	m6A-dependent TNF receptor-associated factor 4 (TRAF4) expression upregulation by ALKBH5 and YTHDF1 contributes to curcumin-induced obesity prevention.
item1618	REG00007	M6ATAR00675	Up	M6ADIS0007	.	32892348	LINC00035 (ABHD11-AS1) was upregulated in NSCLC tissue specimens and cells and the ectopic overexpression was closely correlated with unfavorable prognosis of NSCLC patients.METTL3 installed the m6 A modification and enhanced ABHD11-AS1 transcript stability to increase its expression.
item1619	REG00001	M6ATAR00676	Up	M6ADIS0007	M6ADRUG0030	33563765	Not only FTO knockdown enhanced the gefitinib sensitivity of GR cells but also FTO reduction in donor exosomes alleviated the acquired resistance of recipient non-small cell lung cancer PC9 cells. FTO/YTHDF2/ATP-binding cassette sub-family C member 10 (ABCC10) axis played a role in intercellular transmission of GR cell-derived exosome-mediated gefitinib resistance.
item1620	REG00007	.	.	M6ADIS0001	.	32615646	Functional genetic variants in the METTL3 gene will contribute to neuroblastoma risk.
item1621	REG00008	M6ATAR00676	Down	M6ADIS0007	M6ADRUG0030	33563765	Not only FTO knockdown enhanced the gefitinib sensitivity of GR cells but also FTO reduction in donor exosomes alleviated the acquired resistance of recipient non-small cell lung cancer PC9 cells. FTO/YTHDF2/ATP-binding cassette sub-family C member 10 (ABCC10) axis played a role in intercellular transmission of GR cell-derived exosome-mediated gefitinib resistance.
item1622	REG00007	M6ATAR00451	Up	M6ADIS0057	.	34394353	The expression of m6A and METTL3 was upregulated in human gastric cancer tissues and gastric cancer cell lines. m6A methyltransferase METTL3 promoted the proliferation and migration of gastric cancer cells through the m6A modification of Transcriptional coactivator YAP1 (YAP1).
item1623	REG00013	M6ATAR00677	Up	M6ADIS0055	.	34980207	"Mechanistic investigations revealed that Zinc finger protein SNAI2 (Slug), a key EMT-related transcriptional factor, is the direct target of IGF2BP2, and essential for IGF2BP2-regulated EMT and metastasis in HNSCC."
item1624	REG00007	M6ATAR00295	Up	M6ADIS0006	.	34491544	"ILF3-AS1 expression was significantly elevated in HCC tissues,mechanistically, ILF3-AS1 associated with Interleukin enhancer-binding factor 3 (ILF3) mRNA and inhibited its degradation. ILF3-AS1 increased ILF3 m6A level via recruiting N6-methyladenosine (m6A) RNA methyltransferase METTL3. Moreover, IFL3-AS1 enhanced the interaction between ILF3 mRNA and m6A reader IGF2BP1."
item1625	REG00012	M6ATAR00295	Up	M6ADIS0006	.	34491544	"ILF3-AS1 expression was significantly elevated in HCC tissues,mechanistically, ILF3-AS1 associated with Interleukin enhancer-binding factor 3 (ILF3) mRNA and inhibited its degradation. ILF3-AS1 increased ILF3 m6A level via recruiting N6-methyladenosine (m6A) RNA methyltransferase METTL3. Moreover, IFL3-AS1 enhanced the interaction between ILF3 mRNA and m6A reader IGF2BP1."
item1626	REG00005	M6ATAR00678	Down	M6ADIS0006	.	32772918	"ALKBH5 suppressed the proliferation and invasion capabilities of HCC cells in vitro and in vivo. Mechanistically, ALKBH5-mediated m6A demethylation led to a post-transcriptional inhibition of Ly6/PLAUR domain-containing protein 1 (LYPD1)."
item1627	REG00001	M6ATAR00679	Down	M6ADIS0057	.	35064107	"This study demonstrated that the key demethylase of m6A FTO promoted the proliferation and metastasis of gastric cancer via regulating the mitochondrial fission/fusion and metabolism. In terms of mechanism, FTO improved the degradation of Caveolin-1 (CAV1) mRNA via its demethylation."
item1628	REG00005	M6ATAR00420	Down	M6ADIS0007	.	34016959	"ALKBH5 gain- or loss-of function could effectively reverse Serine/threonine-protein kinase STK11 (STK11/LKB1) regulated cell proliferation, colony formation, and migration of KRAS-mutated lung cancer cells."
item1629	REG00007	M6ATAR00680	Down	M6ADIS0059	.	33411363	"METTL3-catalyzed m6A modification in CRC tumorigenesis, wherein it facilitates CRC tumor growth and metastasis through suppressing Protein yippee-like 5 (YPEL5) expression in an m6A-YTHDF2-dependent manner."
item1630	REG00008	M6ATAR00680	Down	M6ADIS0059	.	33411363	"METTL3-catalyzed m6A modification in CRC tumorigenesis, wherein it facilitates CRC tumor growth and metastasis through suppressing Protein yippee-like 5 (YPEL5) expression in an m6A-YTHDF2-dependent manner."
item1631	REG00023	.	.	M6ADIS0018	.	35138268	YTHDC2 is a key regulator of meiosis in humans and pathogenic variants within this gene are associated with POI.
item1632	REG00007	M6ATAR00484	Up	M6ADIS0006	.	35522946	METTL3-mediated Cystine/glutamate transporter (SLC7A11) m6A modification enhances hepatoblastoma ferroptosis resistance. The METTL3/IGF2BP1/m6A modification promotes SLC7A11 mRNA stability and upregulates its expression by inhibiting the deadenylation process.
item1633	REG00012	M6ATAR00484	Up	M6ADIS0006	.	35522946	METTL3-mediated Cystine/glutamate transporter (SLC7A11) m6A modification enhances hepatoblastoma ferroptosis resistance. The METTL3/IGF2BP1/m6A modification promotes SLC7A11 mRNA stability and upregulates its expression by inhibiting the deadenylation process.
item1634	REG00006	M6ATAR00681	Up	M6ADIS0165	.	34452996	"METTL14 knockdown decreases GGR and DNA damage-binding protein 2 (DDB2) abundance. Conversely, overexpression of wild-type METTL14 but not its enzymatically inactive mutant increases GGR and DDB2 abundance. METTL14 is a target for selective autophagy and acts as a critical epitranscriptomic mechanism to regulate GGR and suppress UVB-induced skin tumorigenesis."
item1635	REG00005	M6ATAR00159	Up	M6ADIS0046	.	35579750	"Bioactive peptides can inhibit acute myeloid leukemia cell proliferation by downregulating ALKBH5-mediated m6A demethylation of eIF4E-binding protein 1 (4EBP1/EIF4EBP1) and MLST8 mRNAs, which have potential to prevent and treat this disease."
item1636	REG00005	M6ATAR00682	Up	M6ADIS0046	.	35579750	"Bioactive peptides can inhibit acute myeloid leukemia cell proliferation by downregulating ALKBH5-mediated m6A demethylation of EIF4EBP1 and Target of rapamycin complex subunit LST8 (MLST8) mRNAs, which have potential to prevent and treat this disease."
item1637	REG00006	M6ATAR00683	Down	M6ADIS0155	.	35333576	"Colonic mucosal barrier dysfunction is one of the major causes of inflammatory bowel disease (IBD). Mettl14 restricted colonic epithelial cell death by regulating the stability of NF-kappa-B inhibitor alpha (Nfkbia) mRNA and modulating the NF-Kappa-B pathway,suggesting that m6A modification could be a potential therapeutic target for IBD."
item1638	REG00006	M6ATAR00237	Down	M6ADIS0006	.	33380825	"METTL14 was found to inhibit HCC cell migration, invasion, and EMT through modulating Epidermal growth factor receptor (EGFR)/PI3K/AKT signaling pathway in an m6A-dependent manner."
item1639	REG00006	M6ATAR00368	Down	M6ADIS0006	.	33380825	"METTL14 was found to inhibit HCC cell migration, invasion, and EMT through modulating EGFR/PI3-kinase subunit alpha (PI3k/PIK3CA)/AKT signaling pathway in an m6A-dependent manner."
item1640	REG00006	M6ATAR00175	Down	M6ADIS0006	.	33380825	"METTL14 was found to inhibit HCC cell migration, invasion, and EMT through modulating EGFR/PI3K/RAC-alpha serine/threonine-protein kinase (AKT1) signaling pathway in an m6A-dependent manner."
item1641	REG00007	M6ATAR00684	Up	M6ADIS0055	.	34476262	METTL3 intensified the metastasis and proliferation of OSCC by modulating the m6A amounts of Protein arginine N-methyltransferase 5 (PRMT5) and PD-L1.
item1642	REG00001	M6ATAR00685	Down	M6ADIS0110	.	34737423	"FTO-mediated N6-methyladenosine demethylation downregulated AC008440.5 (AC008) transcription, while lower FTO expression led to upregulation of AC008 transcription in OA."
item1643	REG00007	M6ATAR00360	Up	M6ADIS0055	.	34476262	METTL3 intensified the metastasis and proliferation of OSCC by modulating the m6A amounts of PRMT5 and Programmed cell death 1 ligand 1 (CD274/PD-L1).
item1644	REG00006	M6ATAR00310	Up	M6ADIS0059	.	34097350	The expression of METTL14 was downregulated in CRC cells and METTL14 could inhibit the metastasis of CRC cells. MeCP2 could bind to METTL14 to coregulate tumor suppressor Krueppel-like factor 4 (KLF4) expression through changing m6 A methylation modification.
item1645	REG00006	M6ATAR00686	Up	M6ADIS0150	.	33708859	"The overexpression of miR-4729 in vascular endothelial cells decreased the global mRNA methylation and TIE1 mRNA 3'UTR-specific site methylation by silencing METTL14 expression, reducing Tyrosine-protein kinase receptor Tie-1 (TIE1) mRNA stability, down-regulating the TIE1/VEGFA signal molecular loop expression, and weakening angiogenesis ability. MiR-4729 regulates TIE1 mRNA m6A modification and angiogenesis in hemorrhoids by targeting METTL14."
item1646	REG00007	.	.	M6ADIS0089	.	32847866	"An accumulation of METTL3, but not RBM15B, in the insoluble fractions, which positively correlated with the levels of insoluble Tau protein in the postmortem human Alzheimer's Disease samples."
item1647	REG00001	M6ATAR00687	Up	M6ADIS0161	.	33995105	"FTO was colocalized with Matrix metalloproteinase-24 (MMP24) in spinal neurons and shown increased binding to the Mmp24 mRNA in the spinal cord after SNL. SNL promoted the m6A eraser FTO binding to the Mmp24 mRNA, which subsequently facilitated the translation of MMP24 in the spinal cord, and ultimately contributed to neuropathic pain genesis."
item1648	REG00007	M6ATAR00688	Up	M6ADIS0051	.	35396379	Higher METTL3 expression indicated poorer prognosis. METTL3 upregulated Histone deacetylase 5 (HDAC5) expression in osteosarcoma cells by increasing the m6A level.
item1649	REG00014	M6ATAR00274	Up	M6ADIS0057	.	34621671	IGF2BP3 positively regulated Hypoxia-inducible factor 1-alpha (HIF-1-Alpha/HIF1A) expression by directly binding to a specific m6A site in the coding region of HIF1A mRNA in gastric cancer cells. IGF2BP3 and HIF1A were highly expressed in GC tissues and hypoxia-treated GC cells.
item1650	REG00007	M6ATAR00404	Up	M6ADIS0065	.	34076991	"Knockdown of METTL3 downregulated protein levels of Transcription factor SOX-2 (SOX2), CD133 and CD44 in MCF-7 cells. METTL3 is upregulated in breast cancer, and it promotes the stemness and malignant progression of BCa through mediating m6A modification on SOX2 mRNA."
item1651	REG00007	M6ATAR00689	Up	M6ADIS0065	.	34076991	"Knockdown of METTL3 downregulated protein levels of SOX2, Prominin-1 (CD133) and CD44 in MCF-7 cells. METTL3 is upregulated in breast cancer, and it promotes the stemness and malignant progression of BCa through mediating m6A modification on SOX2 mRNA."
item1652	REG00007	M6ATAR00574	Up	M6ADIS0065	.	34076991	"Knockdown of METTL3 downregulated protein levels of SOX2, CD133 and CD44 antigen (CD44) in MCF-7 cells. METTL3 is upregulated in breast cancer, and it promotes the stemness and malignant progression of BCa through mediating m6A modification on SOX2 mRNA."
item1653	REG00015	M6ATAR00690	Down	M6ADIS0007	.	34520821	High expression of KIAA1429 was testified in patients with non-small cell lung cancer and predicted worse prognosis in patients. KIAA1429-guided m6A modifications promoted NSCLC progression via m6A-dependent degradation of Death-associated protein kinase 3 (DAPK3) mRNA.
item1654	REG00007	M6ATAR00691	Up	M6ADIS0007	.	35441574	m6A transferase METTL3-induced Long intergenic non-protein coding RNA 1833 (LINC01833) m6A methylation promotes NSCLC progression through modulating HNRNPA2B1 expression.
item1655	REG00005	M6ATAR00260	Up	M6ADIS0142	.	35339477	ALKBH5 was upregulated in the cardiomyocytes of diabetic cardiomyopathy mice and posttranscriptionally activated Forkhead box protein O3 (FOXO3) by m6A demethylation in an m6A-YTHDF2-dependent manner.This work reveals the key function of the ALKBH5-FOXO3-CDR1as/Hippo signaling pathway in DCM and provides insight into the critical roles of m6A methylation in DCM.
item1656	REG00007	M6ATAR00401	Down	M6ADIS0057	.	32782536	"METTL3-KO in gastric cancer cells resulted in the suppression of cell proliferation by inducing Suppressor of cytokine signaling 2 (SOCS2), suggesting a potential role of elevated METTL3 expression in gastric cancer progression."
item1657	REG00007	M6ATAR00441	Up	M6ADIS0006	.	35035685	"METTL3 regulates the expression of Ubiquitin carboxyl-terminal hydrolase 7 (USP7) through m6A methylation and facilitate the invasion, migration and proliferation of HCC cells. Besides, the elevated METTL3 expression was related to worse overall survival."
item1658	REG00007	M6ATAR00692	Up	M6ADIS0068	.	34537760	"METTL3 induced m6A modification on Kinesin-like protein KIF3C (KIF3C), promoting the stabilization of KIF3C-mRNA by IGF2BP1. KIF3C was overexpressed in prostate cancer, promoting its growth migration and invasion was induced by miR-320d/METTL3 in an m6A dependent process."
item1659	REG00005	M6ATAR00140	Up	M6ADIS0154	.	35182329	"ALKBH5 knockdown suppressed cell proliferation, migration and invasion of infantile hemangioma cells, while promoting cell apoptosis. ALKBH5 promoted lncRNA Nuclear paraspeckle assembly transcript 1 (NEAT1) expression by reducing the m6A modification of lncRNA NEAT1."
item1660	REG00017	M6ATAR00206	Up	M6ADIS0057	.	34075693	METTL16-mediated m6A methylation promotes proliferation of gastric cancer cells through enhancing G1/S-specific cyclin-D1 (CCND1) expression.
item1661	REG00001	M6ATAR00693	Down	M6ADIS0051	.	35121825	"FTO could reduce the mRNA stability of Dapper homolog 1 (DACT1) via m6A demethylation, which decreased DACT1 expression and further activated the Wnt signaling pathway. The oncogenic effect of FTO on osteosarcoma was dependent on DACT1."
item1662	REG00006	M6ATAR00694	Up	M6ADIS0096	.	35004673	"Mettl14 resulted in enhanced levels of Proto-oncogene Wnt-1 (Wnt1) m6A modification and Wnt1 protein but not its transcript level. Furthermore, Mettl14 overexpression blocked I/R-induced downregulation of Wnt1 and Bete-catenin proteins, whereas Mettl14 hearts exhibited the opposite results. Mettl14 attenuates cardiac I/R injury by activating Wnt/Bete-catenin in an m6A-dependent manner, providing a novel therapeutic target for ischemic heart disease."
item1663	REG00013	M6ATAR00308	Up	M6ADIS0007	.	33758932	"In lung cancer, IGF2BP2 modified m6A to increase the expression of Thymidine kinase, cytosolic (TK1), thus promoting angiogenesis."
item1664	REG00006	M6ATAR00222	Up	M6ADIS0096	.	35004673	"Mettl14 resulted in enhanced levels of Wnt1 m6A modification and Wnt1 protein but not its transcript level.Furthermore, Mettl14 overexpression blocked I/R-induced downregulation of Wnt1 and Catenin beta-1 (CTNNB1/Beta-catenin) proteins, whereas Mettl14 hearts exhibited the opposite results. Mettl14 attenuates cardiac I/R injury by activating Wnt/Bete-catenin in an m6A-dependent manner, providing a novel therapeutic target for ischemic heart disease."
item1665	REG00014	M6ATAR00446	Up	M6ADIS0058	.	32993738	Knockdown of IGF2BP3 repressed DNA replication in the S phase of cell cycle and angiogenesis via reading m6A modification of CCND1 and Vascular endothelial growth factor A (VEGFA) respectively. Knockdown of IGF2BP3 repressed angiogenesis in colon cancer via regulating VEGF.
item1666	REG00001	M6ATAR00245	Up	M6ADIS0056	.	35524932	"Knockdown of FTO drastically suppressed the proliferation, migration, and invasion of ESCC cells,and Receptor tyrosine-protein kinase erbB-2 (ERBB2) is the target of FTO, which acts in concert in ESCC tumorigenesis and metastasis."
item1667	REG00026	M6ATAR00695	Down	M6ADIS0061	.	35033590	"DNA damage repair is a major barrier for chemotherapy efficacy of pancreatic cancer, it's the first time that PHD finger protein 10 (PHF10) was found and involved in the DNA damage response. ZC3H13 knockdown downregulated the m6A methylation of PHF10 and decreased PHF10 translation in a YTHDF1-dependent manner."
item1668	REG00008	M6ATAR00537	.	M6ADIS0104	.	35468611	"YTHDF2 regulates the stability of MAP kinase kinase 4 (MAP2K4) and MAP4K4 mRNAs.This study identified that dasatinib and quercetin alleviate LPS-induced senescence in HUVECs via the TRAF6-MAPK-NF-Kappa-B axis in a YTHDF2-dependent manner, providing novel ideas for clinical treatment of age-related cardiovascular diseases."
item1669	REG00008	M6ATAR00538	.	M6ADIS0104	.	35468611	"YTHDF2 regulates the stability of MAP2K4 and HPK/GCK-like kinase HGK (MAP4K4) mRNAs.This study identified that dasatinib and quercetin alleviate LPS-induced senescence in HUVECs via the TRAF6-MAPK-NF-Kappa-B axis in a YTHDF2-dependent manner, providing novel ideas for clinical treatment of age-related cardiovascular diseases."
item1670	REG00001	M6ATAR00513	Down	M6ADIS0115	.	34496349	RNA N6-methyladenosine demethylase FTO promotes osteoporosis through demethylating Runt-related transcription factor 2 (Runx2) mRNA and inhibiting osteogenic differentiation.
item1671	REG00007	M6ATAR00696	.	M6ADIS0016	.	34735003	PM2.5 exposure increased the levels of METTL3-mediated m6A modification of Cadherin-1 (CDH1) mRNA. PM2.5 exposure triggered EMT progression to promote the pulmonary fibrosis via miR-494-3p/YTHDF2 recognized and METTL3 mediated m6A modification.
item1672	REG00005	M6ATAR00697	Down	M6ADIS0056	.	34312488	ALKBH5 demethylated pri-miR-194-2 and inhibited miR-194-2 biogenesis through an m6A/DGCR8-dependent manner. ALKBH5/miR-194-2/RAI1 axis was also validated in clinical samples. This study revealed ALKBH5 in miRNAs biogenesis and provide novel insight for developing treatment strategies in esophageal cancer.
item1673	REG00005	M6ATAR00698	Down	M6ADIS0056	.	34312488	ALKBH5 demethylated pri-miR-194-2 and inhibited miR-194-2 biogenesis through an m6A/DGCR8-dependent manner. ALKBH5/miR-194-2/Retinoic acid-induced protein 1 (RAI1) axis was also validated in clinical samples. This study revealed ALKBH5 in miRNAs biogenesis and provide novel insight for developing treatment strategies in esophageal cancer.
item1674	REG00007	M6ATAR00401	Down	M6ADIS0001	.	34586733	"MiR-302a was identified to target METTL3, which could inhibit Suppressor of cytokine signaling 2 (SOCS2) expression via m6A modification in glioma."
item1675	REG00006	M6ATAR00375	Up	M6ADIS0057	.	34476213	"METTL14 inhibits tumor growth and metastasis of Stomach Adenocarcinoma via stabilization of Mutated in multiple advanced cancers 1 (PTEN) mRNA expression. Therefore, METTL14 is a potential biomarker of prognosis and therapeutic targets for Stomach Adenocarcinoma."
item1676	REG00026	M6ATAR00699	Up	M6ADIS0008	.	35418160	"The study revealed firm links between m6A modification patterns and cervical cancer prognosis, especially through ZC3H13-mediated m6A modification of Centromere protein K (CENPK) mRNA."
item1677	REG00008	.	.	M6ADIS0002	.	33577677	"SUMOylation of YTHDF2 has little impact on its ubiquitination and localization, but significantly increases its binding affinity of m6A-modified mRNAs and subsequently results in deregulated gene expressions which accounts for cancer progression."
item1678	REG00007	M6ATAR00700	Down	M6ADIS0073	.	33484966	METTL3 played a pivotal tumor-suppressor role in papillary thyroid cancer carcinogenesis through Proto-oncogene c-Rel (c-Rel) and RelA inactivation of the nuclear factor Kappa-B (NF-Kappa-B) pathway by cooperating with YTHDF2 and altered TAN infiltration to regulate tumor growth.
item1679	REG00008	M6ATAR00700	Down	M6ADIS0073	.	33484966	METTL3 played a pivotal tumor-suppressor role in papillary thyroid cancer carcinogenesis through Proto-oncogene c-Rel (c-Rel) and RelA inactivation of the nuclear factor Kappa-B (NF-Kappa-B) pathway by cooperating with YTHDF2 and altered TAN infiltration to regulate tumor growth.
item1680	REG00007	M6ATAR00425	Down	M6ADIS0073	.	33484966	METTL3 played a pivotal tumor-suppressor role in papillary thyroid cancer carcinogenesis through c-Rel and Transcription factor p65 (RELA) inactivation of the nuclear factor Kappa-B (NF-Kappa-B) pathway by cooperating with YTHDF2 and altered TAN infiltration to regulate tumor growth.
item1681	REG00008	M6ATAR00425	Down	M6ADIS0073	.	33484966	METTL3 played a pivotal tumor-suppressor role in papillary thyroid cancer carcinogenesis through c-Rel and Transcription factor p65 (RELA) inactivation of the nuclear factor Kappa-B (NF-Kappa-B) pathway by cooperating with YTHDF2 and altered TAN infiltration to regulate tumor growth.
item1682	REG00005	.	.	M6ADIS0056	.	34491904	The loss of ALKBH5 expression contributes to esophageal squamous cell carcinoma malignancy.
item1683	REG00007	M6ATAR00701	Up	M6ADIS0006	.	34398984	The N6-methyladenosine (m6A) modification of ASPM mRNA mediated by METTL3 promoted its expression in liver hepatocellular carcinoma.
item1684	REG00001	M6ATAR00702	Down	M6ADIS0068	.	34787056	"FTO was downregulated in PCa and its expression level showed a relevance to the prognosis of PCa patients. Additionally, FTO could regulate the proliferation, migration and invasion of PCa via regulating the expression level of Melanocortin receptor 4 (MC4R)."
item1685	REG00001	.	.	M6ADIS0010	.	33563180	"Dysregulated FTO and METTL3 are involved in the disease development and progression, affecting immune response in CCRCC. FTO and METTL3 expression and DNA methylation are potential prognostic markers of CCRCC."
item1686	REG00015	M6ATAR00703	Up	M6ADIS0065	.	34976433	"KIAA1429 could significantly promote the migration and invasion of breast cancer cells. KIAA1429 could bind to the motif in the 3' UTR of SMC protein 1A (SMC1A) mRNA directly and enhance SMC1A mRNA stability. In conclusion, the study revealed a novel mechanism of the KIAA1429/SMC1A/SNAIL axis in the regulation of metastasis of breast cancer."
item1687	REG00015	M6ATAR00399	Up	M6ADIS0065	.	34976433	"KIAA1429 could significantly promote the migration and invasion of breast cancer cells. KIAA1429 could bind to the motif in the 3' UTR of SMC1A mRNA directly and enhance SMC1A mRNA stability. In conclusion, the study revealed a novel mechanism of the KIAA1429/SMC1A/Zinc finger protein SNAI1 (SNAI1) axis in the regulation of metastasis of breast cancer."
item1688	REG00007	M6ATAR00341	Up	M6ADIS0057	.	33048840	"Expressions of HBXIP, METTL3 and Myc proto-oncogene protein (MYC) were all determined to be upregulated in both GC tissues and cells. HBXIP plays an oncogenic role in GC via METTL3-mediated MYC mRNA m6A modification."
item1689	REG00007	M6ATAR00704	Up	M6ADIS0068	.	35405116	METTL3-stabilized lncRNA Small nucleolar RNA host gene (SNHG7) accelerates glycolysis in PCa via SRSF1/c-Myc axis and inspires the understanding of m6A roles in lncRNA metabolism and tumor progression.
item1690	REG00001	M6ATAR00491	Up	M6ADIS0067	.	33103587	"This study found high expression of FTO in metastatic endometrial cancer and that this action promote both metastasis and invasion in vivo and in vitro. Mechanistically, FTO can catalyse demethylation modification in 3'UTR region of Homeobox protein Hox-B13 (HOXB13) mRNA, thereby abolishing m6A modification recognition with the YTHDF2 protein."
item1691	REG00006	M6ATAR00705	Down	M6ADIS0142	.	35013106	"METTL14 suppressed pyroptosis and diabetic cardiomyopathy via downregulating lncRNA Ubiquitin domain-containing protein TINC (TINCR), which further decreased the expression of key pyroptosis-related protein, NLRP3."
item1692	REG00005	M6ATAR00299	Up	M6ADIS0053	M6ADRUG0047	34496932	"The ALKBH5-HOXA10 loop jointly activates the JAK2/STAT3 signaling pathway by mediating Tyrosine-protein kinase JAK2 (JAK2) m6A demethylation, promoting epithelial ovarian cancer resistance to cisplatin."
item1693	REG00007	M6ATAR00289	Down	M6ADIS0006	.	35094011	METTL3 was upregulated and predicted poor prognosis of patients with intrahepatic cholangiocarcinoma(ICC). H3K4me3 activation-driven METTL3 transcription promotes ICC progression by YTHDF2-mediated Interferon-induced 54 kDa protein (IFIT2) mRNA degradation.
item1694	REG00006	M6ATAR00141	Up	M6ADIS0055	.	35467063	"METTL14 and lncRNA Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) were upregulated, and miR-224-5p was downregulated in OSCC tissues and cells. METTL14 induced m6A modification of MALAT1 to upregulate MALAT1."
item1695	REG00007	M6ATAR00706	Up	M6ADIS0073	.	35436987	"Metalloreductase STEAP2 (STEAP2) overexpression inhibited papillary thyroid cancer cell proliferation, migration, and invasion in vitro and inhibited lung metastasis and tumorigenicity in vivo. METTL3 stabilized STEAP2 mRNA and regulated STEAP2 expression positively in an m6A-dependent manner."
item1696	REG00007	.	.	M6ADIS0010	.	33563180	"Dysregulated FTO and METTL3 are involved in the disease development and progression, affecting immune response in CCRCC. FTO and METTL3 expression and DNA methylation are potential prognostic markers of CCRCC."
item1697	REG00001	M6ATAR00451	Up	M6ADIS0055	.	34779644	"Stable knockdown of FTO inhibited OSCC cell viability, colony formation, and tumor growth. Further, FTO depletion increased Transcriptional coactivator YAP1 (YAP1) m6A modification at mRNA 3'-untranslated region, accelerating the degradation of YAP1 mRNA, a well-documented oncogene promoting OSCC progression."
item1698	REG00006	.	.	M6ADIS0070	.	35048498	"METTL14 as a key component for m6 A RNA deposit and that it is closely related to BlCa progression, playing an important role in tumor aggressiveness."
item1699	REG00007	M6ATAR00567	Down	M6ADIS0141	.	33961823	"In SARS-CoV-2 infection, depletion of the host cell m6A methyltransferase METTL3 decreases m6A levels in SARS-CoV-2 and host genes, and m6A reduction in viral RNA increases RIG-I-like receptor 1 (RIG-I) binding and subsequently enhances the downstream innate immune signaling pathway and inflammatory gene expression."
item1700	REG00007	M6ATAR00441	Up	M6ADIS0006	.	35571490	"Ubiquitin carboxyl-terminal hydrolase 7 (USP7) was upregulated in HCC and associated with METTL3 level positively. USP7 silencing decreased proliferation, migration, and invasion rates of HCC cells. METTL3 promotes HCC to proliferate, migrate, and invade by regulating m6A methylation of USP7."
item1701	REG00007	M6ATAR00330	Up	M6ADIS0055	.	34479400	"High METTL3 expression was positively correlated with more severe clinical features of OSCC tumors. Furthermore, METTL3-KD and cycloleucine, a methylation inhibitor, decreased m6A levels and down-regulated Mitogen-activated protein kinase 14 (p38/MAPK14) expression in OSCC cells."
item1702	REG00024	M6ATAR00175	Down	M6ADIS0006	.	34088349	YTHDF1 contributes to the progression of HCC by activating PI3K/RAC-alpha serine/threonine-protein kinase (AKT1)/mTOR signaling pathway and inducing EMT.
item1703	REG00024	M6ATAR00339	Down	M6ADIS0006	.	34088349	YTHDF1 contributes to the progression of HCC by activating PI3K/AKT/Serine/threonine-protein kinase mTOR (MTOR) signaling pathway and inducing EMT.
item1704	REG00005	M6ATAR00707	Up	M6ADIS0065	M6ADRUG0022	35278676	ALKBH5 removed the m6A methylation of Breast cancer type 1 susceptibility protein (BRCA1) for mRNA stabilization and further enhanced DNA repair competency to decrease doxorubicin efficacy in breast cancer cells.
item1705	REG00007	M6ATAR00708	Up	M6ADIS0099	.	33579825	"In the in vivo atherosclerosis model,partial ligation of the carotid artery led to plaque formation and up-regulation of METTL3 and NACHT/LRR/PYD domains-containing protein 1 (NLRP1), with down-regulation of KLF4; knockdown of METTL3 via repetitive shRNA administration prevented the atherogenic process, NLRP3 up-regulation, and KLF4 down-regulation. Collectively, it has demonstrated that METTL3 serves a central role in the atherogenesis induced by oscillatory stress and disturbed blood flow."
item1706	REG00007	M6ATAR00605	Up	M6ADIS0099	.	33579825	"In the in vivo atherosclerosis model,partial ligation of the carotid artery led to plaque formation and up-regulation of METTL3 and NLRP1, with down-regulation of KLF4; knockdown of METTL3 via repetitive shRNA administration prevented the atherogenic process, NACHT, LRR and PYD domains-containing protein 3 (NLRP3) up-regulation, and KLF4 down-regulation. Collectively, it has demonstrated that METTL3 serves a central role in the atherogenesis induced by oscillatory stress and disturbed blood flow."
item1707	REG00001	M6ATAR00709	Up	M6ADIS0006	.	33783988	"AMD1 could stabilize the interaction of Ras GTPase-activating-like protein IQGAP1 (IQGAP1) with FTO, which then promotes FTO expression and increases HCC stemness."
item1708	REG00007	M6ATAR00310	Down	M6ADIS0099	.	33579825	"In the in vivo atherosclerosis model,partial ligation of the carotid artery led to plaque formation and up-regulation of METTL3 and NLRP1, with down-regulation of KLF4; knockdown of METTL3 via repetitive shRNA administration prevented the atherogenic process, NLRP1 up-regulation, and Krueppel-like factor 4 (KLF4) down-regulation. Collectively, it has demonstrated that METTL3 serves a central role in the atherogenesis induced by oscillatory stress and disturbed blood flow."
item1709	REG00007	M6ATAR00710	Up	M6ADIS0055	.	35287752	"METTL3 enhanced the m6A modification of M-phase inducer phosphatase 2 (CDC25B) mRNA, which maintained its stability and upregulated its expression, thereby activating G2/M phase of cell cycle and leading to HNSCC malignant progression."
item1710	REG00007	M6ATAR00711	.	M6ADIS0061	M6ADRUG0024	35433957	DBH antisense RNA 1 (Lnc_DBH-AS1) expression in pancreatic cancer(PC) was found to be linked to the METTL3-dependent m6A methylation of the lncRNA. MechanisticallyDBH-AS1 was able to increase PC cell sensitivity to gemcitabine by sequestering miR-3163 and thus upregulating USP44 in these tumor cells.
item1711	REG00007	M6ATAR00712	Up	M6ADIS0065	M6ADRUG0022	35502895	"Knockdown of METTL3 sensitized these breast cancer cells to Adriamycin (ADR; also named as doxorubicin) treatment and increased accumulation of DNA damage. Mechanically, we demonstrated that inhibition of METTL3 impaired HR efficiency and increased ADR-induced DNA damage by regulating m6A modification of Pro-epidermal growth factor (EGF)/RAD51 axis. METTL3 promoted EGF expression through m6A modification, which further upregulated RAD51 expression, resulting in enhanced HR activity."
item1712	REG00007	M6ATAR00713	Up	M6ADIS0065	M6ADRUG0022	35502895	"Knockdown of METTL3 sensitized these breast cancer cells to Adriamycin (ADR; also named as doxorubicin) treatment and increased accumulation of DNA damage. Mechanically, we demonstrated that inhibition of METTL3 impaired HR efficiency and increased ADR-induced DNA damage by regulating m6A modification of EGF/RAD51 axis. METTL3 promoted EGF expression through m6A modification, which further upregulated DNA repair protein RAD51 homolog 1 (RAD51) expression, resulting in enhanced HR activity."
item1713	REG00001	M6ATAR00487	Up	M6ADIS0104	M6ADRUG0103	35296150	"FTO overexpression significantly upregulated the mRNA and protein levels of Vascular cell adhesion protein 1 (VCAM1) and ICAM-1, downregulated those of KLF2 and eNOS, and strongly attenuated the atorvastatin-mediated induction of KLF2 and eNOS expression. FTO could serve as a novel molecular target to modulate endothelial function in vascular diseases."
item1714	REG00001	M6ATAR00284	Up	M6ADIS0104	M6ADRUG0103	35296150	"FTO overexpression significantly upregulated the mRNA and protein levels of VCAM-1 and Intercellular adhesion molecule 1 (ICAM1), downregulated those of KLF2 and eNOS, and strongly attenuated the atorvastatin-mediated induction of KLF2 and eNOS expression. FTO could serve as a novel molecular target to modulate endothelial function in vascular diseases."
item1715	REG00001	M6ATAR00714	Down	M6ADIS0104	M6ADRUG0103	35296150	"FTO overexpression significantly upregulated the mRNA and protein levels of VCAM-1 and ICAM-1, downregulated those of Krueppel-like factor 2 (KLF2) and eNOS, and strongly attenuated the atorvastatin-mediated induction of KLF2 and eNOS expression. FTO could serve as a novel molecular target to modulate endothelial function in vascular diseases."
item1716	REG00001	M6ATAR00715	Down	M6ADIS0104	M6ADRUG0103	35296150	"FTO overexpression significantly upregulated the mRNA and protein levels of VCAM-1 and ICAM-1, downregulated those of KLF2 and Constitutive NOS (eNOS), and strongly attenuated the atorvastatin-mediated induction of KLF2 and eNOS expression. FTO could serve as a novel molecular target to modulate endothelial function in vascular diseases."
item1717	REG00007	M6ATAR00716	.	M6ADIS0059	.	35595748	Ephrin type-A receptor 2 (EphA2) and VEGFA targeted by METTL3 via different IGF2BP-dependent mechanisms were found to promote vasculogenic mimicry (VM) formation via PI3K/AKT/mTOR and ERK1/2 signaling in CRC.
item1718	REG00006	M6ATAR00484	Down	M6ADIS0065	M6ADRUG0091	35562334	m6A-hypomethylation regulated FGFR4 phosphorylates GSK-3beta and activates beta-catenin/TCF4-Cystine/glutamate transporter (SLC7A11)/FPN1 signaling to drive anti-HER2 resistance. Knockdown of METTL14 significantly increased the expression level of FGFR4 in HER2-positive breast cancer cells. FGFR4 reduced the sensitivity of HER2-positive breast cancer to trastuzumab plus pertuzumab or tucatinib. These results pinpoint a mechanism of anti-HER2 resistance and provide a strategy for overcoming resistance via FGFR4 inhibition in recalcitrant HER2-positive breast cancer.
item1719	REG00007	M6ATAR00717	Up	M6ADIS0159	.	35452193	"Hypoxia induced rapid H3K4 methylation of the promoter of the methyltransferase-like 3 gene (METTL3) and resulted in its overexpression. METTL3 overexpression evokes N6-methyladenosine (m6A)-dependent miR-503 biogenesis in endothelial cells. In summary, this study highlights a novel endogenous mechanism wherein EVs aggravate myocardial injury during the onset of AMI via endothelial cell-secreted miR-503 shuttling."
item1720	REG00007	M6ATAR00446	.	M6ADIS0059	.	35595748	EphA2 and Vascular endothelial growth factor A (VEGFA) targeted by METTL3 via different IGF2BP-dependent mechanisms were found to promote vasculogenic mimicry (VM) formation via PI3K/AKT/mTOR and ERK1/2 signaling in CRC.
item1721	REG00014	M6ATAR00716	Up	M6ADIS0059	.	35595748	Ephrin type-A receptor 2 (EphA2) and VEGFA targeted by METTL3 via different IGF2BP3-dependent mechanisms were found to promote vasculogenic mimicry (VM) formation via PI3K/AKT/mTOR and ERK1/2 signaling in CRC.
item1722	REG00014	M6ATAR00446	Up	M6ADIS0059	.	35595748	EphA2 and Vascular endothelial growth factor A (VEGFA) targeted by METTL3 via different IGF2BP3-dependent mechanisms were found to promote vasculogenic mimicry (VM) formation via PI3K/AKT/mTOR and ERK1/2 signaling in CRC.
item1723	REG00013	M6ATAR00716	Up	M6ADIS0059	.	35595748	Ephrin type-A receptor 2 (EphA2) and VEGFA targeted by METTL3 via different IGF2BP2-dependent mechanisms were found to promote vasculogenic mimicry (VM) formation via PI3K/AKT/mTOR and ERK1/2 signaling in CRC.
item1724	REG00013	M6ATAR00446	Up	M6ADIS0059	.	35595748	EphA2 and Vascular endothelial growth factor A (VEGFA) targeted by METTL3 via different IGF2BP2-dependent mechanisms were found to promote vasculogenic mimicry (VM) formation via PI3K/AKT/mTOR and ERK1/2 signaling in CRC.
item1725	REG00024	M6ATAR00718	Up	M6ADIS0057	.	32788173	"Mutated YTHDF1 enhanced expression of Frizzled-7 (FZD7), leading to hyperactivation of the Wnt/Bete-catenin pathway and promotion of gastric cancer carcinogenesis."
item1726	REG00006	M6ATAR00719	Down	M6ADIS0166	.	35013140	Silencing METTL14 repressed apoptosis of spinal cord neurons and attenuated spinal cord injury by inhibiting m6A modification of Elongation factor 1-alpha 2 (EEF1A2) and activating the Akt/mTOR pathway.
item1727	REG00022	M6ATAR00375	Down	M6ADIS0091	.	33188203	"YTHDC1 promoted Mutated in multiple advanced cancers 1 (PTEN) mRNA degradation to increase Akt phosphorylation, thus facilitating neuronal survival in particular after ischemia, modulating m6A reader YTHDC1 provide a potential therapeutic target for ischemic stroke."
item1728	REG00006	.	.	M6ADIS0007	.	34733365	Silencing of METTL14 suppressed non-small cell lung cancer malignancy by inhibiting Twist-mediated activation of AKT signaling.
item1729	REG00001	M6ATAR00720	Up	M6ADIS0007	.	34169146	"FTO upregulated the expression of E2F1 by inhibiting the m6A modification of E2F1. The FTO/E2F1/Protein kinase C-binding protein NELL2 (NELL2) axis modulated NSCLC cell viability, migration, and invasion in vitro as well as affected NSCLC tumor growth and metastasis in vivo."
item1730	REG00001	M6ATAR00721	Down	.	.	35169043	"In FTO-depleted cells, we find that the canonical WNT/Bete-Catenin signaling is attenuated in a non-cell autonomous manner via the up-regulation of Dickkopf-related protein 1 (DKK1)."
item1731	REG00001	M6ATAR00234	Up	M6ADIS0007	.	34169146	"FTO upregulated the expression of Transcription factor E2F1 (E2F1) by inhibiting the m6A modification of E2F1. The FTO/E2F1/NELL2 axis modulated NSCLC cell viability, migration, and invasion in vitro as well as affected NSCLC tumor growth and metastasis in vivo."
item1732	REG00015	M6ATAR00722	Up	M6ADIS0007	.	33249400	"KIAA1429 regulates Mucin-3A (MUC3A) expression through m6A modification to modulate LUAD cells to proliferate, migrate, invade, and induce cell cycle arrest."
item1733	REG00001	M6ATAR00723	Up	M6ADIS0056	.	35568876	FTO relys on the reading protein YTHDF1 to affect the translation pathway of the Estradiol 17-beta-dehydrogenase 11 (HSD17B11) gene to regulate the formation of lipid droplets in esophageal cancer cells.
item1734	REG00015	M6ATAR00724	Down	M6ADIS0059	.	34819634	KIAA1429 plays an oncogenic role in CRC cells by inhibiting the expression of Wee1-like protein kinase (WEE1) in an m6A-independent manner and is associated with poor survival in CRC patients.
item1735	REG00022	M6ATAR00725	.	M6ADIS0142	.	34716659	This study suggests that YTHDC1 plays crucial role in regulating the normal contractile function and the development of dilated cardiomyopathy.
item1736	REG00024	M6ATAR00258	Up	M6ADIS0065	.	35197112	"Forkhead box protein M1 (FOXM1) is a target of YTHDF1. Through recognizing and binding to the m6A-modified mRNA of FOXM1, YTHDF1 accelerated the translation process of FOXM1 and promoted breast cancer metastasis."
item1737	REG00025	M6ATAR00726	Up	M6ADIS0065	.	33125861	"Mechanistically, YTHDF3 enhances the translation of m6A-enriched transcripts for GD1 alpha synthase (ST6GALNAC5), GJA1, and EGFR, all associated with breast cancer brain metastasis. This work uncovers an essential role of YTHDF3 in controlling the interaction between cancer cells and brain microenvironment, thereby inducing brain metastatic competence."
item1738	REG00025	M6ATAR00727	Up	M6ADIS0065	.	33125861	"Mechanistically, YTHDF3 enhances the translation of m6A-enriched transcripts for ST6GALNAC5, Gap junction alpha-1 protein (GJA1), and EGFR, all associated with breast cancer brain metastasis. This work uncovers an essential role of YTHDF3 in controlling the interaction between cancer cells and brain microenvironment, thereby inducing brain metastatic competence."
item1739	REG00025	M6ATAR00237	Up	M6ADIS0065	.	33125861	"Mechanistically, YTHDF3 enhances the translation of m6A-enriched transcripts for ST6GALNAC5, GJA1, and Epidermal growth factor receptor (EGFR), all associated with breast cancer brain metastasis. This work uncovers an essential role of YTHDF3 in controlling the interaction between cancer cells and brain microenvironment, thereby inducing brain metastatic competence."
item1740	REG00001	M6ATAR00728	Up	M6ADIS0068	.	35397614	FTO suppresses PCa proliferation and metastasis through reducing the degradation of Chloride intracellular channel protein 4 (CLIC4) mRNA in an m6A dependent manner.
item1741	REG00001	M6ATAR00373	Up	M6ADIS0092	.	28333151	"FTO downregulation suppressed mitochondria biogenesis and energy production, showing as the decreased mitochondria mass and mitochondrial DNA (mtDNA) content, the downregulated expression of mtDNA-encoding genes and PPAR-gamma coactivator 1-alpha (PGC-1a/PPARGC1A) gene, together with declined ATP level. These findings provide the first evidence for the contribution of FTO for skeletal muscle differentiation."
item1742	REG00018	M6ATAR00341	.	M6ADIS0061	.	34970694	The study revealed important roles for METTL5 in the development of pancreatic cancer and present the METTL5/Myc proto-oncogene protein (MYC) axis as a novel therapeutic strategy for treatment.
item1743	REG00006	M6ATAR00375	Up	M6ADIS0010	.	35249103	"Upregulation of METTL14 inhibited ccRCC cells proliferation and migration in vitro. Overexpression of METTL14 increased the m6A enrichment of Mutated in multiple advanced cancers 1 (PTEN), and promoted Pten expression. METTL14-enhanced Pten mRNA stability was dependent on YTHDF1."
item1744	REG00024	M6ATAR00375	Up	M6ADIS0010	.	35249103	"Upregulation of METTL14 inhibited ccRCC cells proliferation and migration in vitro. Overexpression of METTL14 increased the m6A enrichment of Mutated in multiple advanced cancers 1 (PTEN), and promoted Pten expression. METTL14-enhanced Pten mRNA stability was dependent on YTHDF1."
item1745	REG00001	M6ATAR00360	Up	M6ADIS0055	.	35289035	"Arecoline-induced FTO promotes the stability and expression levels of Programmed cell death 1 ligand 1 (CD274/PD-L1) transcripts through mediating m6A modification and MYC activity, respectively. PD-L1 upregulation confers superior cell proliferation, migration, and resistance to T-cell killing to OSCC cells."
item1746	REG00007	M6ATAR00112	Up	M6ADIS0054	.	34980191	"Knockout of METTL3 can reduce the total expression of ZNFX1 antisense RNA 1 (ZFAS1). ZFAS1 is used as an oncogenic lncRNA, which can promote NPCcell proliferation, migration and tumor growth."
item1747	REG00025	M6ATAR00453	Up	M6ADIS0065	.	35282088	"YTHDF3 positively regulated cell migration, invasion, and EMT in triple-negative breast cancer cells. Moreover, Zinc finger E-box-binding homeobox 1 (ZEB1) was identified as a key downstream target for YTHDF3 and YTHDF3 could enhance ZEB1 mRNA stability in an m6A-dependent manner."
item1748	REG00006	.	.	M6ADIS0008	.	35116983	Up-regulation of METTL14 acted as an adverse prognostic factor for overall survival in cervical cancer patients. These study suggest an important oncogenic role of METTL14 in the growth and invasion of both HPV-positive and HPV-negative cervical cancer cells.
item1749	REG00007	M6ATAR00729	.	M6ADIS0008	.	35638109	"DARS-AS1 was validated to facilitate DARS translation via recruiting METTL3 and METTL14, which bound with DARS mRNA Aspartate--tRNA ligase, cytoplasmic (DARS) mRNA 5' untranslated region (5'UTR) and promoting its translation. The present study demonstrated that the 'HIF1-Alpha/DARS-AS1/DARS/ATG5/ATG3' pathway regulated the hypoxia-induced cytoprotective autophagy of cervical cancer(CC) and is a promising target of therapeutic strategies for patients afflicted with CC."
item1750	REG00006	M6ATAR00729	.	M6ADIS0008	.	35638109	"DARS-AS1 was validated to facilitate DARS translation via recruiting METTL3 and METTL14, which bound with DARS mRNA Aspartate--tRNA ligase, cytoplasmic (DARS) mRNA 5' untranslated region (5'UTR) and promoting its translation. The present study demonstrated that the 'HIF1-Alpha/DARS-AS1/DARS/ATG5/ATG3' pathway regulated the hypoxia-induced cytoprotective autophagy of cervical cancer(CC) and is a promising target of therapeutic strategies for patients afflicted with CC."
item1751	REG00013	M6ATAR00497	Up	M6ADIS0057	.	35306138	"IGF2BP2, as a m6A reader, was proved to increase the expression of Insulin-like growth factor 1 receptor (IGF1R) by identifying m6A methylation modification sites in IGF1R mRNA, thus activating RhoA-ROCK pathway. The oncogenic role of IGF2BP2 in gastric cancer carcinogenesis and confirmed its activation is partly due to the activation of IGF1R-RhoA-ROCK signaling pathway."
item1752	REG00008	M6ATAR00524	Down	.	.	32248017	"RBM4 interacts with YTH N6-methyladenosine RNA binding protein 2 (YTHDF2) to degrade m6A modified Transcription factor ISGF-3 components p91/p84 (Stat1) mRNA, thereby regulating glycolysis and M1 macrophage polarization."
item1753	REG00025	M6ATAR00730	.	M6ADIS0061	.	35183226	Theses results implicate a negative feedback of m6A reader YTHDF3 and glycolytic lncRNA DICER1-AS1 is involved in glycolysis and tumorigenesis of pancreatic cancer. YTHDF3 and lncRNA DICER1-AS1 promotes glycolysis of pancreatic cancer through inhibiting maturation of hsa-miR-5586-5p.
item1754	REG00008	M6ATAR00731	Down	M6ADIS0001	.	34246306	"YTHDF2 accelerated UBX domain-containing protein 1 (UBXN1) mRNA degradation via METTL3-mediated m6A, which, in turn, promoted NF-Kappa-B activation. YTHDF2 promotes the malignant progression of gliomas and revealed important insight into the upstream regulatory mechanism of NF-Kappa-B activation via UBXN1 with a primary focus on m6A modification."
item1755	REG00008	M6ATAR00054	Up	M6ADIS0001	.	34246306	"YTHDF2 accelerated UBXN1 mRNA degradation via METTL3-mediated m6A, which, in turn, promoted Nuclear factor NF-kappa-B p105 subunit (NF-Kappa-B/NFKB1) activation. YTHDF2 promotes the malignant progression of gliomas and revealed important insight into the upstream regulatory mechanism of NF-Kappa-B activation via UBXN1 with a primary focus on m6A modification."
item1756	REG00007	M6ATAR00731	Down	M6ADIS0001	.	34246306	"YTHDF2 accelerated UBX domain-containing protein 1 (UBXN1) mRNA degradation via METTL3-mediated m6A, which, in turn, promoted NF-Kappa-B activation. YTHDF2 promotes the malignant progression of gliomas and revealed important insight into the upstream regulatory mechanism of NF-Kappa-B activation via UBXN1 with a primary focus on m6A modification."
item1757	REG00007	M6ATAR00054	Up	M6ADIS0001	.	34246306	"YTHDF2 accelerated UBXN1 mRNA degradation via METTL3-mediated m6A, which, in turn, promoted Nuclear factor NF-kappa-B p105 subunit (NF-Kappa-B/NFKB1) activation. YTHDF2 promotes the malignant progression of gliomas and revealed important insight into the upstream regulatory mechanism of NF-Kappa-B activation via UBXN1 with a primary focus on m6A modification."
item1758	REG00005	M6ATAR00732	Down	M6ADIS0057	.	35114989	"Myt1 kinase (PKMYT1), as a downstream target of ALKBH5, promoted invasion and migration in GC. Moreover IGF2BP3 helped stabilize the mRNA stability of PKMYT1 via its m6A modification site."
item1759	REG00014	M6ATAR00732	Up	M6ADIS0057	.	35114989	"Myt1 kinase (PKMYT1), as a downstream target of ALKBH5, promoted invasion and migration in GC. Moreover IGF2BP3 helped stabilize the mRNA stability of PKMYT1 via its m6A modification site."
item1760	REG00007	M6ATAR00733	Up	M6ADIS0073	.	34562008	"Silencing METTL3 suppresses hsa-miR-222-3p expression and thus stimulates STK4 expression, thereby repressing the malignancy and metastasis of Thyroid Carcinoma."
item1761	REG00007	M6ATAR00734	Down	M6ADIS0073	.	34562008	"Silencing METTL3 suppresses miR-222-3p expression and thus stimulates Serine/threonine-protein kinase 4 (STK4) expression, thereby repressing the malignancy and metastasis of Thyroid Carcinoma."
item1762	REG00007	M6ATAR00735	Up	M6ADIS0006	.	35348293	"METTL3 up-regulated the expression of hsa-miR-589-5p and promoted the maturation of miR-589-5p. Overexpressed miR-589-5p and METTL3 promoted the viability, migration and invasion of liver cancer cells."
item1763	REG00001	.	.	M6ADIS0057	.	33122917	The prediction model was established based on the expression of m6A RNA methylation regulators FTO (fat mass and obesity-associated) and RBM15 (RNA binding motif protein 15). The two-methylase combination model was an independent prognostic factor of GC.
item1764	REG00008	M6ATAR00736	Down	M6ADIS0048	.	35075244	"The analyses of m6A-RIP-seq and RIP-PCR indicated that Signal transducer and activator of transcription 5A (STAT5A) was the downstream target of YTHDF2, which was binding to the m6A modification site of STAT5A to promote its mRNA degradation. ChIP-seq and PCR assays revealed that STAT5A suppressed multiple myelomacell proliferation by occupying the transcription site of MAP2K2 to decrease ERK phosphorylation."
item1765	REG00001	M6ATAR00402	Down	M6ADIS0048	M6ADRUG0102	35145273	"FTO promotes Bortezomib resistance via m6A-dependent destabilization of Superoxide dismutase [Mn], mitochondrial (SOD2) expression in multiple myeloma."
item1766	REG00013	M6ATAR00141	Up	M6ADIS0007	.	35111811	"IGF2BP2 promotes Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) stability in an m6A-dependent mechanism, thus promoting its downstream target autophagy-related (ATG)12 expression and NSCLC proliferation."
item1767	REG00005	M6ATAR00737	Down	M6ADIS0007	.	35344216	"ALKBH5 weakens YTHDF1/3-mediated TGF-beta receptor type-2 (TGF-Beta-R2) and SMAD3 mRNA stabilization, and abolishes YTHDF2-mediated SMAD6 mRNA degradation, supporting the notion that ALKBH5 inhibits TGF-Beta-induced EMT and invasion of NSCLC cells via YTHD1/2/3-mediated mechanism."
item1768	REG00005	M6ATAR00396	Down	M6ADIS0007	.	35344216	"ALKBH5 weakens YTHDF1/3-mediated TGF-Beta-R2 and Mothers against decapentaplegic homolog 3 (SMAD3) mRNA stabilization, and abolishes YTHDF2-mediated SMAD6 mRNA degradation, supporting the notion that ALKBH5 inhibits TGF-Beta-induced EMT and invasion of NSCLC cells via YTHD1/2/3-mediated mechanism."
item1769	REG00005	M6ATAR00738	Up	M6ADIS0007	.	35344216	"ALKBH5 weakens YTHDF1/3-mediated TGF-Beta-R2 and SMAD3 mRNA stabilization, and abolishes YTHDF2-mediated Mothers against decapentaplegic homolog 6 (SMAD6) mRNA degradation, supporting the notion that ALKBH5 inhibits TGF-Beta-induced EMT and invasion of NSCLC cells via YTHD1/2/3-mediated mechanism."
item1770	REG00001	M6ATAR00739	.	M6ADIS0070	.	35418191	"FTO proved as an N6-methyladenosine (m6A) demethylase in decreasing m6A modification was confirmed to regulate the migration and proliferation in Bca, overexpressing hsa-miR-5581-3p partially rescued the effects of the overexpressing SMAD3 and FTO in BCa cells."
item1771	REG00024	M6ATAR00605	Up	.	.	35649302	"YTHDF1 promotes pro-inflammatory IL-1-Beta production in macrophages during bacterial infections. YTHDF1 overexpression promotes NACHT, LRR and PYD domains-containing protein 3 (NLRP3) translation.YTHDF1 participates in inflammatory responses and subsequent injuries, serving as a new potential therapeutic target in clinical treatment of inflammatory diseases."
item1772	REG00024	M6ATAR00294	Up	.	.	35649302	"YTHDF1 promotes pro-inflammatory Interleukin-1 beta (IL1B) production in macrophages during bacterial infections. YTHDF1 overexpression promotes NLRP3 translation. YTHDF1 participates in inflammatory responses and subsequent injuries, serving as a new potential therapeutic target in clinical treatment of inflammatory diseases."
item1773	REG00007	M6ATAR00740	Down	M6ADIS0146	.	34799724	METTL3-mediated m6A-modification profile in gallbladder-cancer cells and identified Dual specificity protein phosphatase 5 (DUSP5) as the downstream gene of METTL3. METTL3 promoted the degradation of DUSP5 mRNA in a YTHDF2-dependent manner.
item1774	REG00020	.	.	M6ADIS0057	.	33122917	The prediction model was established based on the expression of m6A RNA methylation regulators FTO (fat mass and obesity-associated) and RBM15 (RNA binding motif protein 15). The two-methylase combination model was an independent prognostic factor of GC.
item1775	REG00007	M6ATAR00741	Down	M6ADIS0057	.	32650804	N6-methyladenosine (m6A) modification of Basic leucine zipper transcriptional factor ATF-like 2 (BATF2) mRNA by METTL3 repressed its expression in gastric cancer.
item1776	REG00008	M6ATAR00742	Down	M6ADIS0007	M6ADRUG0100	34656164	"In lung adenocarcinoma, The miR-146a/Notch signaling was sustained highly activated in a m6A dependent manner, and the m6A regulator of YTHDF2 suppressed LINC00902 (TUSC7), both of which contributed to the resistant features. Functionally, the sponge type of TUSC7 regulation of miR-146a inhibited Notch signaling functions, and affected the cancer progression and stem cells' renewal in Erlotinib resistant PC9 cells (PC9ER) and Erlotinib resistant HCC827 cells (HCC827ER) cells."
item1777	REG00022	M6ATAR00743	.	M6ADIS0061	.	34021267	"MiR-30d is a novel target for YTHDC1 through m6A modification, and hsa-miR-30d represses pancreatic ductal adenocarcinoma tumorigenesis via suppressing aerobic glycolysis."
item1778	REG00009	M6ATAR00679	Down	M6ADIS0067	.	33559954	"WTAP could methylate 3'-UTR of Caveolin-1 (CAV1) and downregulate CAV-1 expression to activate NF-Kappa-B signaling pathway in EC, which promoted EC progression."
item1779	REG00009	M6ATAR00054	.	M6ADIS0067	.	33559954	"WTAP could methylate 3'-UTR of CAV-1 and downregulate CAV-1 expression to activate Nuclear factor NF-kappa-B p105 subunit (NF-Kappa-B/NFKB1) signaling pathway in EC, which promoted EC progression."
item1780	REG00007	M6ATAR00325	Up	M6ADIS0007	M6ADRUG0106	32792859	"Chidamide could decrease Hepatocyte growth factor receptor (c-Met/MET) expression by inhibiting mRNA N6-methyladenosine (m6A) modification through the downregulation of METTL3 and WTAP expression, subsequently increasing the crizotinib sensitivity of NSCLC cells in a c-MET-/HGF-dependent manner."
item1781	REG00009	M6ATAR00325	Up	M6ADIS0007	M6ADRUG0106	32792859	"Chidamide could decrease Hepatocyte growth factor receptor (c-Met/MET) expression by inhibiting mRNA N6-methyladenosine (m6A) modification through the downregulation of METTL3 and WTAP expression, subsequently increasing the crizotinib sensitivity of NSCLC cells in a c-MET-/HGF-dependent manner."
item1782	REG00007	M6ATAR00744	Up	M6ADIS0110	.	33894271	METTL3 is involved in OA probably by regulating the inflammatory response. METTL3 overexpression affects extracellular matrix degradation in OA by adjusting the balance between TIMPs and Interstitial collagenase (MMP1).
item1783	REG00007	M6ATAR00744	Up	M6ADIS0110	.	33894271	METTL3 is involved in OA probably by regulating the inflammatory response. METTL3 overexpression affects extracellular matrix degradation in OA by adjusting the balance between TIMPs and Interstitial collagenase (MMP1).
item1784	REG00007	M6ATAR00333	Down	M6ADIS0110	.	33894271	METTL3 is involved in OA probably by regulating the inflammatory response. METTL3 overexpression affects extracellular matrix degradation in OA by adjusting the balance between TIMPs and Collagenase 3 (MMP13).
item1785	REG00007	M6ATAR00745	Down	M6ADIS0110	.	33894271	METTL3 is involved in OA probably by regulating the inflammatory response. METTL3 overexpression affects extracellular matrix degradation in OA by adjusting the balance between Metalloproteinase inhibitor 1 (TIMP-1) and MMPs.
item1786	REG00006	M6ATAR00498	Down	M6ADIS0065	M6ADRUG0091	35562334	m6A-hypomethylation regulated FGFR4 phosphorylates GSK-3beta and activates beta-catenin/TCF4-SLC7A11/Solute carrier family 40 member 1 (FPN1) signaling to drive anti-HER2 resistance. Knockdown of METTL14 significantly increased the expression level of FGFR4 in HER2-positive breast cancer cells. FGFR4 reduced the sensitivity of HER2-positive breast cancer to trastuzumab plus pertuzumab or tucatinib. These results pinpoint a mechanism of anti-HER2 resistance and provide a strategy for overcoming resistance via FGFR4 inhibition in recalcitrant HER2-positive breast cancer.
item1787	REG00007	M6ATAR00648	Down	M6ADIS0110	.	33894271	METTL3 is involved in OA probably by regulating the inflammatory response. METTL3 overexpression affects extracellular matrix degradation in OA by adjusting the balance between Metalloproteinase inhibitor 2 (TIMP2) and MMPs.
item1788	REG00012	M6ATAR00249	Up	M6ADIS0160	.	35565249	"This data identify IGF2BP1 as an important driver of tumor progression in NEN, and indicate that disruption of the IGF2BP1-Myc-Histone-lysine N-methyltransferase EZH2 (EZH2) axis represents a promising approach for targeted therapy of neuroendocrine neoplasms."
item1789	REG00007	M6ATAR00746	Down	M6ADIS0004	.	34561421	m6A methyltransferase complex METTL3/METTL14 is upregulated in CML patients and that is required for proliferation of primary CML cells and CML cell lines sensitive and resistant to the TKI imatinib. METTL3 directly regulates the level of Pescadillo homolog (PES1) protein identified as an oncogene in several tumors. These results point to METTL3 as a novel relevant oncogene in CML and as a promising therapeutic target for TKI resistant CML.
item1790	REG00006	M6ATAR00746	Down	M6ADIS0004	.	34561421	m6A methyltransferase complex METTL3/METTL14 is upregulated in CML patients and that is required for proliferation of primary CML cells and CML cell lines sensitive and resistant to the TKI imatinib. METTL3 directly regulates the level of Pescadillo homolog (PES1) protein identified as an oncogene in several tumors. These results point to METTL3 as a novel relevant oncogene in CML and as a promising therapeutic target for TKI resistant CML.
item1791	REG00008	M6ATAR00424	Down	.	.	32905781	"YTHDF3 recruits the PAN2-PAN3 deadenylase complex and conduces to reprogramming by promoting mRNA clearance of somatic genes, including Tead2 and Tgfb1, which parallels the activity of the YTHDF2-CCR4-NOT deadenylase complex. YTHDF2/3 deficiency suppressed the mRNA clearance of MEF-related genes, especially Transcriptional enhancer factor TEF-4 (TEAD2). YTHDF2/3 couples RNA deadenylation and regulation with the clearance of somatic genes and provides insights into iPSC reprogramming at the posttranscriptional level."
item1792	REG00025	M6ATAR00424	Down	.	.	32905781	"YTHDF3 recruits the PAN2-PAN3 deadenylase complex and conduces to reprogramming by promoting mRNA clearance of somatic genes, including Tead2 and Tgfb1, which parallels the activity of the YTHDF2-CCR4-NOT deadenylase complex. YTHDF2/3 deficiency suppressed the mRNA clearance of MEF-related genes, especially Transcriptional enhancer factor TEF-4 (TEAD2). YTHDF2/3 couples RNA deadenylation and regulation with the clearance of somatic genes and provides insights into iPSC reprogramming at the posttranscriptional level."
item1793	REG00008	.	.	M6ADIS0067	.	35512522	YTHDF2 expression can accurately assess the depth of myometrial invasion (DMI) in EMAC when EMAC coexists with adenomyosis.
item1794	REG00007	M6ATAR00228	Up	M6ADIS0056	.	34729394	"METTL3 could interact with Microprocessor complex subunit DGCR8 (DGCR8) protein and positively modulate pri-miR-320b maturation process in an N6-methyladenosine (m6A)-dependent manner. Therefore, our findings uncover a VEGF-C-independent mechanism of exosomal and intracellular miR-320b-mediated LN metastasis and identify miR-320b as a novel predictive marker and therapeutic target for LN metastasis in ESCC."
item1795	REG00007	M6ATAR00047	Up	M6ADIS0056	.	34729394	"METTL3 could interact with DGCR8 protein and positively modulate pri-miR-320b maturation process in an N6-methyladenosine (m6A)-dependent manner. Therefore, our findings uncover a VEGF-C-independent mechanism of exosomal and intracellular hsa-miR-320b-mediated LN metastasis and identify miR-320b as a novel predictive marker and therapeutic target for LN metastasis in ESCC."
item1796	REG00008	M6ATAR00747	Up	M6ADIS0057	.	35499052	"CBSLR interacted with YTHDF2 to form a CBSLR/YTHDF2/CBS signaling axis that decreased the stability of CBS mRNA by enhancing the binding of YTHDF2 with the m6A-modified coding sequence (CDS) of CBS mRNA. Reveal a novel mechanism in how HIF1-Alpha/CBSLR modulates ferroptosis/chemoresistance in GC, illuminating potential therapeutic targets for refractory hypoxic tumors."
item1797	REG00006	M6ATAR00526	Down	M6ADIS0065	M6ADRUG0092	35562334	m6A-hypomethylation regulated Fibroblast growth factor receptor 4 (FGFR4) phosphorylates GSK-3beta and activates beta-catenin/TCF4-SLC7A11/FPN1 signaling to drive anti-HER2 resistance. Knockdown of METTL14 significantly increased the expression level of FGFR4 in HER2-positive breast cancer cells. FGFR4 reduced the sensitivity of HER2-positive breast cancer to trastuzumab plus pertuzumab or tucatinib. These results pinpoint a mechanism of anti-HER2 resistance and provide a strategy for overcoming resistance via FGFR4 inhibition in recalcitrant HER2-positive breast cancer.
item1798	REG00008	M6ATAR00748	Down	M6ADIS0057	.	35499052	"CBSLR interacted with YTHDF2 to form a CBSLR/YTHDF2/CBS signaling axis that decreased the stability of Cystathionine beta-synthase (CBS) mRNA by enhancing the binding of YTHDF2 with the m6A-modified coding sequence (CDS) of CBS mRNA. Reveal a novel mechanism in how HIF1-Alpha/CBSLR modulates ferroptosis/chemoresistance in GC, illuminating potential therapeutic targets for refractory hypoxic tumors."
item1799	REG00007	.	Up	M6ADIS0006	.	35122073	"The N6-methyladenosine (m6A) modification was mediated by N6-adenosine-methyltransferase 70-kDa subunit (METTL3) and recognized by insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1)/IGF2BP3, which maintained lnc-CTHCC stability and increased its expression in HCC."
item1800	REG00007	.	Up	M6ADIS0006	.	35122073	"The N6-methyladenosine (m6A) modification was mediated by N6-adenosine-methyltransferase 70-kDa subunit (METTL3) and recognized by insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1)/IGF2BP3, which maintained lnc-CTHCC stability and increased its expression in HCC."
item1801	REG00007	.	Up	M6ADIS0006	.	35122073	"The N6-methyladenosine (m6A) modification was mediated by N6-adenosine-methyltransferase 70-kDa subunit (METTL3) and recognized by insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1)/IGF2BP3, which maintained lnc-CTHCC stability and increased its expression in HCC."
item1802	REG00007	M6ATAR00750	Down	M6ADIS0056	.	34155197	"m6A-RNA immunoprecipitation sequencing revealed that METTL3 upregulates the m6A modification of Adenomatous polyposis coli protein (APC), which recruits YTHDF for APC mRNA degradation. Our findings reveal a mechanism by which the Wnt/Bete-catenin pathway is upregulated in ESCC via METTL3/YTHDF-coupled epitranscriptomal downregulation of APC."
item1803	REG00014	M6ATAR00751	Up	M6ADIS0137	.	34953789	hsa_circ_0004287 was upregulated in peripheral blood mononuclear cells of both AD and psoriasis patients. hsa_circ_0004287 reduced the stability of its host gene metastasis associated lung adenocarcinoma transcript 1 (MALAT1) by competitively binding to IGF2BP3 with MALAT1 in an N6-methyladenosine (m6A)-dependent manner.
item1804	REG00014	M6ATAR00141	Up	M6ADIS0137	.	34953789	CircRNA hsa_circ_0004287 was upregulated in peripheral blood mononuclear cells of both AD and psoriasis patients. hsa_circ_0004287 reduced the stability of its host gene Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) by competitively binding to IGF2BP3 with MALAT1 in an N6-methyladenosine (m6A)-dependent manner.
item1805	REG00006	.	.	M6ADIS0001	.	32891980	Some SNPs in the METTL14 gene are associated with predisposition to neuroblastoma.
item1806	REG00023	M6ATAR00752	Up	M6ADIS0020	.	34822792	"Over-expression (OE) of YTHDC2 increased G2/mitotic-specific cyclin-B2 (CCNB2) levels, reduced cell cycle arrest, and improved reproductive toxicity after Mn exposure."
item1807	REG00024	M6ATAR00753	Down	M6ADIS0057	.	35193930	"Loss of YTHDF1 mediated the overexpression of Interferon gamma receptor 1 (IFNGR1) and JAK/STAT1 signaling pathway in tumor cells, which contributes to restored sensitivity to antitumor immunity. YTHDF1 is overexpressed in GC and promotes GC by inducing cell proliferation and repression of DCs-mediated antitumor immune response."
item1808	REG00006	M6ATAR00268	Down	M6ADIS0065	M6ADRUG0092	35562334	m6A-hypomethylation regulated FGFR4 phosphorylates Glycogen synthase kinase-3 beta (GSK3Beta/GSK3B) and activates beta-catenin/TCF4-SLC7A11/FPN1 signaling to drive anti-HER2 resistance. Knockdown of METTL14 significantly increased the expression level of FGFR4 in HER2-positive breast cancer cells. FGFR4 reduced the sensitivity of HER2-positive breast cancer to trastuzumab plus pertuzumab or tucatinib. These results pinpoint a mechanism of anti-HER2 resistance and provide a strategy for overcoming resistance via FGFR4 inhibition in recalcitrant HER2-positive breast cancer.
item1809	REG00005	M6ATAR00140	Up	M6ADIS0006	.	35357550	"ALKBH5 could up-regulate Nuclear paraspeckle assembly transcript 1 (NEAT1) expression by inhibiting m6A enrichment. ALKBH5-induced NEAT1 promoted cell proliferation and migration of HCC by sponging miR-214 in vitro, which provided a potential therapeutic target for HCC."
item1810	REG00024	M6ATAR00022	Up	.	.	33733063	"YTHDF1 binds the m6A-modified POU domain, class 5, transcription factor 1 (POU5F1) mRNA."
item1811	REG00008	M6ATAR00514	Up	M6ADIS0167	.	35120571	MiR-19a regulated TNF alpha-induced protein 3 (TNFAIP3) degradation by downregulating the expression of YTH N6-methyladenosine RNA-binding protein 2 (YTHDF2). The circGARS sponges miR-19a to regulate YTHDF2 expression to promote SLE progression through the A20/NF-Kappa-B axis and acts as an independent biomarker to help the treatment of SLE patients.
item1812	REG00014	.	.	M6ADIS0007	.	33493403	IGF2BP3 is an oncogene and potential prognostic biomarker of LUAD.
item1813	REG00012	M6ATAR00404	Up	M6ADIS0067	.	33747724	"Dysregulation of IGF2BP1 by PADI2/MEK1/ERK signaling results in abnormal accumulation of oncogenic Transcription factor SOX-2 (SOX2) expression, therefore supporting the malignant state of EC."
item1814	REG00005	.	.	M6ADIS0001	.	35444654	"ALKBH5 promoted proliferation, migration, and invasion of glioma cells and recruited the M2 macrophage to glioma cells."
item1815	REG00006	M6ATAR00484	Down	M6ADIS0006	.	34609072	"METTL14 induced m6A modification at 5'UTR of Cystine/glutamate transporter (SLC7A11) mRNA, which in turn underwent degradation relied on the YTHDF2-dependent pathway. Identify the HIF-1alpha /METTL14/YTHDF2/SLC7A11 axis as a potential therapeutic target for the HCC interventional embolization treatment."
item1816	REG00003	.	.	M6ADIS0007	.	33569346	"High HNRNPC expression is significantly related to poor overall survival in patients with LUAD, suggesting that HNRNPC is a cancer-promoting factor and a potential prognostic biomarker in LUAD."
item1817	REG00008	.	.	M6ADIS0167	.	32583611	"These findings suggested decreased YTHDF2 that was associated with disease activity play an important role in the pathogenesis of SLE, METTL14 and ALKBH5 were concomitantly decreased."
item1818	REG00006	.	.	M6ADIS0167	.	32583611	"These findings suggested decreased YTHDF2 that was associated with disease activity play an important role in the pathogenesis of SLE, METTL14 and ALKBH5 were concomitantly decreased."
item1819	REG00008	M6ATAR00803	.	.	.	36070699	.
item1820	REG00008	M6ATAR00804	.	.	.	36070699	.
item1821	REG00008	M6ATAR00805	.	.	.	36070699	.
item1822	REG00007	M6ATAR00213	Up	M6ADIS0094	.	28247949	"NSUN2-mediated m5C and METTL3/METTL14-mediated m6A methylation synergistically enhance p21 expression at the translational level, leading to elevated expression of p21 in oxidative stress-induced cellular senescence."
item1823	REG00006	M6ATAR00213	Up	M6ADIS0094	.	28247949	"NSUN2-mediated m5C and METTL3/METTL14-mediated m6A methylation synergistically enhance p21 expression at the translational level, leading to elevated expression of p21 in oxidative stress-induced cellular senescence."
item1824	REG00021	M6ATAR01414	Up	M6ADIS0058	.	38065948	RBM15B- and IGFBP2-mediated N6-methyladenosine (m6A) modification and NSUN5-mediated 5-methylcytosine (m5C) modification of GPX4 facilitated anticancer immunity via activation of cyclic GMP-AMP synthase (cGAS)-stimulator of interferon (STING) signaling by maintaining redox homeostasis in COAD.
item1825	REG00034	M6ATAR01414	Up	M6ADIS0058	.	38065948	RBM15B- and IGFBP2-mediated N6-methyladenosine (m6A) modification and NSUN5-mediated 5-methylcytosine (m5C) modification of GPX4 facilitated anticancer immunity via activation of cyclic GMP-AMP synthase (cGAS)-stimulator of interferon (STING) signaling by maintaining redox homeostasis in COAD.
item1826	REG00007	M6ATAR00493	Down	M6ADIS0006	.	35274813	"NKILA facilitated CCA growth and metastasis in vitro and in vivo. The 5-methylcytosine (m5C) methyltransferase NSUN2 interacts with NKILA, increasing its m5C level and promoting its interaction with YBX1. Moreover, NKILA physically interacted with and suppressed miR-582-3p, which was regulated by METTL3-mediated N6-methyladenosine (m6A) modification."
item1827	REG00007	M6ATAR00393	Down	M6ADIS0144	.	37353804	"METTL3-mediated m6A methylation epigenetically regulates the ectopic implantation of ESCs, resulting in the progression of endometriosis.METTL3 expression significantly downregulates m6A RNA methylation levels in ESCs. Silencing m6A modifications mediated by METTL3 accelerates ESCs viability, proliferation, migration, and invasion in vitro. The m6A reader protein YTHDF2 binds to m6A modifications to induce the degradation of SIRT1 mRNA. SIRT1/FOXO3a signalling pathway activation is subsequently inhibited, promoting the cellular senescence of ESCs and inhibiting the ectopic implantation of ESCs in vitro and in vivo."
item1828	REG00008	M6ATAR00393	Down	M6ADIS0144	.	37353804	"METTL3-mediated m6A methylation epigenetically regulates the ectopic implantation of ESCs, resulting in the progression of endometriosis.METTL3 expression significantly downregulates m6A RNA methylation levels in ESCs. Silencing m6A modifications mediated by METTL3 accelerates ESCs viability, proliferation, migration, and invasion in vitro. The m6A reader protein YTHDF2 binds to m6A modifications to induce the degradation of SIRT1 mRNA. SIRT1/FOXO3a signalling pathway activation is subsequently inhibited, promoting the cellular senescence of ESCs and inhibiting the ectopic implantation of ESCs in vitro and in vivo."
item1829	REG00012	M6ATAR01415	Up	M6ADIS0065	.	36632454	"IGF2BP1 directly recognized and bound to the m6A sites on CPT1A mRNA and enhanced its stability, which ultimately mediated IGF2BP1-induced breast cancer metastasis."
item1830	REG00012	M6ATAR00234	Up	M6ADIS0038	.	36632449	IGF2BP1 upregulated MIF through directly upregulating E2F1 expression via m6A modification.
item1831	REG00007	M6ATAR01416	Up	M6ADIS0051	M6ADRUG0108	37121538	"METTL3 aberration, the resultant ZBTB7C m6A modification and persistent ZBTB7C activation likely form an important epigenetic regulatory loop that drives OS progression via promoting OS growth and blocking OS cell apoptosis."
item1832	REG00007	M6ATAR01417	Down	M6ADIS0073	.	37648786	"The treatment options for advanced papillary thyroid cancer (PTC) and anaplastic thyroid cancer (ATC) refractory to standard therapies are limited.Downregulation of METTL3 promoted demethylation of CD70 mRNA, which prevented YTHDF2-mediated degradation of the transcripts.blocking CD70 using cusatuzumab, a high-affinity monoclonal antibody, reversed the anti-PD-1 therapy resistance induced by M2 EVs in vivo."
item1833	REG00008	M6ATAR01417	Down	M6ADIS0073	.	37648786	"The treatment options for advanced papillary thyroid cancer (PTC) and anaplastic thyroid cancer (ATC) refractory to standard therapies are limited.Downregulation of METTL3 promoted demethylation of CD70 mRNA, which prevented YTHDF2-mediated degradation of the transcripts.blocking CD70 using cusatuzumab, a high-affinity monoclonal antibody, reversed the anti-PD-1 therapy resistance induced by M2 EVs in vivo."
item1834	REG00007	M6ATAR01417	Down	M6ADIS0073	M6ADRUG0167	37648786	"The treatment options for advanced papillary thyroid cancer (PTC) and anaplastic thyroid cancer (ATC) refractory to standard therapies are limited.Downregulation of METTL3 promoted demethylation of CD70 mRNA, which prevented YTHDF2-mediated degradation of the transcripts.blocking CD70 using cusatuzumab, a high-affinity monoclonal antibody, reversed the anti-PD-1 therapy resistance induced by M2 EVs in vivo."
item1835	REG00008	M6ATAR01417	Down	M6ADIS0073	M6ADRUG0167	37648786	"The treatment options for advanced papillary thyroid cancer (PTC) and anaplastic thyroid cancer (ATC) refractory to standard therapies are limited.Downregulation of METTL3 promoted demethylation of CD70 mRNA, which prevented YTHDF2-mediated degradation of the transcripts.blocking CD70 using cusatuzumab, a high-affinity monoclonal antibody, reversed the anti-PD-1 therapy resistance induced by M2 EVs in vivo."
item1836	REG00013	M6ATAR00806	Up	M6ADIS0059	.	37986103	BACE1-AS as a novel target of IGF2BP2 through m6A modification. m6A modified BACE1-AS promotes CRC liver metastasis through TUFT1 dependent activation of Wnt signaling pathway.
item1837	REG00007	M6ATAR00341	Up	M6ADIS0056	.	37619934	"METTL3 promoted c-Myc mRNA methylation in the 3'-untranslated Region (3'-UTR) and enhanced its mRNA stability in a YTH N6-Methyladenosine RNA binding protein 1(YTHDF1)-dependent manner, which contributes to Fn induced ESCC proliferation and metastasis."
item1838	REG00001	M6ATAR00807	Down	M6ADIS0380	M6ADRUG0164	37996930	"Daa reduced overall m6A levels in healthy skeletal muscles, which reduced skeletal muscle mass. On the contrary, the increase in m6A levels mediated by R-2HG alleviated denervation induced muscle atrophy. The m6A RNA methylation regulated skeletal muscle mass through ubiquitin-proteasome pathway."
item1839	REG00001	M6ATAR00807	Down	M6ADIS0380	M6ADRUG0066	37996930	"Daa reduced overall m6A levels in healthy skeletal muscles, which reduced skeletal muscle mass. On the contrary, the increase in m6A levels mediated by R-2HG alleviated denervation induced muscle atrophy. The m6A RNA methylation regulated skeletal muscle mass through ubiquitin-proteasome pathway."
item1840	REG00014	.	.	M6ADIS0110	.	37217897	"The functions of m6A regulators in OA synovium and highlighted the association between IGF2BP3 and enhanced M1 polarization and inflammation in OA macrophages, providing novel molecular targets for OA diagnosis and treatment."
item1841	REG00009	M6ATAR00260	Up	M6ADIS0159	.	36894806	"Knockdown of WTAP released the proliferation and reduced the apoptosis and inflammatory cytokines. WTAP catalyzes the m6A modification on FOXO3a mRNA and enhances its stability. Exercise training reduced the WTAP expression, thereby impeding the myocardial I/R injury through targeting FOXO3a, which provides new insights for the treatment of myocardial exercise rehabilitation."
item1842	REG00024	M6ATAR00260	Up	M6ADIS0159	.	36894806	"Knockdown of WTAP released the proliferation and reduced the apoptosis and inflammatory cytokines. WTAP catalyzes the m6A modification on FOXO3a mRNA and enhances its stability. Exercise training reduced the WTAP expression, thereby impeding the myocardial I/R injury through targeting FOXO3a, which provides new insights for the treatment of myocardial exercise rehabilitation."
item1843	REG00009	.	.	M6ADIS0205	.	37892219	"The downregulation of m6A modification in cochlear tissues is related to ARHL and found that the expression of the m6A methylation regulators Wilms tumour suppressor-1-associated protein (WTAP), methyltransferase-like 3 (METTL3), ALKB homologous protein 5 (ALKBH5) and fat mass and obesity-associated protein (FTO) is decreased significantly at the mRNA and protein levels in ARHL mice."
item1844	REG00007	.	.	M6ADIS0205	.	37892219	"The downregulation of m6A modification in cochlear tissues is related to ARHL and found that the expression of the m6A methylation regulators Wilms tumour suppressor-1-associated protein (WTAP), methyltransferase-like 3 (METTL3), ALKB homologous protein 5 (ALKBH6) and fat mass and obesity-associated protein (FTO) is decreased significantly at the mRNA and protein levels in ARHL mice."
item1845	REG00005	.	.	M6ADIS0205	.	37892219	"The downregulation of m6A modification in cochlear tissues is related to ARHL and found that the expression of the m6A methylation regulators Wilms tumour suppressor-1-associated protein (WTAP), methyltransferase-like 3 (METTL3), ALKB homologous protein 5 (ALKBH7) and fat mass and obesity-associated protein (FTO) is decreased significantly at the mRNA and protein levels in ARHL mice."
item1846	REG00001	.	.	M6ADIS0205	.	37892219	"The downregulation of m6A modification in cochlear tissues is related to ARHL and found that the expression of the m6A methylation regulators Wilms tumour suppressor-1-associated protein (WTAP), methyltransferase-like 3 (METTL3), ALKB homologous protein 5 (ALKBH8) and fat mass and obesity-associated protein (FTO) is decreased significantly at the mRNA and protein levels in ARHL mice."
item1847	REG00007	.	Up	M6ADIS0198	.	36963346	A regulation paradigm in which rotifers acquire more DNA damage and age faster due to reduced NHEJ repair pathway caused by METTL3-mediated decrease in m6A modification.
item1848	REG00007	M6ATAR00808	Up	M6ADIS0144	.	36445237	METTL3 could inhibit the E2 level and alter related lipoprotein levels in EMs mice through the upregulation of MIR17HG. The present study highlighted that the m6A methylation transferase METTL3 prevents EMs progression by upregulating MIR17HG expression.
item1849	REG00001	M6ATAR01418	Up	M6ADIS0132	.	36760238	The m6A demethylase FTO promotes keloid formation by up-regulating COL1A1.
item1850	REG00007	M6ATAR00713	Up	M6ADIS0246	.	36423848	"METTL3 upregulated m6A, which facilitated the DDR via stabilizing the DNA damage repair factors (Rad51 and Xrcc5) mRNA to maintain the pro-survival state."
item1851	REG00007	M6ATAR00809	Up	M6ADIS0246	.	36423848	"METTL3 upregulated m6A, which facilitated the DDR via stabilizing the DNA damage repair factors (Rad51 and Xrcc5) mRNA to maintain the pro-survival state."
item1852	REG00032	.	.	M6ADIS0220	.	36864526	.
item1853	REG00020	.	.	M6ADIS0220	.	36864526	.
item1854	REG00024	.	.	M6ADIS0220	.	36864526	.
item1855	REG00008	M6ATAR01419	Up	M6ADIS0006	M6ADRUG0129	36765030	"YTHDF2 stabilized minichromosome maintenance protein 2 (MCM2) and MCM5 transcripts in an m6A-dependent manner, thus promoting cell cycle progression and HBV-related HCC tumorigenesis. Moreover, targeting YTHDF2 O-GlcNAcylation by the OGT inhibitor OSMI-1 significantly suppressed HCC progression."
item1856	REG00008	M6ATAR00321	Up	M6ADIS0006	M6ADRUG0129	36765030	"YTHDF2 stabilized minichromosome maintenance protein 2 (MCM2) and MCM5 transcripts in an m6A-dependent manner, thus promoting cell cycle progression and HBV-related HCC tumorigenesis. Moreover, targeting YTHDF2 O-GlcNAcylation by the OGT inhibitor OSMI-1 significantly suppressed HCC progression."
item1857	REG00007	M6ATAR00259	Down	M6ADIS0019	.	37891533	"METTL3-regulated m6A promotes YTHDF2-mediated decay of FOXO1 mRNA, thereby affecting cellular decidualization and embryo implantation."
item1858	REG00008	M6ATAR00259	Down	M6ADIS0019	.	37891533	"METTL3-regulated m6A promotes YTHDF2-mediated decay of FOXO1 mRNA, thereby affecting cellular decidualization and embryo implantation."
item1859	REG00007	M6ATAR00334	Up	M6ADIS0015	.	37819742	"METTL3-mediated m6A modification promotes the angiogenic behaviors of RECs by targeting MMP2 and TIE2, suggesting its significance in retinal angiogenesis and METTL3 as a potential therapeutic target."
item1860	REG00007	M6ATAR00644	Up	M6ADIS0015	.	37819742	"METTL3-mediated m6A modification promotes the angiogenic behaviors of RECs by targeting MMP2 and TIE2, suggesting its significance in retinal angiogenesis and METTL3 as a potential therapeutic target."
item1861	REG00032	M6ATAR00530	Down	M6ADIS0091	M6ADRUG0117	37332938	m6A modification promotes BBB breakdown in cerebral I/R injury through promoting MMP3 expression.
item1862	REG00015	M6ATAR00811	Up	M6ADIS0099	.	36463391	The regulation of KIAA1429 on ox-LDL-induced HUVECs via m6A/ROCK2 pathway.
item1863	.	M6ATAR00812	.	M6ADIS0061	.	36992083	The m6A-lncRNA TRAF3IP2-AS1 was proved to be a tumor suppressor in PDAC.
item1864	REG00007	M6ATAR00823	Up	M6ADIS0366	.	37455557	.
item1865	REG00023	M6ATAR01422	Up	M6ADIS0007	M6ADRUG0047	37065597	YTHDC2-mediated m6A mRNA modification of Id3 suppresses cisplatin resistance in non-small cell lung cancer.
item1866	REG00023	M6ATAR01422	Up	M6ADIS0007	M6ADRUG0164	37065597	"Overexpression of YTHDC2 increased the expression of Id3, and the methylation inhibitor 3-deazaadenosine abrogated the regulatory effect of YTHDC2 on Id3."
item1867	REG00009	M6ATAR00348	Up	M6ADIS0070	.	36719469	"Mechanistically, there was a remarkable m6A modification site on 3'-UTR of endogenous antioxidant factor NRF2 RNA and WTAP could install its methylation. Moreover, m6A reader YTHDF1 recognized the m6A site on NRF2 mRNA and enhanced its mRNA stability."
item1868	REG00024	M6ATAR00348	Up	M6ADIS0070	.	36719469	"Mechanistically, there was a remarkable m6A modification site on 3'-UTR of endogenous antioxidant factor NRF2 RNA and WTAP could install its methylation. Moreover, m6A reader YTHDF1 recognized the m6A site on NRF2 mRNA and enhanced its mRNA stability."
item1869	REG00007	M6ATAR00610	Down	M6ADIS0268	M6ADRUG0166	37275442	Mettl3-mediated m6A RNA methylation modification modulates CSE-induced EMT by targeting SOCS3 mRNA and ultimately serves as a crucial regulator in the emergence of COPD.Mettl3 silence and cycloleucine treatment inhibited the EMT process of HBECs caused by CSE.
item1870	REG00008	M6ATAR00813	Down	M6ADIS0110	M6ADRUG0142	35733354	"CircRERE exerted chondroprotective effects by targeting miR-195-5p/IRF2BPL, thus regulating the ubiquitination and degradation of beta-catenin. CircRere (mouse homologue) overexpression by IA-injection of AAV-circRere into mice attenuated the severity of DMM-induced OA, whereas AAV-miR-195a-5p or AAV-sh-Irf2bpl reduced the protective effects. The detrimental effects of AAV-sh-Irf2bpl on DMM-induced OA were substantially counteracted by ICG-001, an inhibitor of beta-catenin."
item1871	REG00006	M6ATAR01423	Up	M6ADIS0103	.	36864027	"Exposure to LPS upregulates the lysine acetyltransferase, KAT2B, to promote METTL14 protein stability through acetylation at K398, leading to the increased m6A methylation of Spi2a in macrophages."
item1872	REG00007	M6ATAR00814	Up	M6ADIS0125	.	38065069	"SON rescues MYC and suppresses the METTL3-HSC inflammatory gene expression program, including CCL5, through transcriptional regulation. Thus, our findings define a m6A-SON-CCL5 axis that controls inflammation and HSC fate."
item1873	REG00022	M6ATAR00815	Down	M6ADIS0373	.	36780989	"The m6A ""reader"" protein YTHDC1 was found to reduce circMPP1 expression via m6A modification. In conclusion, this study demonstrates that YTHDC1 maintains trophoblasts function by promoting degradation of m6A-mediated circMPP1."
item1874	REG00022	M6ATAR00816	Down	M6ADIS0135	.	37365312	"By elevating m6A methylation, we could significantly reduce repeat RNA levels from both strands and the derived poly-dipeptides, rescue global mRNA homeostasis and improve survival of C9ORF72-ALS/FTD patient iPSC-derived neurons."
item1875	REG00022	M6ATAR00816	Down	M6ADIS0358	.	37365312	"By elevating m6A methylation, we could significantly reduce repeat RNA levels from both strands and the derived poly-dipeptides, rescue global mRNA homeostasis and improve survival of C9ORF72-ALS/FTD patient iPSC-derived neurons."
item1876	.	M6ATAR00817	.	M6ADIS0245	.	35871232	"Functional significance of LINREP in human GBM for its dual regulation of PTBP1-induced AS and its m6A modification modality, implicating that HuR/LINREP/PTBP1 axis might serve as a potential therapeutic target for GBM."
item1877	REG00023	M6ATAR01332	Down	M6ADIS0007	.	38129673	YTHDC2 suppressed tumor growth in the lung adenocarcinoma mouse model via downregulating MRPL12.
item1878	REG00015	M6ATAR00818	.	M6ADIS0006	.	38058614	"A KIAA1429-HPN modulatory model based on m6A modifications, that offers insights into the occurrence and development of LIHC."
item1879	.	M6ATAR00819	.	M6ADIS0066	M6ADRUG0089	36703541	"LINC02489 regulates the invasion ability of OC cells through the PTEN/mTOR signaling pathway, thereby regulating the sensitivity of SKOV3 cells to paclitaxel. This result provides a potential therapeutic target for chemoresistant OC."
item1880	REG00008	M6ATAR00348	Up	M6ADIS0392	.	36878272	"AhR transcriptionally regulated FTO, and then FTO regulated Nrf2 in a m6A-modified manner through YTHDF2, thereby affecting apoptosis in BPF-exposed TM3 cells to induce reproductive damage."
item1881	REG00001	M6ATAR00348	Down	M6ADIS0392	.	36878272	"AhR transcriptionally regulated FTO, and then FTO regulated Nrf2 in a m6A-modified manner through YTHDF2, thereby affecting apoptosis in BPF-exposed TM3 cells to induce reproductive damage."
item1882	REG00007	M6ATAR00820	Up	M6ADIS0174	M6ADRUG0115	36528756	"N6-methyladenosine methyltransferase-like 3 (METTL3) mediated stabilization of USP13 mRNA that required the m6A reader IGF2BP2. Moreover, an inhibitor of USP13 caused ATG5 decay and co-administration of this inhibitor with 3-methyladenine boosted treatment efficacy of IM in murine xenograft models derived from GIST cells."
item1883	REG00013	M6ATAR00820	Up	M6ADIS0174	M6ADRUG0115	36528756	"N6-methyladenosine methyltransferase-like 3 (METTL3) mediated stabilization of USP13 mRNA that required the m6A reader IGF2BP2. Moreover, an inhibitor of USP13 caused ATG5 decay and co-administration of this inhibitor with 3-methyladenine boosted treatment efficacy of IM in murine xenograft models derived from GIST cells."
item1884	REG00007	M6ATAR00820	Up	M6ADIS0174	M6ADRUG0059	36528756	"N6-methyladenosine methyltransferase-like 3 (METTL3) mediated stabilization of USP13 mRNA that required the m6A reader IGF2BP2. Moreover, an inhibitor of USP13 caused ATG5 decay and co-administration of this inhibitor with 3-methyladenine boosted treatment efficacy of IM in murine xenograft models derived from GIST cells."
item1885	REG00013	M6ATAR00820	Up	M6ADIS0174	M6ADRUG0059	36528756	"N6-methyladenosine methyltransferase-like 3 (METTL3) mediated stabilization of USP13 mRNA that required the m6A reader IGF2BP2. Moreover, an inhibitor of USP13 caused ATG5 decay and co-administration of this inhibitor with 3-methyladenine boosted treatment efficacy of IM in murine xenograft models derived from GIST cells."
item1886	REG00007	M6ATAR00821	Up	M6ADIS0087	M6ADRUG0181	37495067	"Inhibition of METTL3 either by STM or shRNA restored BPA induced downregulation of Chrna4, suggesting that Chrna4 may be a potential target involved in BPA induced neurotoxicity that modified by m6A."
item1887	REG00007	M6ATAR00821	Up	M6ADIS0087	M6ADRUG0108	37495067	"Inhibition of METTL3 either by STM or shRNA restored BPA induced downregulation of Chrna4, suggesting that Chrna4 may be a potential target involved in BPA induced neurotoxicity that modified by m6A."
item1888	REG00005	M6ATAR00484	Down	M6ADIS0059	.	36820954	"ALKBH5 was downregulated in CRC and ALKBH5 overexpression promoted ROS release and ferroptosis. ALKBH5 erased the m6A modification on SLC7A11 mRNA to reduce the mRNA stability of SLC7A11, further reducing SLC7A11 expression. SLC7A11 overexpression reversed the promotive role of ALKBH5 overexpression in ferroptosis. ALKBH5 upregulation mitigated tumor growth in vivo."
item1889	REG00009	M6ATAR00822	Down	M6ADIS0051	.	36988233	"WTAP modulated ALB expression in an m6A-dependent manner. Silencing of WTAP retarded the development of OS via inhibiting cell viability, migration, invasion, and tumor growth."
item1890	REG00007	M6ATAR00823	Up	.	.	36917263	METTL3 is dynamically expressed in goat uterus and can affect EEC proliferation by regulating CTGF in an m6A-dependent manner.
item1891	REG00039	.	Up	M6ADIS0061	.	37816727	"CSTF2-regulated m6As have positive effects on the RNA level of host genes, and CSTF2-regulated m6As are mainly recognized by IGF2BP2, an m6A reader that stabilizes mRNAs."
item1892	REG00013	.	Up	M6ADIS0061	.	37816727	"CSTF2-regulated m6As have positive effects on the RNA level of host genes, and CSTF2-regulated m6As are mainly recognized by IGF2BP2, an m6A reader that stabilizes mRNAs."
item1893	REG00007	M6ATAR00824	Down	M6ADIS0396	.	37696947	"Knockdown of N-Myc rescues pausing in Mettl3-/-ES cells, and forced demethylation and stabilization of Mycn mRNA in paused wild-type ES cells largely recapitulates the transcriptional defects of Mettl3-/-ES cells."
item1894	REG00007	M6ATAR00196	Down	M6ADIS0166	M6ADRUG0108	37401082	"Inhibition of METTL3 activity or expression can inhibit the apoptosis of spinal cord neurons after SCI through the m6A/Bcl-2 signaling pathway.the mRNA and protein levels of Bcl-2, inhibited neuronal apoptosis, and improved neuronal viability in the spinal cord."
item1895	REG00007	M6ATAR01425	Up	M6ADIS0059	.	37626036	"The malignant behaviors governed by REG1alpha could be effectively abolished by silencing of Wnt/beta-catenin/MYC axis or glycolysis process using specific inhibitors. Besides, REG1alpha expression was mediated by METTL3 in an m6A-dependent manner."
item1896	REG00007	M6ATAR00141	Up	M6ADIS0051	.	37897586	"In osteosarcoma cells, METTL3, acting as an oncogene, promoted m6A modification of MALAT1, increased the stability of MALAT, and enhanced MALAT1-mediated oncogenic function."
item1897	REG00018	M6ATAR00826	Up	M6ADIS0054	.	36800991	"METTL5 enhances HSF4b translation to activate the transcription of HSP90B1, which binds with oncogenic mutant p53 (mutp53) protein and prevents it from undergoing ubiquitination-dependent degradation, therefore facilitating NPC tumorigenesis and chemoresistance."
item1898	REG00007	M6ATAR00351	Down	M6ADIS0102	.	37675298	NOTCH1 mRNA m6A modification site and METTL3 overexpression promoted NOTCH1 mRNA degradation. YTHDF2-RIP further demonstrated that the binding ability of YTHDF2 and NOTCH1 mRNA was enhanced after METTL3 overexpression.
item1899	REG00008	M6ATAR00351	Down	M6ADIS0102	.	37675298	NOTCH1 mRNA m6A modification site and METTL3 overexpression promoted NOTCH1 mRNA degradation. YTHDF2-RIP further demonstrated that the binding ability of YTHDF2 and NOTCH1 mRNA was enhanced after METTL3 overexpression.
item1900	REG00009	M6ATAR00827	Up	M6ADIS0057	.	37477820	WTAP-mediated FAM83H-AS1 promotes GC development via m6A modification.
item1901	REG00001	M6ATAR01426	Down	M6ADIS0270	.	37822879	Overexpression of FTO inhibits excessive proliferation and promotes the apoptosis of human glomerular mesangial cells by alleviating FOXO6 m6A modification via YTHDF3-dependent mechanisms.
item1902	REG00025	M6ATAR01426	Down	M6ADIS0270	.	37822879	Overexpression of FTO inhibits excessive proliferation and promotes the apoptosis of human glomerular mesangial cells by alleviating FOXO6 m6A modification via YTHDF3-dependent mechanisms.
item1903	REG00001	M6ATAR00148	Down	M6ADIS0007	.	37120495	GAS5 suppressed by FTO could promote the autophagic death of NSCLC cells in vitro and inhibit NSCLC tumor growth in vivo.
item1904	REG00007	M6ATAR00513	Up	M6ADIS0223	.	36705430	"The novel roles of METTL3 in BMSCs osteogenic differentiation via the IGF2BP1/m6A/RUNX2 signaling axis of m6A-dependent manner, providing a potential therapeutic target for maxillofacial bone defects treatment."
item1905	REG00012	M6ATAR00513	Up	M6ADIS0223	.	36705430	"The novel roles of METTL3 in BMSCs osteogenic differentiation via the IGF2BP1/m6A/RUNX2 signaling axis of m6A-dependent manner, providing a potential therapeutic target for maxillofacial bone defects treatment."
item1906	REG00006	M6ATAR00388	Down	M6ADIS0058	.	37592151	METTL14 might impede the tumorigenic process of CC through SCD1 mediated Wnt/beta-catenin signaling.
item1907	REG00022	M6ATAR00153	Up	M6ADIS0383	.	37917328	"PVT1 positively regulated IL-33 expression by recruiting YTHDC1 to mediate m6A modification of IL-33. In conclusion, silencing PVT1 demonstrated beneficial effects in alleviating BPD by facilitating YTHDC1-mediated m6A modification of IL-33."
item1908	REG00022	M6ATAR01427	Up	M6ADIS0383	.	37917328	"PVT1 positively regulated IL-33 expression by recruiting YTHDC1 to mediate m6A modification of IL-33. In conclusion, silencing PVT1 demonstrated beneficial effects in alleviating BPD by facilitating YTHDC1-mediated m6A modification of IL-33."
item1909	REG00017	M6ATAR00828	Up	M6ADIS0059	.	38084791	METTL16 exerts its oncogenic effects by enhancing the expression of suppressor of glucose by autophagy 1 (Soga1) in an m6A-dependent manner.
item1910	REG00024	M6ATAR01428	Up	M6ADIS0194	.	36996116	"Three m6A modification sites of HRAS 3' UTR, which is regulated by FTO and bound by YTHDF1, but not YTHDF2 nor YTHDF3, promote its protein expression by the enhanced translational elongation. In addition, targeting HRAS m6A modification decreases cancer proliferation and metastasis."
item1911	REG00001	M6ATAR01428	Up	M6ADIS0194	.	36996116	"Three m6A modification sites of HRAS 3' UTR, which is regulated by FTO and bound by YTHDF1, but not YTHDF2 nor YTHDF3, promote its protein expression by the enhanced translational elongation. In addition, targeting HRAS m6A modification decreases cancer proliferation and metastasis."
item1912	REG00009	M6ATAR00341	Up	M6ADIS0061	M6ADRUG0024	37591781	Gemcitabine Inhibits the Progression of Pancreatic Cancer by Restraining the WTAP/MYC Chain in an m6A-Dependent Manner.
item1913	REG00012	M6ATAR00341	Up	M6ADIS0061	M6ADRUG0024	37591781	Gemcitabine Inhibits the Progression of Pancreatic Cancer by Restraining the WTAP/MYC Chain in an m6A-Dependent Manner.
item1914	REG00007	M6ATAR01429	Up	.	M6ADRUG0108	38142659	"During arsenic-induced cell transformation, METTL3-upregulated m6A on the mRNAs of SOD1, SOD2, CAT, TXN, and GPX1 promoted the mRNA translation and protein expressions of these antioxidant enzymes by increasing YTHDF1-mediated mRNA stability. Meanwhile, FTO-downregulated m6A on PRDX5 mRNA increased PRDX5 translation and expression by reducing YTHDF2-mediated mRNA decay."
item1915	REG00007	M6ATAR01430	Up	.	M6ADRUG0108	38142659	"During arsenic-induced cell transformation, METTL3-upregulated m6A on the mRNAs of SOD1, SOD2, CAT, TXN, and GPX1 promoted the mRNA translation and protein expressions of these antioxidant enzymes by increasing YTHDF1-mediated mRNA stability. Meanwhile, FTO-downregulated m6A on PRDX5 mRNA increased PRDX5 translation and expression by reducing YTHDF3-mediated mRNA decay."
item1916	REG00007	M6ATAR00430	Up	.	M6ADRUG0108	38142659	"During arsenic-induced cell transformation, METTL3-upregulated m6A on the mRNAs of SOD1, SOD2, CAT, TXN, and GPX1 promoted the mRNA translation and protein expressions of these antioxidant enzymes by increasing YTHDF1-mediated mRNA stability. Meanwhile, FTO-downregulated m6A on PRDX5 mRNA increased PRDX5 translation and expression by reducing YTHDF4-mediated mRNA decay."
item1917	REG00007	M6ATAR00829	Up	.	M6ADRUG0108	38142659	"During arsenic-induced cell transformation, METTL3-upregulated m6A on the mRNAs of SOD1, SOD2, CAT, TXN, and GPX1 promoted the mRNA translation and protein expressions of these antioxidant enzymes by increasing YTHDF1-mediated mRNA stability. Meanwhile, FTO-downregulated m6A on PRDX5 mRNA increased PRDX5 translation and expression by reducing YTHDF5-mediated mRNA decay."
item1918	REG00024	M6ATAR01429	Up	.	.	38142659	"During arsenic-induced cell transformation, METTL3-upregulated m6A on the mRNAs of SOD1, SOD2, CAT, TXN, and GPX1 promoted the mRNA translation and protein expressions of these antioxidant enzymes by increasing YTHDF1-mediated mRNA stability. Meanwhile, FTO-downregulated m6A on PRDX5 mRNA increased PRDX5 translation and expression by reducing YTHDF6-mediated mRNA decay."
item1919	REG00024	M6ATAR01430	Up	.	.	38142659	"During arsenic-induced cell transformation, METTL3-upregulated m6A on the mRNAs of SOD1, SOD2, CAT, TXN, and GPX1 promoted the mRNA translation and protein expressions of these antioxidant enzymes by increasing YTHDF1-mediated mRNA stability. Meanwhile, FTO-downregulated m6A on PRDX5 mRNA increased PRDX5 translation and expression by reducing YTHDF7-mediated mRNA decay."
item1920	REG00024	M6ATAR00430	Up	.	.	38142659	"During arsenic-induced cell transformation, METTL3-upregulated m6A on the mRNAs of SOD1, SOD2, CAT, TXN, and GPX1 promoted the mRNA translation and protein expressions of these antioxidant enzymes by increasing YTHDF1-mediated mRNA stability. Meanwhile, FTO-downregulated m6A on PRDX5 mRNA increased PRDX5 translation and expression by reducing YTHDF8-mediated mRNA decay."
item1921	REG00024	M6ATAR00829	Up	.	.	38142659	"During arsenic-induced cell transformation, METTL3-upregulated m6A on the mRNAs of SOD1, SOD2, CAT, TXN, and GPX1 promoted the mRNA translation and protein expressions of these antioxidant enzymes by increasing YTHDF1-mediated mRNA stability. Meanwhile, FTO-downregulated m6A on PRDX5 mRNA increased PRDX5 translation and expression by reducing YTHDF9-mediated mRNA decay."
item1922	REG00001	M6ATAR00830	Down	.	M6ADRUG0152	38142659	"During arsenic-induced cell transformation, METTL3-upregulated m6A on the mRNAs of SOD1, SOD2, CAT, TXN, and GPX1 promoted the mRNA translation and protein expressions of these antioxidant enzymes by increasing YTHDF1-mediated mRNA stability. Meanwhile, FTO-downregulated m6A on PRDX5 mRNA increased PRDX5 translation and expression by reducing YTHDF10-mediated mRNA decay."
item1923	REG00008	M6ATAR00830	Up	.	M6ADRUG0152	38142659	"During arsenic-induced cell transformation, METTL3-upregulated m6A on the mRNAs of SOD1, SOD2, CAT, TXN, and GPX1 promoted the mRNA translation and protein expressions of these antioxidant enzymes by increasing YTHDF1-mediated mRNA stability. Meanwhile, FTO-downregulated m6A on PRDX5 mRNA increased PRDX5 translation and expression by reducing YTHDF10-mediated mRNA decay."
item1924	REG00007	M6ATAR01431	Up	M6ADIS0006	.	36923927	"The expression of Anillin actin-binding protein (ANLN) was dramatically higher in HCC with BM tissues, and its messenger RNA (mRNA) stability was enhanced via m6A epitranscriptomic regulation by METTL3 and YTHDF1. High METTL3 and YTHDF1 expression along with nuclear ANLN protein was clinically correlated with BM in HCC patients."
item1925	REG00024	M6ATAR01431	Up	M6ADIS0006	.	36923927	"The expression of Anillin actin-binding protein (ANLN) was dramatically higher in HCC with BM tissues, and its messenger RNA (mRNA) stability was enhanced via m6A epitranscriptomic regulation by METTL3 and YTHDF1. High METTL3 and YTHDF1 expression along with nuclear ANLN protein was clinically correlated with BM in HCC patients."
item1926	REG00007	M6ATAR00831	Up	M6ADIS0055	.	38063205	"N6'methyladenosine (m6A) writer, methyltransferase like 3, catalyzed m6A modification of the HOXC10 transcript, m6A reader insulin like growth factor 2 mRNA binding protein (IGF2BP)1 and IGF2BP3 involved in recognizing and stabilizing m6A-tagged HOXC10 mRNA. In summary, the present study identified HOXC10 as a promising candidate oncogene in HNSCC. The m6A modification-mediated HOXC10 promoted proliferation, migration, and invasion of HNSCC through co-activation of ADAM17/EGFR and Wnt/beta-catenin signaling, providing a novel diagnostic and prognostic biomarker and a potential therapeutic target for HNSCC."
item1927	REG00012	M6ATAR00831	Up	M6ADIS0055	.	38063205	"N6'methyladenosine (m6A) writer, methyltransferase like 3, catalyzed m6A modification of the HOXC10 transcript, m6A reader insulin like growth factor 2 mRNA binding protein (IGF2BP)1 and IGF2BP3 involved in recognizing and stabilizing m6A-tagged HOXC10 mRNA. In summary, the present study identified HOXC10 as a promising candidate oncogene in HNSCC. The m6A modification-mediated HOXC10 promoted proliferation, migration, and invasion of HNSCC through co-activation of ADAM17/EGFR and Wnt/beta-catenin signaling, providing a novel diagnostic and prognostic biomarker and a potential therapeutic target for HNSCC."
item1928	REG00014	M6ATAR00831	Up	M6ADIS0055	.	38063205	"N6'methyladenosine (m6A) writer, methyltransferase-like 3, catalyzed m6A modification of the HOXC10 transcript, m6A reader insulin like growth factor 2 mRNA binding protein (IGF2BP)1 and IGF2BP3 involved in recognizing and stabilizing m6A-tagged HOXC10 mRNA. In summary, the present study identified HOXC10 as a promising candidate oncogene in HNSCC. The m6A modification-mediated HOXC10 promoted proliferation, migration, and invasion of HNSCC through co-activation of ADAM17/EGFR and Wnt/beta-catenin signaling, providing a novel diagnostic and prognostic biomarker and a potential therapeutic target for HNSCC."
item1929	REG00024	M6ATAR00832	Up	M6ADIS0185	.	37914905	"YTHDF1 suppressed autophagy to induce HT22 cell apoptosis through increasing m6A-mediated stability of Cdc25A, a newly identified autophagy inhibitor."
item1930	REG00007	M6ATAR01432	Down	M6ADIS0142	.	37245538	"Downregulation of METTL3 reversed LPS-induced myocardial cell and tissue damage and reduced cardiac function, mainly by increasing Myh3 stability."
item1931	REG00007	M6ATAR00833	.	.	.	37267102	"Conditional targeting of Creb1 in DP thymocytes results in similar phenotypes of iNKT cells lacking Mettl3. Importantly, ectopic expression of Creb1 largely rectifies such developmental defects in Mettl3-deficient iNKT cells."
item1932	REG00007	M6ATAR00856	Up	M6ADIS0007	.	37820733	"METTL3 potentially methylates 7SK to aberrantly activate RNA Pol II transcription in cancer cells, our study provides the molecular basis for potential therapeutics that modulate m6A-7SK for NSCLC treatment."
item1933	REG00005	M6ATAR00856	Down	M6ADIS0007	.	37820733	"METTL3 potentially methylates 7SK to aberrantly activate RNA Pol II transcription in cancer cells, our study provides the molecular basis for potential therapeutics that modulate m6A-7SK for NSCLC treatment."
item1934	REG00007	M6ATAR00348	Up	.	.	36917877	"METTL3 mediated m6A modification of Nrf2 mRNA and promoted Nrf2 translation in mice and 16HBE cells after PM2.5 exposure. Mechanistically, three m6A-modified sites (1317, 1376 and 935; numbered relative to the first nucleotide of 3'UTR) of Nrf2 mRNA were identified in PM2.5-treatment 16HBE cells. Furthermore, the m6A binding proteins YTHDF1/IGF2BP1 promoted Nrf2 translation by binding to m6A residues of Nrf2 mRNA. Our results revealed the mechanism of m6A mediated Nrf2 signaling pathway against oxidative stress, which affected the development of PM2.5-induced PF."
item1935	REG00024	M6ATAR00348	Up	.	.	36917877	"METTL3 mediated m6A modification of Nrf2 mRNA and promoted Nrf2 translation in mice and 16HBE cells after PM2.5 exposure. Mechanistically, three m6A-modified sites (1317, 1376 and 935; numbered relative to the first nucleotide of 3'UTR) of Nrf2 mRNA were identified in PM2.5-treatment 16HBE cells. Furthermore, the m6A binding proteins YTHDF1/IGF2BP1 promoted Nrf2 translation by binding to m6A residues of Nrf2 mRNA. Our results revealed the mechanism of m6A mediated Nrf2 signaling pathway against oxidative stress, which affected the development of PM2.6-induced PF."
item1936	REG00012	M6ATAR00348	Up	.	.	36917877	"METTL3 mediated m6A modification of Nrf2 mRNA and promoted Nrf2 translation in mice and 16HBE cells after PM2.5 exposure. Mechanistically, three m6A-modified sites (1317, 1376 and 935; numbered relative to the first nucleotide of 3'UTR) of Nrf2 mRNA were identified in PM2.5-treatment 16HBE cells. Furthermore, the m6A binding proteins YTHDF1/IGF2BP1 promoted Nrf2 translation by binding to m6A residues of Nrf2 mRNA. Our results revealed the mechanism of m6A mediated Nrf2 signaling pathway against oxidative stress, which affected the development of PM2.7-induced PF."
item1937	REG00008	M6ATAR00834	Down	M6ADIS0017	.	37467831	"YTHDF2 recognized m6A-modified circIRF2 and diminished circIRF2 stability, partly accounting for the decreased circIRF2 in liver fibrosis."
item1938	REG00001	M6ATAR00135	Down	M6ADIS0185	.	37437797	Downregulation of FTO expression contributes to increased m6A RNA modification in cerebral I/R injury.
item1939	REG00013	M6ATAR00835	Up	M6ADIS0020	.	37670228	"IGF2BP2 binds to the m6A-modified 3' untranslated region (3'-UTR) of PLOD2 mRNA, thereby positively regulating its mRNA stability. Targeted specific demethylation of PLOD2 m6A by CRISPR/dCas13b-ALKBH5 system can significantly decrease the m6A and expression level of PLOD2."
item1940	REG00005	M6ATAR00835	Down	M6ADIS0020	.	37670228	"IGF2BP2 binds to the m6A-modified 3' untranslated region (3'-UTR) of PLOD2 mRNA, thereby positively regulating its mRNA stability. Targeted specific demethylation of PLOD2 m6A by CRISPR/dCas13b-ALKBH5 system can significantly decrease the m6A and expression level of PLOD2."
item1941	REG00007	M6ATAR00836	Up	M6ADIS0059	.	36745568	Tl increased the level of aberrant N6-methyladenosine (m6A) modification of ATP13A3 via the METLL3/METTL14/ALKBH5-ATP13A3 axis to promote colorectal tumorigenesis.
item1942	REG00006	M6ATAR00836	Up	M6ADIS0059	.	36745568	Tl increased the level of aberrant N6-methyladenosine (m6A) modification of ATP13A3 via the METLL3/METTL14/ALKBH5-ATP13A4 axis to promote colorectal tumorigenesis.
item1943	REG00005	M6ATAR00836	Up	M6ADIS0059	.	36745568	Tl increased the level of aberrant N6-methyladenosine (m6A) modification of ATP13A3 via the METLL3/METTL14/ALKBH5-ATP13A5 axis to promote colorectal tumorigenesis.
item1944	REG00024	M6ATAR00837	Up	M6ADIS0083	.	36914671	YTHDF1 facilitates the translation of bone morphogenetic protein 8b (Bmp8b) in an m6A-dependent manner to induce the beiging process.
item1945	REG00036	M6ATAR00141	Up	.	.	37669863	"RNA immunoprecipitation and mass spectrometry revealed 12 new synapse-specific learning-induced m6A readers in the mPFC of male C57/BL6 mice, with m6A-modified Malat1 binding to a subset of these, including CYFIP2 and DPYSL2. In addition, a cell type- and synapse-specific, and state-dependent, reduction of m6A on Malat1 impairs fear-extinction memory; an effect that likely occurs through a disruption in the interaction between Malat1 and DPYSL2 and an associated decrease in dendritic spine formation."
item1946	REG00037	M6ATAR00141	Up	.	.	37669863	"RNA immunoprecipitation and mass spectrometry revealed 12 new synapse-specific learning-induced m6A readers in the mPFC of male C57/BL6 mice, with m6A-modified Malat1 binding to a subset of these, including CYFIP2 and DPYSL2. In addition, a cell type- and synapse-specific, and state-dependent, reduction of m6A on Malat1 impairs fear-extinction memory; an effect that likely occurs through a disruption in the interaction between Malat1 and DPYSL2 and an associated decrease in dendritic spine formation."
item1947	REG00009	M6ATAR00838	Up	M6ADIS0137	.	38029838	WTAP-mediated m6A modification promoted the expression of S100A9 and SERPINB3 to aggravate human epidermal keratinocyte proliferation and dysdifferentiation contributing to the pathophysiological development of AD.
item1948	REG00009	M6ATAR00839	Up	M6ADIS0137	.	38029838	WTAP-mediated m6A modification promoted the expression of S100A9 and SERPINB3 to aggravate human epidermal keratinocyte proliferation and dysdifferentiation contributing to the pathophysiological development of AD.
item1949	REG00005	M6ATAR00840	Up	M6ADIS0254	.	37998339	ALKBH5 stabilizes m6A-modified LOC4191 to suppress E. coli-induced apoptosis.
item1950	REG00007	M6ATAR00841	Up	M6ADIS0097	.	36980863	METTL3 led to enhanced m6A levels of TNC mRNA and promoted TNC mRNA stability.
item1951	REG00001	M6ATAR01433	Up	M6ADIS0257	.	37925419	"FTO regulated m6A modification on SOST transcripts, and AGEs affected the binding of FTO to SOST transcripts. FTO knockdown accelerated the degradation of SOST mRNA in presence of AGEs. Interference with SOST expression in AGE-treated BMSCs partially rescued the osteogenesis by activating Wnt Signaling."
item1952	REG00008	M6ATAR00484	Down	M6ADIS0099	.	37792239	"YTHDF2 promoted the degradation of SLC7A11 mRNA, thereby reducing its mRNA stability. Taken together, these findings suggest that YTHDF2 accelerates endothelial cells ferroptosis in cerebrovascular atherosclerosis, helping us enhance our comprehension on cerebrovascular disease pathological physiology."
item1953	REG00017	M6ATAR00842	Down	M6ADIS0051	.	37357526	"VPS33B knockdown markedly attenuated shMETTL16-mediated inhibition on OS progression. Finally, METTL16/VPS33B might facilitate OS progression through PI3K/AKT pathway."
item1954	REG00007	M6ATAR00843	Up	M6ADIS0066	M6ADRUG0047	38112021	The regulation of its expression and the stability of its mRNA were influenced by m6A modifications involving both METTL3 and IGF2BP1.
item1955	REG00012	M6ATAR00843	Up	M6ADIS0066	M6ADRUG0047	38112021	The regulation of its expression and the stability of its mRNA were influenced by m6A modifications involving both METTL3 and IGF2BP1.
item1956	REG00006	M6ATAR00844	Up	M6ADIS0185	M6ADRUG0109	37348798	"XFZYD improves neurological deficits, spatial learning and memory impairments in rats post-TBI probably through increasing the expression of METTL14 and BDNF in the cortex."
item1957	REG00008	M6ATAR01434	.	M6ADIS0243	.	37315764	The eucaryotic elongation factor 2 as post-transcriptionally regulated by Ythdf2 using cell type specific Ribo-seq data. Our study expands our understanding on the regulatory functions of m6A methylation in cardiomyocytes and how cardiac function is controlled by the m6A reader protein Ythdf2.
item1958	REG00007	M6ATAR00845	Down	M6ADIS0237	.	37508433	Manipulation of the m6A 'eraser' fat mass and obesity-associated protein (FTO) and m6A 'writer' protein methyltransferase-like 3 (METTL3) directly affects the expression of CD40L. The m6A 'reader' protein YT521-B homology domain family-2 (YTHDF2) is hypothesized to be able to recognize and bind m6A specific sequences on the CD40L mRNA and promotes its degradation.
item1959	REG00001	M6ATAR00845	Up	M6ADIS0237	.	37508433	Manipulation of the m6A 'eraser' fat mass and obesity-associated protein (FTO) and m6A 'writer' protein methyltransferase-like 3 (METTL3) directly affects the expression of CD40L. The m6A 'reader' protein YT521-B homology domain family-2 (YTHDF2) is hypothesized to be able to recognize and bind m6A specific sequences on the CD40L mRNA and promotes its degradation.
item1960	REG00008	M6ATAR00845	Down	M6ADIS0237	.	37508433	Manipulation of the m6A 'eraser' fat mass and obesity-associated protein (FTO) and m6A 'writer' protein methyltransferase-like 3 (METTL3) directly affects the expression of CD40L. The m6A 'reader' protein YT521-B homology domain family-2 (YTHDF2) is hypothesized to be able to recognize and bind m6A specific sequences on the CD40L mRNA and promotes its degradation.
item1961	REG00007	M6ATAR01436	Up	M6ADIS0393	M6ADRUG0164	36819040	"Knockdown of cellular m6A methyltransferases METTL3 and METTL14 and the specific binding proteins YTHDF2 and YTHDF3 inhibited PRV replication, while silencing of demethylase ALKBH5 promoted PRV output. The overexpression of METTL14 induced more efficient virus proliferation in PRV-infected PK15 cells. Inhibition of m6A modification by 3-deazaadenosine (3-DAA), a m6A modification inhibitor, could significantly reduce viral replication."
item1962	REG00006	M6ATAR01436	Up	M6ADIS0393	M6ADRUG0164	36819040	"Knockdown of cellular m6A methyltransferases METTL3 and METTL14 and the specific binding proteins YTHDF2 and YTHDF3 inhibited PRV replication, while silencing of demethylase ALKBH5 promoted PRV output. The overexpression of METTL14 induced more efficient virus proliferation in PRV-infected PK15 cells. Inhibition of m6A modification by 3-deazaadenosine (3-DAA), a m6A modification inhibitor, could significantly reduce viral replication."
item1963	REG00008	M6ATAR01436	Up	M6ADIS0393	M6ADRUG0164	36819040	"Knockdown of cellular m6A methyltransferases METTL3 and METTL14 and the specific binding proteins YTHDF2 and YTHDF3 inhibited PRV replication, while silencing of demethylase ALKBH5 promoted PRV output. The overexpression of METTL14 induced more efficient virus proliferation in PRV-infected PK15 cells. Inhibition of m6A modification by 3-deazaadenosine (3-DAA), a m6A modification inhibitor, could significantly reduce viral replication."
item1964	REG00025	M6ATAR01436	Up	M6ADIS0393	M6ADRUG0164	36819040	"Knockdown of cellular m6A methyltransferases METTL3 and METTL14 and the specific binding proteins YTHDF2 and YTHDF3 inhibited PRV replication, while silencing of demethylase ALKBH5 promoted PRV output. The overexpression of METTL14 induced more efficient virus proliferation in PRV-infected PK15 cells. Inhibition of m6A modification by 3-deazaadenosine (3-DAA), a m6A modification inhibitor, could significantly reduce viral replication."
item1965	REG00005	M6ATAR01436	Down	M6ADIS0393	M6ADRUG0164	36819040	"Knockdown of cellular m6A methyltransferases METTL3 and METTL14 and the specific binding proteins YTHDF2 and YTHDF3 inhibited PRV replication, while silencing of demethylase ALKBH5 promoted PRV output. The overexpression of METTL14 induced more efficient virus proliferation in PRV-infected PK15 cells. Inhibition of m6A modification by 3-deazaadenosine (3-DAA), a m6A modification inhibitor, could significantly reduce viral replication."
item1966	REG00012	M6ATAR00771	Up	M6ADIS0010	.	36691477	"IGF2BP1 recognized the m6A modified sites on LDHA mRNA and enhanced its mRNA stability, thereby accelerating tumor energy metabolism."
item1967	REG00007	M6ATAR00846	Up	M6ADIS0210	.	36516331	"Overexpression of methyltransferase like 3 (METTL3) promoted the osteogenic differentiation of PPDLSCs, while knocking down METTL3 showed an inhibitory effect. Furthermore, METTL3 overexpression promotes the stability of lncRNA4114 to upregulate the expression level. Moreover, lncRNA4114 overexpression promoted the osteogenic differentiation of PPDLSCs."
item1968	REG00001	M6ATAR00847	.	M6ADIS0066	M6ADRUG0047	36622754	NNMT was upregulated and demethylated in FTO-overexpressing cells. Treatment with an NNMT inhibitor or NNMT knockdown restored sensitivity to Pt in FTO-overexpressing cells.
item1969	REG00009	M6ATAR00848	Up	M6ADIS0006	.	37926706	Enhanced expression of WTAP or METTL16 upregulated m6A modification level of AC026356.1 in HCC cells.
item1970	REG00007	M6ATAR00848	Up	M6ADIS0006	.	37926706	Enhanced expression of WTAP or METTL16 upregulated m6A modification level of AC026356.1 in HCC cells.
item1971	REG00012	M6ATAR00293	Up	M6ADIS0006	.	37926706	"m6A-modified AC026356.1 promoted HCC cellular proliferation, migration, and liver metastasis.6A-modified AC026356.1 bound to IGF2BP1. The interaction between m6A-modified AC026356.1 and IGF2BP1 promoted the binding of IL11 mRNA to IGF2BP1, leading to increased IL11 mRNA stability and IL11 secretion."
item1972	REG00007	M6ATAR00297	Up	M6ADIS0070	.	37003532	Targeted m6A demethylation of ITGA6 mRNA by the multisite dCasRx-m6A editor significantly reduced BCa cell proliferation and migration in vitro and in vivo.
item1973	REG00005	M6ATAR00297	Up	M6ADIS0070	.	37003532	Targeted m6A demethylation of ITGA6 mRNA by the multisite dCasRx-m6A editor significantly reduced BCa cell proliferation and migration in vitro and in vivo.
item1974	REG00007	M6ATAR01437	.	M6ADIS0110	.	37724835	METTL3 in combination with NEK7 inhibited the progression of OA by promoting chondrocytes pyroptosis.
item1975	REG00007	M6ATAR00287	Up	M6ADIS0032	.	37973667	"EIF2alpha is markedly upregulated in monocrotaline (MCT)-induced PAH rats, eIF2alpha can be upregulated by mRNA methylation, and upregulated eIF2alpha can promote PASMC proliferation in MCT-PAH rats."
item1976	REG00009	M6ATAR00287	Up	M6ADIS0032	.	37973667	"EIF2alpha is markedly upregulated in monocrotaline (MCT)-induced PAH rats, eIF2alpha can be upregulated by mRNA methylation, and upregulated eIF2alpha can promote PASMC proliferation in MCT-PAH rats."
item1977	REG00024	M6ATAR00287	Up	M6ADIS0032	.	37973667	"EIF2alpha is markedly upregulated in monocrotaline (MCT)-induced PAH rats, eIF2alpha can be upregulated by mRNA methylation, and upregulated eIF2alpha can promote PASMC proliferation in MCT-PAH rats."
item1978	REG00015	M6ATAR01438	Up	M6ADIS0055	.	37517144	KIAA1429 promoted the OSCC aerobic glycolysis and inhibited the ferroptosis of OSCC through YTHDF1-mediated PGK1 mRNA stability.
item1979	REG00024	M6ATAR01438	Up	M6ADIS0055	.	37517144	KIAA1429 promoted the OSCC aerobic glycolysis and inhibited the ferroptosis of OSCC through YTHDF1-mediated PGK1 mRNA stability.
item1980	REG00007	M6ATAR00850	Up	M6ADIS0162	.	36260529	"METTL3 overexpression increased total m6A, circSETD2 m6A, and circSETD2 levels. m6A modification mediated circSETD2 upregulation. circSETD2 was a sponge of miR-181a-5p to elevate MCL1 transcription. miR-181a-5p overexpression or MCL1 silencing annulled the role of m6A-modified circSETD2. circSETD2 inhibition negated suppression of METTL3 overexpression on chorionic trophoblast apoptosis in vivo. Collectively, m6A modification of circSETD2 suppressed miR-181a-5p and increased MCL1 transcription, thus regulating trophoblasts."
item1981	REG00001	M6ATAR00850	Down	M6ADIS0162	.	36260529	"METTL3 overexpression increased total m6A, circSETD2 m6A, and circSETD2 levels. m6A modification mediated circSETD2 upregulation. circSETD2 was a sponge of miR-181a-5p to elevate MCL1 transcription. miR-181a-5p overexpression or MCL1 silencing annulled the role of m6A-modified circSETD2. circSETD2 inhibition negated suppression of METTL3 overexpression on chorionic trophoblast apoptosis in vivo. Collectively, m6A modification of circSETD2 suppressed miR-181a-5p and increased MCL1 transcription, thus regulating trophoblasts."
item1982	REG00015	M6ATAR00258	Up	M6ADIS0057	M6ADRUG0048	36326914	KIAA1429 facilitated the GC OXA resistance in GC cells by promoting FOXM1 mRNA stability.
item1983	REG00001	M6ATAR00851	Up	M6ADIS0083	.	35904284	FTO promoted adipocyte differentiation by regulating ADRB1 gene through m6A modification in Hycole rabbits.
item1984	REG00001	M6ATAR00488	Up	.	.	37048078	"The targeted specific demethylation of TGFbeta1 m6A using dCas13b-FTO significantly increased the TGFbeta1-mediated activity of the SMAD2 signaling pathway, promoting myoblast proliferation."
item1985	REG00007	M6ATAR00853	.	M6ADIS0161	.	37482304	"In the process of NPP, METTL3 may inhibit the expression of MOR by regulating the methylation level of OPRM1 gene RNA encoding MOR, and ultimately promote the occurrence and development of NPP."
item1986	REG00026	M6ATAR00473	Up	M6ADIS0132	.	37752292	ZC3H13 accelerated keloid formation by mediating the m6A modification of HIPK2 mRNA and maintaining its stability.
item1987	REG00022	M6ATAR00854	Up	M6ADIS0006	.	37954496	"m6A-modified LEAWBIH binds to the m6A reader YTHDC1, which further interacts with and recruits H3K9me2 demethylase KDM3B to CTNNB1 promoter, leading to H3K9me2 demethylation and CTNNB1 transcription activation. Functional rescue assays showed that blocking Wnt/beta-catenin signaling abolished the role of LEAWBIH in HCC."
item1988	REG00022	M6ATAR00360	Up	M6ADIS0068	.	37698736	N6-methyladenosine regulator YTHDF1 represses the CD8 + T cell-mediated antitumor immunity and ferroptosis in prostate cancer via m6A/PD-L1 manner.
item1989	REG00025	M6ATAR01438	Up	M6ADIS0051	.	36171455	"YTHDF3 functioned as an oncogene in osteosarcoma tumorigenesis through m6A/PGK1 manner, providing a therapeutic strategy for human osteosarcoma."
item1990	REG00007	M6ATAR00175	Up	.	.	36444808	"METTL3-upregulated m6A promotes AKT1 expression by YTHDF1-mediated stability.
FTO-downregulated m6A elevates AKT1 level by inhibiting YTHDF2-mediated degradation.
m6A promotes AKT phosphorylated activation by affecting AKT regulator PHLPP2 and PDK1."
item1991	REG00022	M6ATAR00175	Up	.	.	36444808	"METTL3-upregulated m6A promotes AKT1 expression by YTHDF1-mediated stability.
FTO-downregulated m6A elevates AKT1 level by inhibiting YTHDF2-mediated degradation.
m6A promotes AKT phosphorylated activation by affecting AKT regulator PHLPP2 and PDK2."
item1992	REG00001	M6ATAR00175	Up	.	.	36444808	"METTL3-upregulated m6A promotes AKT1 expression by YTHDF1-mediated stability.
FTO-downregulated m6A elevates AKT1 level by inhibiting YTHDF2-mediated degradation.
m6A promotes AKT phosphorylated activation by affecting AKT regulator PHLPP2 and PDK3."
item1993	REG00023	M6ATAR00175	Down	.	.	36444808	"METTL3-upregulated m6A promotes AKT1 expression by YTHDF1-mediated stability.
FTO-downregulated m6A elevates AKT1 level by inhibiting YTHDF2-mediated degradation.
m6A promotes AKT phosphorylated activation by affecting AKT regulator PHLPP2 and PDK4."
item1994	REG00014	M6ATAR00856	Up	.	M6ADRUG0132	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL1)."
item1995	REG00007	M6ATAR00856	Up	.	M6ADRUG0132	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL1)."
item1996	REG00023	M6ATAR00856	Up	.	M6ADRUG0132	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL1)."
item1997	REG00014	M6ATAR01517	Down	.	M6ADRUG0132	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL4)."
item1998	REG00040	M6ATAR01517	Down	.	M6ADRUG0132	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL4)."
item1999	REG00041	M6ATAR01517	Down	.	M6ADRUG0132	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL4)."
item2000	REG00014	M6ATAR00856	Up	.	M6ADRUG0144	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL1)."
item2001	REG00007	M6ATAR00856	Up	.	M6ADRUG0144	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL1)."
item2002	REG00023	M6ATAR00856	Up	.	M6ADRUG0144	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL1)."
item2003	REG00014	M6ATAR01517	Down	.	M6ADRUG0144	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL4)."
item2004	REG00040	M6ATAR01517	Down	.	M6ADRUG0144	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL4)."
item2005	REG00041	M6ATAR01517	Down	.	M6ADRUG0144	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL4)."
item2006	REG00014	M6ATAR00856	Up	.	M6ADRUG0123	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL1)."
item2007	REG00007	M6ATAR00856	Up	.	M6ADRUG0123	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL1)."
item2008	REG00023	M6ATAR00856	Up	.	M6ADRUG0123	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL1)."
item2009	REG00014	M6ATAR01517	Down	.	M6ADRUG0123	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL4)."
item2010	REG00040	M6ATAR01517	Down	.	M6ADRUG0123	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL4)."
item2011	REG00041	M6ATAR01517	Down	.	M6ADRUG0123	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL4)."
item2012	REG00014	M6ATAR00856	Up	.	M6ADRUG0048	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL1)."
item2013	REG00007	M6ATAR00856	Up	.	M6ADRUG0048	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL1)."
item2014	REG00023	M6ATAR00856	Up	.	M6ADRUG0048	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL1)."
item2015	REG00014	M6ATAR01517	Down	.	M6ADRUG0048	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL4)."
item2016	REG00040	M6ATAR01517	Down	.	M6ADRUG0048	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL4)."
item2017	REG00041	M6ATAR01517	Down	.	M6ADRUG0048	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL4)."
item2018	REG00014	M6ATAR00856	Up	.	M6ADRUG0154	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL1)."
item2019	REG00007	M6ATAR00856	Up	.	M6ADRUG0154	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL1)."
item2020	REG00023	M6ATAR00856	Up	.	M6ADRUG0154	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL1)."
item2021	REG00014	M6ATAR01517	Down	.	M6ADRUG0154	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL4)."
item2022	REG00040	M6ATAR01517	Down	.	M6ADRUG0154	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL4)."
item2023	REG00041	M6ATAR01517	Down	.	M6ADRUG0154	36566349	"RN7SK was identified as a small nuclear RNA that interacts with m6A readers. m6A readers recognized and facilitated secondary structure formation of m6A-modified RN7SK, which in turn prevented m6A reader mRNA degradation from exonucleases. Thus, a positive feedback circuit between RN7SK and m6A readers is established in tumor cells. From findings on the interaction with RN7SK, new m6A readers, such as EWS RNA binding protein 1 (EWSR1) and KH RNA binding domain containing, signal transduction-associated 1 (KHDRBS1), were identified and shown to boost Wnt/beta-catenin signaling and tumorigenesis by suppressing translation of Cullin1 (CUL4)."
item2024	REG00007	M6ATAR00610	Up	M6ADIS0257	.	36873555	"METTL3 targeted the m6A site on SOCS3 mRNA, which positively regulated the mRNA stability of SOCS3. In conclusion, METTL3 silencing attenuated the HG-induced vascular endothelium cells injury via promoting SOCS3 stability."
item2025	REG00007	M6ATAR00477	Up	M6ADIS0057	.	37823387	METTL3-mediated m6A modification of lncRNA SNHG3 accelerates GC progression by modulating miR-186-5p/cyclinD2 axis.
item2026	REG00022	M6ATAR00860	Up	M6ADIS0006	.	37701563	"m6A-modified ATP8B1-AS1 interacts with and recruits m6A reader YTHDC1 and histone demethylase KDM3B to MYC promoter region, leading to the reduction of H3K9me2 level at MYC promoter region and activation of MYC transcription. Functional rescue assays showed that depletion of MYC largely abolished the oncogenic roles of ATP8B1-AS1."
item2027	REG00007	M6ATAR00530	Up	.	.	36793308	"The reduction of METTL3 decreased the expression of MMP3, MMP13, and GATA3.the molecular mechanisms of METTL3-mediated m6A post-transcriptional change in the modulation of SMSCs differentiating into chondrocytes, thus highlighting the potential therapeutic effect of SMSCs for cartilage regeneration."
item2028	REG00007	M6ATAR00333	Up	.	.	36793308	"The reduction of METTL3 decreased the expression of MMP3, MMP13, and GATA3.the molecular mechanisms of METTL3-mediated m6A post-transcriptional change in the modulation of SMSCs differentiating into chondrocytes, thus highlighting the potential therapeutic effect of SMSCs for cartilage regeneration."
item2029	REG00007	M6ATAR00265	Up	.	.	36793308	"The reduction of METTL3 decreased the expression of MMP3, MMP13, and GATA3.the molecular mechanisms of METTL3-mediated m6A post-transcriptional change in the modulation of SMSCs differentiating into chondrocytes, thus highlighting the potential therapeutic effect of SMSCs for cartilage regeneration."
item2030	REG00024	M6ATAR00206	Up	M6ADIS0164	.	36992945	"There was a m6A modification site on cyclin D1 RNA (CCND1 genome) and YTHDF1 combined with cyclin D1 mRNA, thereby enhancing its mRNA stability via m6A-dependent manner. Collectively, these findings reveal a novel axis of YTHDF1/m6A/cyclin D1 in asthma's airway remodeling, which may provide novel therapeutic strategy for asthma."
item2031	REG00009	M6ATAR00555	Down	M6ADIS0059	.	36154586	WTAP Mediated the N6-methyladenosine Modification of PDK4 to Regulate the Malignant Behaviors of Colorectal Cancer Cells In Vitro and I n Vivo.
item2032	REG00005	M6ATAR00393	Up	M6ADIS0159	.	37193033	Results using overexpression or knockdown of SIRT1 confirmed the protective effect of SIRT1 on H/R induced CMs apoptosis.
item2033	REG00007	M6ATAR01439	Up	M6ADIS0233	M6ADRUG0108	37710320	"Interference with METTL3 expression and exposure to STM2457 inhibited METTL3 activity, which in turn interfered with the phosphorylated insulin receptor substrate (pIRS)-glucose transporter 2 (GLUT2) insulin signaling pathway; overexpression of CYP2B6 hindered IRS phosphorylation and translocation of GLUT2 to membranes, which ultimately exacerbated IR."
item2034	REG00007	M6ATAR00862	.	M6ADIS0055	.	37249063	Mettl3 mediated the m6A modification of ALDH1A3 and ALDH7A1 mRNA in Bmi1+HNSCC CSCs.
item2035	REG00007	M6ATAR00863	.	M6ADIS0055	.	37249063	Mettl3 mediated the m6A modification of ALDH1A3 and ALDH7A1 mRNA in Bmi1+HNSCC CSCs.
item2036	REG00005	M6ATAR00864	Down	M6ADIS0275	.	36625590	"The knockdown of the m6A eraser ALKBH5 increases the DUSP1 transcript m6A level, resulting in accelerated transcript degradation, the activation of p38 and JNK, and the enhanced expression of IL-1beta, CSF3, TGM2, and SRC. These results demonstrate that m6A and the reader protein YTHDF2 orchestrate optimal innate immune responses during viral and bacterial infections by downregulating the expression of a negative regulator, DUSP1, of the p38 and JNK pathways that are central to innate immune responses against pathogenic infections."
item2037	REG00008	M6ATAR00864	Down	M6ADIS0275	.	36625590	"The knockdown of the m6A eraser ALKBH5 increases the DUSP1 transcript m6A level, resulting in accelerated transcript degradation, the activation of p38 and JNK, and the enhanced expression of IL-1beta, CSF3, TGM2, and SRC. These results demonstrate that m6A and the reader protein YTHDF2 orchestrate optimal innate immune responses during viral and bacterial infections by downregulating the expression of a negative regulator, DUSP1, of the p38 and JNK pathways that are central to innate immune responses against pathogenic infections."
item2038	REG00024	M6ATAR01440	Up	M6ADIS0087	.	37572160	YTHDF1 improved sevoflurane-induced neuronal pyroptosis and cognitive dysfunction through activating CREB-BDNF signaling.
item2039	REG00005	M6ATAR00865	Up	.	M6ADRUG0182	37573961	Benzo[a]pyrene-induced up-regulation of circ_0003552 via ALKBH5-mediated m6A modification promotes DNA damage in human bronchial epithelial cells.
item2040	REG00007	M6ATAR00866	Up	M6ADIS0067	M6ADRUG0089	37755125	METTL3 could upregulate FGD5-AS1 expression via N6-methyladenosine (m6A) modification.research has shed light on the involvement of the METTL3/FGD5-AS1 axis in the development of PTX resistance in EC.
item2041	REG00006	M6ATAR00867	Up	.	.	37449516	METTL14 mediates m6A modification on osteogenic proliferation and differentiation of bone marrow mesenchymal stem cells by regulating the processing of pri-miR-873.
item2042	REG00007	M6ATAR00868	.	M6ADIS0067	.	35971034	m6A mRNA methylation regulates the ERK/NF-kappaB/AKT signaling pathway through the PAPPA/IGFBP4 axis to promote proliferation and tumor formation in endometrial cancer.
item2043	REG00007	M6ATAR00869	.	M6ADIS0067	.	35971034	m6A mRNA methylation regulates the ERK/NF-kappaB/AKT signaling pathway through the PAPPA/IGFBP4 axis to promote proliferation and tumor formation in endometrial cancer.
item2044	REG00024	M6ATAR00868	.	M6ADIS0067	.	35971034	m6A mRNA methylation regulates the ERK/NF-kappaB/AKT signaling pathway through the PAPPA/IGFBP4 axis to promote proliferation and tumor formation in endometrial cancer.
item2045	REG00024	M6ATAR00869	.	M6ADIS0067	.	35971034	m6A mRNA methylation regulates the ERK/NF-kappaB/AKT signaling pathway through the PAPPA/IGFBP4 axis to promote proliferation and tumor formation in endometrial cancer.
item2046	REG00012	M6ATAR00360	Up	M6ADIS0057	.	37817028	"IGF2BP1 overexpression enhanced the stability of PD-L1 mRNA, thereby deteriorating the immune escape of gastric cancer cells."
item2047	REG00008	M6ATAR00870	Down	M6ADIS0008	.	37273106	m6A reader YTHDF2 could recognize m6A-modified CARMN and promote its degradation in CC cells.
item2048	REG00009	M6ATAR00871	.	M6ADIS0046	M6ADRUG0174	37926762	Chidamide treatment suppressed WT1-associated protein (WTAP)-mediated RNA m6A modification of GNAS-AS1. Chidamide downregulated GNAS-AS1 to inhibit glycolysis in AML cells. GNAS-AS1 targeted miR-34a-5p to promote insulin-like growth factor 2 mRNA-binding protein (IGF2BP2) expression. IGF2BP2 inhibition reversed the promoting effect of miR-34a-5p knockdown on glycolysis and RhoA/ROCK pathway in Chidamide-treated cells. GNAS-AS1 overexpression abolished the inhibitory effect of Chidamide on AML tumorigenesis in vivo by modulating the RhoA/ROCK pathway.
item2049	REG00013	M6ATAR00871	.	M6ADIS0046	M6ADRUG0174	37926762	Chidamide treatment suppressed WT1-associated protein (WTAP)-mediated RNA m6A modification of GNAS-AS1. Chidamide downregulated GNAS-AS1 to inhibit glycolysis in AML cells. GNAS-AS1 targeted miR-34a-5p to promote insulin-like growth factor 2 mRNA-binding protein (IGF2BP2) expression. IGF2BP2 inhibition reversed the promoting effect of miR-34a-5p knockdown on glycolysis and RhoA/ROCK pathway in Chidamide-treated cells. GNAS-AS1 overexpression abolished the inhibitory effect of Chidamide on AML tumorigenesis in vivo by modulating the RhoA/ROCK pathway.
item2050	REG00015	M6ATAR00872	Up	M6ADIS0059	.	38103097	KIAA1429 promoted lncRNA POU6F2-AS1 expression via m6A modification.lncRNA POU6F2-AS1 was modulated by KIAA1429 in the form of m6A modification to regulate the malignant phenotype of CRC.
item2051	REG00009	M6ATAR00011	Up	M6ADIS0115	.	37010483	WTAP-mediated m6A modification promoted osteogenic differentiation and inhibited adipogenic differentiation of BMMSCs through the miR-29b-3p/HDAC4 axis.
item2052	REG00001	M6ATAR00873	.	M6ADIS0007	M6ADRUG0160	37919739	"FTO facilitated NSCLC metastasis by modifying the m6A level of FAP in a YTHDF2-dependent manner.FTO promoted cell migration and invasion in NSCLC, and the FAK inhibitor defactinib (VS6063) suppressed NSCLC metastasis induced by overexpression of FTO."
item2053	REG00008	M6ATAR00873	.	M6ADIS0007	M6ADRUG0160	37919739	"FTO facilitated NSCLC metastasis by modifying the m6A level of FAP in a YTHDF2-dependent manner.FTO promoted cell migration and invasion in NSCLC, and the FAK inhibitor defactinib (VS6063) suppressed NSCLC metastasis induced by overexpression of FTO."
item2054	REG00014	M6ATAR01441	Down	M6ADIS0184	.	37743642	TET3-mediated IGF2BP3 accelerated the proliferation of TNBC by destabilising NF1 mRNA via an m6A-dependent manner.
item2055	REG00024	M6ATAR00874	Down	M6ADIS0061	.	37223505	"YTHDF1 serves as a reader for the m6A modified LINC00901 and downregulates the LINC00901 level.LINC00901 positively regulates MYC through upregulation of IGF2BP2, a known RNA binding protein that can enhance MYC mRNA stability."
item2056	REG00013	M6ATAR00341	Up	M6ADIS0061	.	37223505	"YTHDF1 serves as a reader for the m6A modified LINC00901 and downregulates the LINC00901 level.LINC00901 positively regulates MYC through upregulation of IGF2BP2, a known RNA binding protein that can enhance MYC mRNA stability."
item2057	REG00022	M6ATAR00875	Up	M6ADIS0006	.	37809459	The m6A reader YTHDC1-mediated lncRNA CTBP1-AS2 m6A modification accelerates cholangiocarcinoma progression.
item2058	REG00007	M6ATAR00876	Up	.	.	37558013	"EGR1 promotes METTL3 transcription and increases m6A-modified CHI3L1 level, thereby stimulating osteoclast differentiation and osteoporosis development."
item2059	REG00004	M6ATAR00877	Down	M6ADIS0068	.	37215455	Activation of the HNRNPA2B1/ miR-93-5p/FRMD6 axis facilitates prostate cancer progression in an m6A-dependent manner.
item2060	REG00024	M6ATAR00878	Up	M6ADIS0016	.	37742376	"For As-IPF, the global levels of m6A, levels of YTHDF1 and m6A-modified neuronal protein 3.1 (NREP) were elevated in alveolar epithelial cells (AECs). The secretion levels of TGF-beta1 were increased via YTHDF1/m6A/NREP, which promoted the fibroblast-to-myofibroblast transition (FMT)."
item2061	REG00007	M6ATAR00879	Up	M6ADIS0007	.	37742030	METTL3 exerts synergistic effects on m6A methylation and histone modification to regulate the function of VGF in lung adenocarcinoma.
item2062	REG00022	M6ATAR00416	.	M6ADIS0081	.	36878322	"YTHDC1 may regulate mRNA splicing and export by interacting with SRSF3 and CPSF6 to modulate glucose metabolism via regulating insulin secretion, implying YTHDC1 might be a novel potential target for lowing glucose."
item2063	REG00022	M6ATAR00880	.	M6ADIS0081	.	36878322	"YTHDC1 may regulate mRNA splicing and export by interacting with SRSF3 and CPSF6 to modulate glucose metabolism via regulating insulin secretion, implying YTHDC1 might be a novel potential target for lowing glucose."
item2064	REG00007	M6ATAR00881	Down	M6ADIS0362	.	36656457	"In vivo, D26496 overexpression alleviated SNI-induced neuropathic pain and oxidative stress. In conclusion, our results suggested that D26496 m6A modification mediated by METTL3 and recognition of D26496 m6A sites by YTHDF2 induced D26496 degradation, thereby participating in the progression of SNI."
item2065	REG00008	M6ATAR00881	Down	M6ADIS0362	.	36656457	"In vivo, D26496 overexpression alleviated SNI-induced neuropathic pain and oxidative stress. In conclusion, our results suggested that D26496 m6A modification mediated by METTL3 and recognition of D26496 m6A sites by YTHDF2 induced D26496 degradation, thereby participating in the progression of SNI."
item2066	REG00005	M6ATAR00882	Up	M6ADIS0252	.	36918845	"During EBV reactivation the m6A eraser ALKBH5 is significantly downregulated leading to enhanced methylation of the cellular transcripts DTX4 and TYK2, that results in degradation of TYK2 mRNAs and higher efficiency of translation of DTX4 mRNAs."
item2067	REG00005	M6ATAR00883	Up	M6ADIS0252	.	36918845	"During EBV reactivation the m6A eraser ALKBH5 is significantly downregulated leading to enhanced methylation of the cellular transcripts DTX4 and TYK2, that results in degradation of TYK2 mRNAs and higher efficiency of translation of DTX4 mRNAs."
item2068	REG00015	M6ATAR00884	Up	M6ADIS0004	M6ADRUG0118	37692484	"The combined use of rucaparib and imatinib enhanced the sensitivity of CML cells to imatinib. Our study provides evidence that elevated KIAA1429 expression in the blast phase of CML enhances the stability of RAB27B mRNA through the m6A/YTHDF1 axis to up-regulate RAB27B expression, thereby promoting CML progression. Rucaparib exerts inhibitory effects on KIAA1429 expression and thus reduces CML progression."
item2069	REG00024	M6ATAR00884	Up	M6ADIS0004	M6ADRUG0118	37692484	"The combined use of rucaparib and imatinib enhanced the sensitivity of CML cells to imatinib. Our study provides evidence that elevated KIAA1429 expression in the blast phase of CML enhances the stability of RAB27B mRNA through the m6A/YTHDF1 axis to up-regulate RAB27B expression, thereby promoting CML progression. Rucaparib exerts inhibitory effects on KIAA1429 expression and thus reduces CML progression."
item2070	REG00015	M6ATAR00884	Up	M6ADIS0004	M6ADRUG0107	37692484	"The combined use of rucaparib and imatinib enhanced the sensitivity of CML cells to imatinib. Our study provides evidence that elevated KIAA1429 expression in the blast phase of CML enhances the stability of RAB27B mRNA through the m6A/YTHDF1 axis to up-regulate RAB27B expression, thereby promoting CML progression. Rucaparib exerts inhibitory effects on KIAA1429 expression and thus reduces CML progression."
item2071	REG00024	M6ATAR00884	Up	M6ADIS0004	M6ADRUG0107	37692484	"The combined use of rucaparib and imatinib enhanced the sensitivity of CML cells to imatinib. Our study provides evidence that elevated KIAA1429 expression in the blast phase of CML enhances the stability of RAB27B mRNA through the m6A/YTHDF1 axis to up-regulate RAB27B expression, thereby promoting CML progression. Rucaparib exerts inhibitory effects on KIAA1429 expression and thus reduces CML progression."
item2072	REG00007	M6ATAR00885	Up	M6ADIS0379	.	36982798	METTL3-mediated lncRNA EN_42575 exerted a regulatory effect on IPEC-J2 cells exposed to CPB2 toxins.
item2073	REG00007	M6ATAR00484	Down	M6ADIS0159	.	36645573	"METTL3 silencing repressed the ferroptosis phenotype induced by LPS. Mechanistically, METTL3-mediated m6A methylation on solute carrier family 7 member 11 (SLC7A11) empowered its mRNA with high methylation level. Moreover, YTHDF2 directly bound to the m6A modification sites of SLC7A11 to mediate the mRNA degradation. The m6A modified SLC7A11 mRNA was recognized by YTHDF2, which promoted the decay of SLC7A11 mRNA, consequently up-regulating ferroptosis in sepsis-induced myocardial injury. Together, these findings establish a role of METTL3 in the ferroptosis of LPS-induced cardiomyocytes, and provide potential therapeutic target to treat the sepsis-induced myocardial injury."
item2074	REG00008	M6ATAR00484	Down	M6ADIS0159	.	36645573	"METTL3 silencing repressed the ferroptosis phenotype induced by LPS. Mechanistically, METTL3-mediated m6A methylation on solute carrier family 7 member 11 (SLC7A11) empowered its mRNA with high methylation level. Moreover, YTHDF2 directly bound to the m6A modification sites of SLC7A11 to mediate the mRNA degradation. The m6A modified SLC7A11 mRNA was recognized by YTHDF2, which promoted the decay of SLC7A11 mRNA, consequently up-regulating ferroptosis in sepsis-induced myocardial injury. Together, these findings establish a role of METTL3 in the ferroptosis of LPS-induced cardiomyocytes, and provide potential therapeutic target to treat the sepsis-induced myocardial injury."
item2075	REG00013	M6ATAR01442	Up	M6ADIS0061	.	35908253	IGF2BP2 promotes pancreatic carcinoma progression by enhancing the stability of B3GNT6 mRNA via m6A methylation.
item2076	REG00007	M6ATAR00886	Up	M6ADIS0053	M6ADRUG0047	38086167	"METTL3 facilitates m6A modification, and YTHDF1 recognizes the specific m6A-modified site to prevent RIPK4 RNA degradation and upregulate RIPK4 expression. This induces NF-kappaB activation, resulting in tumor growth and DDP resistance in vitro and in vivo."
item2077	REG00024	M6ATAR00886	Up	M6ADIS0053	M6ADRUG0047	38086167	"METTL3 facilitates m6A modification, and YTHDF1 recognizes the specific m6A-modified site to prevent RIPK4 RNA degradation and upregulate RIPK4 expression. This induces NF-kappaB activation, resulting in tumor growth and DDP resistance in vitro and in vivo."
item2078	REG00009	M6ATAR00189	Up	M6ADIS0006	.	38056309	"WTAP upregulates ATG5 expression post-transcriptionally in an m6A-YTHDC2-dependent manner, thereby promoting the translation of ATG5 mRNA during ferroptosis in HCC. These findings have significant implications for the development of innovative and effective therapeutic approaches for HCC treatment."
item2079	REG00023	M6ATAR00189	Up	M6ADIS0006	.	38056309	"WTAP upregulates ATG5 expression post-transcriptionally in an m6A-YTHDC2-dependent manner, thereby promoting the translation of ATG5 mRNA during ferroptosis in HCC. These findings have significant implications for the development of innovative and effective therapeutic approaches for HCC treatment."
item2080	REG00005	M6ATAR01443	Down	M6ADIS0005	.	37612282	"ALKBH5 impaired cell proliferation by regulating human Toll-like receptor 2 (TLR2) in an m6A-dependent manner in HPSCC cells. ALKBH5 decreased TLR2 m6A modification, which could be recognized by the m6A readers IGF2BP2 and YTHDF1. IGF2BP2 facilitates TLR2 mRNA stability, whereas YTHDF1 promotes TLR2 mRNA translation."
item2081	REG00024	M6ATAR01443	Up	M6ADIS0005	.	37612282	"ALKBH5 impaired cell proliferation by regulating human Toll-like receptor 2 (TLR2) in an m6A-dependent manner in HPSCC cells. ALKBH5 decreased TLR2 m6A modification, which could be recognized by the m6A readers IGF2BP2 and YTHDF1. IGF2BP2 facilitates TLR2 mRNA stability, whereas YTHDF1 promotes TLR2 mRNA translation."
item2082	REG00013	M6ATAR01443	Up	M6ADIS0005	.	37612282	"ALKBH5 impaired cell proliferation by regulating human Toll-like receptor 2 (TLR2) in an m6A-dependent manner in HPSCC cells. ALKBH5 decreased TLR2 m6A modification, which could be recognized by the m6A readers IGF2BP2 and YTHDF1. IGF2BP2 facilitates TLR2 mRNA stability, whereas YTHDF1 promotes TLR2 mRNA translation."
item2083	REG00017	M6ATAR00213	Up	M6ADIS0061	.	37182151	METTL16 plays a tumor-suppressive role and suppresses PDAC cell proliferation through the p21 pathway by mediating m6A modification.
item2084	REG00007	M6ATAR00610	Down	M6ADIS0124	M6ADRUG0067	36368553	"Arsenite induces METTL3 upregulation, represses suppressors of cytokine signaling 3 (SOCS3) expression in an m6A- YTH m6A RNA binding protein 2 (YTHDF2)-dependent manner, and leads to the aberrant activation of the Janus kinase (JAK)2/signal transducer and activator of transcription 3(STAT3) signaling pathway.the role of m6A in arsenite-induced skin lesions through the activation of the JAK2/STAT3/Krt signaling axis."
item2085	REG00008	M6ATAR00610	Down	M6ADIS0124	M6ADRUG0067	36368553	"Arsenite induces METTL3 upregulation, represses suppressors of cytokine signaling 3 (SOCS3) expression in an m6A- YTH m6A RNA binding protein 2 (YTHDF2)-dependent manner, and leads to the aberrant activation of the Janus kinase (JAK)2/signal transducer and activator of transcription 3(STAT3) signaling pathway.the role of m6A in arsenite-induced skin lesions through the activation of the JAK2/STAT3/Krt signaling axis."
item2086	REG00004	M6ATAR00150	Up	M6ADIS0007	.	37308993	HNRNPA2B1-mediated m6A modification of lncRNA MEG3 promotes tumorigenesis and metastasis of NSCLC cells by regulating miR-21-5p/PTEN axis and may provide a therapeutic target for NSCLC.
item2087	REG00007	M6ATAR00887	Down	M6ADIS0391	.	37494067	"METTL3 catalyzes m6A in the 3' untranslated region of GATA6 read by YTH N6-Methyladenosine RNA Binding Protein 2 and triggers mRNA degradation. GATA6 knockdown rescues TNF-alpha-induced inflammatory cytokine secretion of epithelial cells, indicating that GATA6 is a main substrate of METTL3 in airway epithelial cells. Overall, this study provides evidence of a novel role for METTL3 in the inflammatory cytokine release of epithelial cells and provides an innovative therapeutic target for ALI."
item2088	REG00008	M6ATAR00887	Down	M6ADIS0391	.	37494067	"METTL3 catalyzes m6A in the 3' untranslated region of GATA6 read by YTH N6-Methyladenosine RNA Binding Protein 2 and triggers mRNA degradation. GATA6 knockdown rescues TNF-alpha-induced inflammatory cytokine secretion of epithelial cells, indicating that GATA6 is a main substrate of METTL3 in airway epithelial cells. Overall, this study provides evidence of a novel role for METTL3 in the inflammatory cytokine release of epithelial cells and provides an innovative therapeutic target for ALI."
item2089	REG00006	M6ATAR01444	Up	M6ADIS0088	.	37309980	Results reveal the potential of METTL14 as a novel diagnostic biomarker for PD and identify modification of pathogenic alpha-syn protein by METTL14 via an m6A-YTHDF2-dependent mechanism.
item2090	REG00008	M6ATAR01444	Up	M6ADIS0088	.	37309980	Results reveal the potential of METTL14 as a novel diagnostic biomarker for PD and identify modification of pathogenic alpha-syn protein by METTL14 via an m6A-YTHDF2-dependent mechanism.
item2091	REG00017	M6ATAR01414	Up	M6ADIS0065	.	36434904	METTL16 epigenetically enhanced GPX4 expression via m6A modification to promote breast cancer progression by inhibiting ferroptosis.
item2092	REG00007	M6ATAR00285	Up	M6ADIS0061	.	37196908	"METTL3 may post-transcriptionally upregulate ID2 expression in an m6A-YTHDF2-dependent manner to further promote the stabilization of ID2 mRNA, which may be a new target for pancreatic cancer treatment."
item2093	REG00008	M6ATAR00285	Up	M6ADIS0061	.	37196908	"METTL3 may post-transcriptionally upregulate ID2 expression in an m6A-YTHDF2-dependent manner to further promote the stabilization of ID2 mRNA, which may be a new target for pancreatic cancer treatment."
item2094	REG00004	M6ATAR00888	Down	M6ADIS0065	M6ADRUG0097	36693492	Overexpression of ATG4B rescued the malignancy driven by HNRNPA2B1 in breast cancer cells and increased the olaparib sensitivity. Our study revealed that the m6A reader HNRNPA2B1 mediated proliferation and autophagy in breast cancer cell lines by facilitating ATG4B mRNA decay and targeting HNRNPA2B1/m6A/ATG4B might enhance the olaparib sensitivity of breast cancer cells.
item2095	REG00006	M6ATAR00514	.	M6ADIS0112	.	37327357	METTL14-Mediated m6A Modification of TNFAIP3 Involved in Inflammation in Patients With Active Rheumatoid Arthritis .
item2096	REG00006	M6ATAR00889	.	.	.	37269288	Mettl14-mediated m6A modification of Zfp292 ensures the cell-cycle progression of late-born retinal progenitor cells.
item2097	REG00007	M6ATAR01445	Up	M6ADIS0109	.	37914138	"Methyltransferase-like 3 (METTL3) acts as a main modulator to promote the methylation and gene expression of TEAD1, leading to STING-NLRP3 signaling activation. Importantly, it was shown that IGF2BP2 functions as an m6A ""reader"" to recognize methylated TEAD1 mRNA and promote its stability."
item2098	REG00013	M6ATAR01445	Up	M6ADIS0109	.	37914138	"Methyltransferase-like 3 (METTL3) acts as a main modulator to promote the methylation and gene expression of TEAD1, leading to STING-NLRP3 signaling activation. Importantly, it was shown that IGF2BP2 functions as an m6A ""reader"" to recognize methylated TEAD1 mRNA and promote its stability."
item2099	REG00007	M6ATAR01446	Up	M6ADIS0066	.	38154356	"The METTL3/YTHDF1 m6A axis directly binds to the mRNA of DDR2, thereby promoting the expression levels of the tumor promoter DDR2 and thus contributing to the progression of ovarian cancer."
item2100	REG00024	M6ATAR01446	Up	M6ADIS0066	.	38154356	"The METTL3/YTHDF1 m6A axis directly binds to the mRNA of DDR2, thereby promoting the expression levels of the tumor promoter DDR2 and thus contributing to the progression of ovarian cancer."
item2101	REG00007	M6ATAR00356	Up	M6ADIS0091	M6ADRUG0121	37809663	Re treatment relieved the H/R induced injury in the L-02 cells through decreasing the METTL3 levels. METTL3 enhanced the mRNA stability and expressions of P53 through m6A modification. Re-METTL3-P53 axis might a new direction for the treatment of liver IRI in the future.
item2102	REG00007	M6ATAR00890	Up	M6ADIS0007	.	38141906	"METTL3 regulates the mRNA stability of SH3BP5 in a YTHDF1-dependent manner, thereby impacting the invasive capacity of lung cancer cells."
item2103	REG00024	M6ATAR00890	Up	M6ADIS0007	.	38141906	"METTL3 regulates the mRNA stability of SH3BP5 in a YTHDF1-dependent manner, thereby impacting the invasive capacity of lung cancer cells."
item2104	REG00025	M6ATAR00260	.	.	.	36374269	"YTHDF3 binding to the m6A modifications at the coding DNA sequence (CDS) and 3' untranslated region (UTR) around the stop codon of Foxo3 mRNA, recruiting EIF3A and EIF4B to facilitate FOXO3 translation, thus boosting autophagy."
item2105	REG00005	M6ATAR00345	Up	M6ADIS0066	.	37818080	Hypoxia-induced m6A demethylase ALKBH5 promotes ovarian cancer tumorigenicity by decreasing methylation of the lncRNA RMRP.
item2106	REG00007	M6ATAR01447	Up	.	.	37041485	METTL3 enhances dentinogenesis differentiation of dental pulp stem cells via increasing GDF6 and STC1 mRNA stability .
item2107	REG00007	M6ATAR01448	Up	.	.	37041485	METTL3 enhances dentinogenesis differentiation of dental pulp stem cells via increasing GDF6 and STC1 mRNA stability .
item2108	REG00022	M6ATAR01449	Up	M6ADIS0066	.	37781028	Low expression of m6A reader YTHDC1 promotes progression of ovarian cancer via PIK3R1/STAT3/GANAB axis.
item2109	REG00005	M6ATAR00892	Up	M6ADIS0008	.	37480971	ALKBH5-mediated m6A demethylation enhanced the expression of PAK5. The m6A reader YTHDF2 bound to PAK5 mRNA and regulated its stability in an m6A-dependent manner.
item2110	REG00008	M6ATAR00892	Down	M6ADIS0008	.	37480971	ALKBH5-mediated m6A demethylation enhanced the expression of PAK5. The m6A reader YTHDF2 bound to PAK5 mRNA and regulated its stability in an m6A-dependent manner.
item2111	REG00017	M6ATAR00893	Down	M6ADIS0061	.	37859814	"Mechanistically, METTL16 regulates DVL2 expression by suppressing its translation via m6A modification, thereby regulating Wnt/beta-catenin signaling."
item2112	REG00007	M6ATAR01450	Up	M6ADIS0008	.	36382580	"METTL3 mediated the m6A modification of cathepsin L (CTSL) mRNA at the 5'-UTR, and the m6A reader protein insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) bound to the m6A sites and enhanced CTSL mRNA stability. Our results indicated that METTL3 enhanced CTSL mRNA stability through an m6A-IGF2BP2-dependent mechanism, thereby promoting cervical cancer cell metastasis."
item2113	REG00013	M6ATAR01450	Up	M6ADIS0008	.	36382580	"METTL3 mediated the m6A modification of cathepsin L (CTSL) mRNA at the 5'-UTR, and the m6A reader protein insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) bound to the m6A sites and enhanced CTSL mRNA stability. Our results indicated that METTL3 enhanced CTSL mRNA stability through an m6A-IGF2BP2-dependent mechanism, thereby promoting cervical cancer cell metastasis."
item2114	REG00007	M6ATAR01451	Down	.	M6ADRUG0044	37599001	"MTORC1 induces m6A modification of MAPK13 mRNA at its 3' untranslated region through the methyltransferase-like 3 (METTL3)-METTL14-Wilms' tumor 1-associating protein(WTAP) methyltransferase complex, facilitating its mRNA degradation via an m6A reader protein YTH domain family protein 2. Rapamycin blunts this process and stabilizes MAPK13."
item2115	REG00006	M6ATAR01451	Down	.	M6ADRUG0044	37599001	"MTORC1 induces m6A modification of MAPK13 mRNA at its 3' untranslated region through the methyltransferase-like 3 (METTL3)-METTL14-Wilms' tumor 1-associating protein(WTAP) methyltransferase complex, facilitating its mRNA degradation via an m6A reader protein YTH domain family protein 2. Rapamycin blunts this process and stabilizes MAPK13."
item2116	REG00009	M6ATAR01451	Down	.	M6ADRUG0044	37599001	"MTORC1 induces m6A modification of MAPK13 mRNA at its 3' untranslated region through the methyltransferase-like 3 (METTL3)-METTL14-Wilms' tumor 1-associating protein(WTAP) methyltransferase complex, facilitating its mRNA degradation via an m6A reader protein YTH domain family protein 2. Rapamycin blunts this process and stabilizes MAPK13."
item2117	REG00008	M6ATAR01451	Down	.	M6ADRUG0044	37599001	"MTORC1 induces m6A modification of MAPK13 mRNA at its 3' untranslated region through the methyltransferase-like 3 (METTL3)-METTL14-Wilms' tumor 1-associating protein(WTAP) methyltransferase complex, facilitating its mRNA degradation via an m6A reader protein YTH domain family protein 2. Rapamycin blunts this process and stabilizes MAPK13."
item2118	REG00013	M6ATAR01414	Up	M6ADIS0183	.	38039694	IGF2BP2 augmented the GPX4 expression by the m6A modification to weaken UC progression via suppressing ferroptosis.
item2119	REG00006	M6ATAR00260	Up	M6ADIS0136	.	37935312	"Expression of METTL14 upregulated the expression of FOXO3a, thereby activating autophagy and alleviating inflammation."
item2120	REG00007	M6ATAR01452	Up	M6ADIS0272	.	37056933	"METTL3 increased m6A level of RAC3 mRNA, resulting in increased stability and translation of RAC3 mRNA. RAC3 was responsible for the CAFs' promoting effect on cell migration via the AKT/NF-kappaB pathway."
item2121	REG00014	M6ATAR00894	Up	M6ADIS0146	.	37643553	IGF2BP3 drives gallbladder cancer progression by m6A-modified CLDN4 and inducing macrophage immunosuppressive polarization.
item2122	REG00005	M6ATAR00895	Down	M6ADIS0006	.	36609413	ALKBH5 decreases PAQR4 mRNA and protein expression in an N6-methyladenosine (m6A)-dependent manner. The study also showed that ALKBH5 changes PAQR4 expression via the m6A reader IGF2BP1.
item2123	REG00012	M6ATAR00895	Down	M6ADIS0006	.	36609413	ALKBH5 decreases PAQR4 mRNA and protein expression in an N6-methyladenosine (m6A)-dependent manner. The study also showed that ALKBH5 changes PAQR4 expression via the m6A reader IGF2BP1.
item2124	REG00001	M6ATAR00375	Down	M6ADIS0238	.	38092760	N6-methyladenosine demethylase FTO regulates synaptic and cognitive impairment by destabilizing PTEN mRNA in hypoxic-ischemic neonatal rats.
item2125	REG00005	M6ATAR00896	Down	M6ADIS0310	.	37827106	"ALKBH5 promoted m6A modification of Slamf7, which decreased Slamf7 mRNA stability in an m6A-dependent manner, ultimately regulating Slamf7 expression. In addition, silica exposure activated PI3K/AKT and induced macrophage autophagy."
item2126	REG00007	M6ATAR00897	Up	M6ADIS0065	M6ADRUG0044	37589705	"N6-methyladenosine (m6A) methylation of RNA by the methyltransferase complex (MTC), with core components including METTL3-METTL14 heterodimers and Wilms' tumor 1-associated protein (WTAP), contributes to breast tumorigenesis.depletion of METTL3a globally disrupts m6A deposition, and METTL3a mediates mammalian target of rapamycin (mTOR) activation via m6A-mediated suppression of TMEM127 expression."
item2127	REG00006	M6ATAR00897	Up	M6ADIS0065	M6ADRUG0044	37589705	"N6-methyladenosine (m6A) methylation of RNA by the methyltransferase complex (MTC), with core components including METTL3-METTL14 heterodimers and Wilms' tumor 1-associated protein (WTAP), contributes to breast tumorigenesis.depletion of METTL3a globally disrupts m6A deposition, and METTL3a mediates mammalian target of rapamycin (mTOR) activation via m6A-mediated suppression of TMEM127 expression."
item2128	REG00009	M6ATAR00897	Up	M6ADIS0065	M6ADRUG0044	37589705	"N6-methyladenosine (m6A) methylation of RNA by the methyltransferase complex (MTC), with core components including METTL3-METTL14 heterodimers and Wilms' tumor 1-associated protein (WTAP), contributes to breast tumorigenesis.depletion of METTL3a globally disrupts m6A deposition, and METTL3a mediates mammalian target of rapamycin (mTOR) activation via m6A-mediated suppression of TMEM127 expression."
item2129	REG00007	M6ATAR00898	Up	M6ADIS0073	.	37824376	"The m6A modification of LINC01125 was mediated by METTL3 and LINC01125 inhibited cell invasion, migration and proliferation, thereby suppressing the development of PTC."
item2130	REG00004	M6ATAR00899	.	M6ADIS0066	.	36259156	"Mechanistically, m6A reader HNRNPA2B1 might regulate CDK19 mRNA stability to alter m6A level.miR-30c-5p inhibits OvCa progression and reduces the m6A level by inhibiting m6A reader HNRNPA2B1, thus providing new insights into the m6A regulatory mechanism in OvCa."
item2131	REG00017	M6ATAR00760	Down	.	.	36795489	"Mechanistically, knocking down METTL16 decreased MCP1 mRNA degradation, which was mediated by the m6A reader YTH N6-methyladenosine RNA-binding protein 2 (YTHDF2). We further revealed that YTHDF2 specifically recognized m6A sites on MCP1 mRNA in the CDS region and thus negatively regulated MCP1 expression."
item2132	REG00008	M6ATAR00760	Down	.	.	36795489	"Mechanistically, knocking down METTL16 decreased MCP1 mRNA degradation, which was mediated by the m6A reader YTH N6-methyladenosine RNA-binding protein 2 (YTHDF2). We further revealed that YTHDF2 specifically recognized m6A sites on MCP1 mRNA in the CDS region and thus negatively regulated MCP1 expression."
item2133	REG00007	M6ATAR00393	Up	M6ADIS0205	.	37087022	"In OC1 cells, METTL3 positively regulated SIRT1 protein levels, while reversely regulated the level of ROS and apoptosis. IGF2BP3 was found to be involved in the regulation of SIRT1 protein expression."
item2134	REG00014	M6ATAR00393	Up	M6ADIS0205	.	37087022	"In OC1 cells, METTL3 positively regulated SIRT1 protein levels, while reversely regulated the level of ROS and apoptosis. IGF2BP3 was found to be involved in the regulation of SIRT1 protein expression."
item2135	REG00006	M6ATAR00325	Up	.	.	37355987	"Aberrant m6A modification destabilizes c-MET mRNA, reducing cell proliferation.the METTL14 R298P mutation affects target recognition for m6A modification, perturbing gene expression patterns and cell growth."
item2136	REG00042	M6ATAR00341	Up	M6ADIS0056	.	37932821	"Functionally, SHMT2 silencing suppressed c-myc expression in an m6A-dependent manner, thereby blocking the proliferation, migration, invasion and immune escape abilities of EC cells. Mechanistically, SHMT2 encouraged the accumulation of methyl donor SAM through a one-carbon metabolic network, thereby regulating the m6A modification and stability of c-myc mRNA in a METTL3/FTO/ALKBH5/IGF2BP2-dependent way."
item2137	REG00007	M6ATAR00341	Up	M6ADIS0056	.	37932821	"Functionally, SHMT2 silencing suppressed c-myc expression in an m6A-dependent manner, thereby blocking the proliferation, migration, invasion and immune escape abilities of EC cells. Mechanistically, SHMT2 encouraged the accumulation of methyl donor SAM through a one-carbon metabolic network, thereby regulating the m6A modification and stability of c-myc mRNA in a METTL3/FTO/ALKBH5/IGF2BP3-dependent way."
item2138	REG00001	M6ATAR00341	Down	M6ADIS0056	.	37932821	"Functionally, SHMT2 silencing suppressed c-myc expression in an m6A-dependent manner, thereby blocking the proliferation, migration, invasion and immune escape abilities of EC cells. Mechanistically, SHMT2 encouraged the accumulation of methyl donor SAM through a one-carbon metabolic network, thereby regulating the m6A modification and stability of c-myc mRNA in a METTL3/FTO/ALKBH5/IGF2BP4-dependent way."
item2139	REG00005	M6ATAR00341	Down	M6ADIS0056	.	37932821	"Functionally, SHMT2 silencing suppressed c-myc expression in an m6A-dependent manner, thereby blocking the proliferation, migration, invasion and immune escape abilities of EC cells. Mechanistically, SHMT2 encouraged the accumulation of methyl donor SAM through a one-carbon metabolic network, thereby regulating the m6A modification and stability of c-myc mRNA in a METTL3/FTO/ALKBH5/IGF2BP5-dependent way."
item2140	REG00013	M6ATAR00341	Up	M6ADIS0056	.	37932821	"Functionally, SHMT2 silencing suppressed c-myc expression in an m6A-dependent manner, thereby blocking the proliferation, migration, invasion and immune escape abilities of EC cells. Mechanistically, SHMT2 encouraged the accumulation of methyl donor SAM through a one-carbon metabolic network, thereby regulating the m6A modification and stability of c-myc mRNA in a METTL3/FTO/ALKBH5/IGF2BP6-dependent way."
item2141	REG00001	M6ATAR00901	Up	.	.	38129517	FTO-mediated m6A demethylation regulates GnRH expression in the hypothalamus via the PLCbeta3/Ca2+/CAMK signalling pathway.
item2142	REG00007	M6ATAR00902	Down	M6ADIS0383	.	37478627	"In conclusion, METTL3-mediated cell pyroptosis promotes BPD by regulating the m6A modification of ATG8."
item2143	.	M6ATAR00679	.	M6ADIS0251	.	38187046	"Importantly, ERalpha stimulates m6A dependent maturation of miR199a-5p, which is elevated in ER+ breast cancer, to inhibit CAV1 translation by antagonizing m6A modification of CAV1 mRNA."
item2144	REG00007	M6ATAR00903	Up	.	.	37482682	PARP1 modulates METTL3 promoter chromatin accessibility and associated LPAR5 RNA m6A methylation to control cancer cell radiosensitivity.
item2145	REG00001	M6ATAR00348	Up	M6ADIS0091	.	36327034	m6A binding protein YT521-B homology (YTH) domain family protein 2 (YTHDF2) promoted the degradation of Nrf2 by promoting the m6A methylation level of Nrf2 mRNA.FTO inhibits oxidative stress by mediating m6A demethylation of Nrf2 to alleviate cerebral ischemia/reperfusion injury.
item2146	REG00008	M6ATAR00348	Down	M6ADIS0091	.	36327034	m6A binding protein YT521-B homology (YTH) domain family protein 2 (YTHDF2) promoted the degradation of Nrf2 by promoting the m6A methylation level of Nrf2 mRNA.FTO inhibits oxidative stress by mediating m6A demethylation of Nrf2 to alleviate cerebral ischemia/reperfusion injury.
item2147	REG00015	M6ATAR00140	Up	M6ADIS0065	.	37208522	"Mechanistically, we reveal that VIRMA overexpression upregulates the m6A-modified long non-coding RNA, NEAT1, which contributes to breast cancer cell growth."
item2148	REG00009	M6ATAR00904	Up	M6ADIS0001	.	37260902	"FLOT1, stabilized by WTAP/IGF2BP2 mediated N6-methyladenosine modification, predicts poor prognosis and promotes growth and invasion in gliomas."
item2149	REG00013	M6ATAR00904	Up	M6ADIS0001	.	37260902	"FLOT1, stabilized by WTAP/IGF2BP2 mediated N6-methyladenosine modification, predicts poor prognosis and promotes growth and invasion in gliomas."
item2150	REG00007	M6ATAR00905	Up	M6ADIS0014	.	36908822	METTL3-mediated m6A modification of has_circ_0007905 promotes age-related cataract progression through miR-6749-3p/EIF4EBP1.
item2151	REG00005	M6ATAR00768	Down	M6ADIS0061	.	37149664	"m6A methylation regulates hypoxia-induced pancreatic cancer glycolytic metabolism through ALKBH5-HDAC4-HIF1alpha positive feedback loop.Mechanistically, m6A methylation recognized by m6A reader-YTHDF2 enhanced the stability of HDAC4, and then promoted glycolytic metabolism and migration of PC cells."
item2152	REG00008	M6ATAR00768	Up	M6ADIS0061	.	37149664	"m6A methylation regulates hypoxia-induced pancreatic cancer glycolytic metabolism through ALKBH5-HDAC4-HIF1alpha positive feedback loop.Mechanistically, m6A methylation recognized by m6A reader-YTHDF2 enhanced the stability of HDAC4, and then promoted glycolytic metabolism and migration of PC cells."
item2153	REG00007	M6ATAR00137	Up	M6ADIS0046	.	37588203	RNA m6A reader YTHDF2 facilitates precursor miR-126 maturation to promote acute myeloid leukemia progression.methyltransferase-like 3 (METTL3) adds m6A in primary microRNAs (pri-miRNAs) and facilitates its processing into precursor miRNAs (pre-miRNAs).
item2154	REG00008	M6ATAR00137	Up	M6ADIS0046	.	37588203	RNA m6A reader YTHDF2 facilitates precursor miR-126 maturation to promote acute myeloid leukemia progression.methyltransferase-like 3 (METTL3) adds m6A in primary microRNAs (pri-miRNAs) and facilitates its processing into precursor miRNAs (pre-miRNAs).
item2155	REG00007	M6ATAR00906	Up	M6ADIS0065	M6ADRUG0022	38103759	METTL3 mediated m6A modification of HYOU1 mRNA promoted the doxorubicin resistance in breast cancer cells.IGF2BP3 participates in the m6A modification of HYOU1 mRNA.
item2156	REG00014	M6ATAR00906	Up	M6ADIS0065	M6ADRUG0022	38103759	METTL3 mediated m6A modification of HYOU1 mRNA promoted the doxorubicin resistance in breast cancer cells.IGF2BP3 participates in the m6A modification of HYOU1 mRNA.
item2157	REG00001	M6ATAR00907	.	M6ADIS0007	M6ADRUG0125	37848553	Phenethyl isothiocyanate inhibits metastasis potential of non-small cell lung cancer cells through FTO mediated TLE1 m6A modification.
item2158	REG00007	M6ATAR01453	Down	M6ADIS0065	.	36609396	Knockout of the protein expression of METTL3 or YTHDF2 increased the expression of LATS1 mRNA and suppressed breast cancer tumorigenesis by activating YAP/TAZ in the Hippo pathway.
item2159	REG00008	M6ATAR01453	Down	M6ADIS0065	.	36609396	Knockout of the protein expression of METTL3 or YTHDF2 increased the expression of LATS1 mRNA and suppressed breast cancer tumorigenesis by activating YAP/TAZ in the Hippo pathway.
item2160	.	M6ATAR00908	.	M6ADIS0068	M6ADRUG0158	37056926	m6A-modified circRBM33 promotes prostate cancer progression via PDHA1-mediated mitochondrial respiration regulation and presents a potential target for ARSI(enzalutamide and darolutamide) therapy .
item2161	.	M6ATAR00908	.	M6ADIS0068	M6ADRUG0161	37056926	m6A-modified circRBM33 promotes prostate cancer progression via PDHA1-mediated mitochondrial respiration regulation and presents a potential target for ARSI(enzalutamide and darolutamide) therapy .
item2162	REG00008	M6ATAR00909	Down	M6ADIS0059	.	37381158	ALKBH5/YTHDF2-mediated m6A modification of circAFF2 enhances radiosensitivity of colorectal cancer by inhibiting Cullin neddylation.
item2163	REG00005	M6ATAR00909	Up	M6ADIS0059	.	37381158	ALKBH5/YTHDF2-mediated m6A modification of circAFF2 enhances radiosensitivity of colorectal cancer by inhibiting Cullin neddylation.
item2164	REG00001	M6ATAR00348	Up	M6ADIS0378	.	37122072	"FTO overexpression decreased the m6A methylation of Nrf2 mRNA. Moreover, YTHDF2 bound to Nrf2 mRNA and decreased its stability."
item2165	REG00008	M6ATAR00348	Down	M6ADIS0378	.	37122072	"FTO overexpression decreased the m6A methylation of Nrf2 mRNA. Moreover, YTHDF2 bound to Nrf2 mRNA and decreased its stability."
item2166	REG00012	M6ATAR00277	Up	M6ADIS0257	.	37009154	m6A reader IGF2BP1 accelerates apoptosis of high glucose-induced vascular endothelial cells in a m6A-HMGB1 dependent manner.
item2167	REG00001	M6ATAR00910	Down	M6ADIS0110	.	37005694	FTO-mediated m6A demethylation of pri-miR-3591 alleviates osteoarthritis progression.
item2168	REG00007	M6ATAR00911	Up	M6ADIS0061	.	36781839	"Mechanistically, circMYO1C cyclization was mediated by m6A methyltransferase METTL3. Moreover, methylated RNA immunoprecipitation sequencing (MeRIP-seq) unveiled the remarkable m6A modification on PD-L1 mRNA. Moreover, circMYO1C targeted the m6A site of PD-L1 mRNA to enhance its stability by cooperating with IGF2BP2, thereby accelerating PDAC immune escape."
item2169	REG00013	M6ATAR00360	Up	M6ADIS0061	.	36781839	"Mechanistically, circMYO1C cyclization was mediated by m6A methyltransferase METTL3. Moreover, methylated RNA immunoprecipitation sequencing (MeRIP-seq) unveiled the remarkable m6A modification on PD-L1 mRNA. Moreover, circMYO1C targeted the m6A site of PD-L1 mRNA to enhance its stability by cooperating with IGF2BP2, thereby accelerating PDAC immune escape."
item2170	.	M6ATAR00912	.	M6ADIS0055	.	36127411	m6A-modified circFOXK2 targets GLUT1 to accelerate oral squamous cell carcinoma aerobic glycolysis.circFOXK2 promoted the GLUT1 mRNA stability through cooperating with insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) in a m6A-dependent manner.
item2171	REG00014	M6ATAR00269	Up	M6ADIS0055	.	36127411	m6A-modified circFOXK2 targets GLUT1 to accelerate oral squamous cell carcinoma aerobic glycolysis.circFOXK2 promoted the GLUT1 mRNA stability through cooperating with insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) in a m6A-dependent manner.
item2172	REG00001	M6ATAR01454	Up	M6ADIS0059	M6ADRUG0005	36307991	"SIVA1, a critical apoptotic gene, as a key downstream target of the FTO-mediated m6A demethylation. The m6A demethylation of SIVA1 at the CDS region induced its mRNA degradation via a YTHDF2-dependent mechanism.FTO inhibition may restore the sensitivity of chemo-resistant CRC cells to 5-FU."
item2173	REG00008	M6ATAR01454	Down	M6ADIS0059	M6ADRUG0005	36307991	"SIVA1, a critical apoptotic gene, as a key downstream target of the FTO-mediated m6A demethylation. The m6A demethylation of SIVA1 at the CDS region induced its mRNA degradation via a YTHDF2-dependent mechanism.FTO inhibition may restore the sensitivity of chemo-resistant CRC cells to 5-FU."
item2174	REG00005	M6ATAR00913	Down	M6ADIS0274	M6ADRUG0022	36876119	"ALKBH5 regulated the expression of Rasal3 in an m6A-dependent manner through posttranscriptional mRNA regulation and reduced Rasal3 mRNA stability, thus activating RAS3, inhibiting apoptosis through the RAS/RAF/ERK signaling pathway, and alleviating DIC injury. These findings indicate the potential therapeutic effect of ALKBH5 on DIC."
item2175	REG00008	M6ATAR00690	Down	M6ADIS0146	M6ADRUG0024	37700438	"The YTHDF2/DAPK3 axis induces the resistance of GBC cells to gemcitabine. In conclusion, we reveal the oncogenic role of YTHDF2 in GBC, demonstrating that YTHDF2 increases the mRNA degradation of the tumor suppressor DAPK3 in an m6A-dependent way, which promotes GBC progression and desensitizes GBC cells to gemcitabine."
item2176	REG00007	M6ATAR01455	Up	M6ADIS0001	.	36086906	"That HOTAIRM1, methyltransferase-like 3 (METTL3), and insulin-like growth factor binding protein 2 (IGFBP2) were upregulated in glioma tissues and cell lines. HOTAIRM1 functions as an oncogene in glioma progression; however, knockdown of HOTAIRM1 significantly reduced cell viability, migration, invasion, and VM formation. Notably, METTL3-dependent m6A modification enhanced HOTAIRM1 mRNA stability, whereas knockdown of METTL3 deficiency significantly suppressed VM in glioma. Moreover, HOTAIRM1 was found to bind IGFBP2, and HOTAIRM1 deficiency blocked glioma progression and VM formation in vivo. Our results indicated that METTL3-dependent m6A-modified HOTAIRM1 promoted VM formation in glioma."
item2177	REG00034	M6ATAR01455	Up	M6ADIS0001	.	36086906	"That HOTAIRM1, methyltransferase-like 3 (METTL3), and insulin-like growth factor binding protein 2 (IGFBP2) were upregulated in glioma tissues and cell lines. HOTAIRM1 functions as an oncogene in glioma progression; however, knockdown of HOTAIRM1 significantly reduced cell viability, migration, invasion, and VM formation. Notably, METTL3-dependent m6A modification enhanced HOTAIRM1 mRNA stability, whereas knockdown of METTL3 deficiency significantly suppressed VM in glioma. Moreover, HOTAIRM1 was found to bind IGFBP2, and HOTAIRM1 deficiency blocked glioma progression and VM formation in vivo. Our results indicated that METTL3-dependent m6A-modified HOTAIRM1 promoted VM formation in glioma."
item2178	REG00006	M6ATAR00605	Up	M6ADIS0233	.	35226250	NLRP3 mRNA stability was enhanced by METTL14-mediated m6A methylation during arsenic-induced hepatic IR.
item2179	REG00005	M6ATAR00298	Up	M6ADIS0053	.	36632222	"ALKBH5 overexpression also reversed the m6A modification in ITGB1 mRNA and suppressed the YTHDF2 protein-mediated m6A-dependent ITGB1 mRNA degradation, which resulted in increased expression of ITGB1 and phosphorylation of the focal adhesion kinase (FAK) and Src proto-oncogene proteins, thereby increasing LN metastasis."
item2180	REG00008	M6ATAR00298	Down	M6ADIS0053	.	36632222	"ALKBH5 overexpression also reversed the m6A modification in ITGB1 mRNA and suppressed the YTHDF2 protein-mediated m6A-dependent ITGB1 mRNA degradation, which resulted in increased expression of ITGB1 and phosphorylation of the focal adhesion kinase (FAK) and Src proto-oncogene proteins, thereby increasing LN metastasis."
item2181	REG00007	M6ATAR00596	Up	M6ADIS0097	.	37898386	"METTL3-mediated m6A modification promotes sympathetic hyperactivity through TRAF6/ECSIT pathway and mitochondrial oxidative stress in the PVN, thereby leading to ventricular arrhythmias post-MI."
item2182	REG00013	M6ATAR01456	Up	M6ADIS0046	.	36574771	"Mechanistically, IGF2BP2 stabilizes PRMT6 mRNA via m6A-mediated manner, which catalyzes H3R2me2a and suppresses lipid transporter MFSD2A expression."
item2183	REG00007	M6ATAR01457	Up	M6ADIS0007	.	37037089	DGUOK-AS1 silencing decreases NSCLC cell growth and metastasis by decreasing METTL3/IGF2BP2-mediated TRPM7 stability.
item2184	REG00013	M6ATAR01457	Up	M6ADIS0007	.	37037089	DGUOK-AS1 silencing decreases NSCLC cell growth and metastasis by decreasing METTL3/IGF2BP2-mediated TRPM7 stability.
item2185	REG00007	M6ATAR00914	Up	M6ADIS0094	.	36608773	METTL3 was able to promote the maturation of miR-181a-5p and then inhibited the expression of NF-kappaB and IL-1alpha.
item2186	REG00007	M6ATAR00404	Up	M6ADIS0087	M6ADRUG0135	36977205	METTL3 relieved the injury of the SH-SY5Y cells induced by LPS treatment and sevoflurane exposure through regulating the m6A and mRNA levels of Sox2.
item2187	REG00012	M6ATAR00484	Up	M6ADIS0026	.	37783915	HIF-1alpha-induced upregulation of m6A reader IGF2BP1 facilitates peripheral nerve injury recovery by enhancing SLC7A11 mRNA stabilization.
item2188	REG00007	M6ATAR00915	Up	M6ADIS0363	M6ADRUG0139	37537731	Genetic and pharmacological inhibition of METTL3 alleviates renal fibrosis by reducing EVL m6A modification through an IGF2BP2-dependent mechanism.Upregulated METTL3 enhanced the m6A modification of EVL mRNA to improve its stability and expression in an insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2)-dependent manner.
item2189	REG00013	M6ATAR00915	Up	M6ADIS0363	M6ADRUG0139	37537731	Genetic and pharmacological inhibition of METTL3 alleviates renal fibrosis by reducing EVL m6A modification through an IGF2BP2-dependent mechanism.Upregulated METTL3 enhanced the m6A modification of EVL mRNA to improve its stability and expression in an insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2)-dependent manner.
item2190	REG00023	M6ATAR00513	Down	.	.	37636387	YTHDC2 inhibits rat bone mesenchymal stem cells osteogenic differentiation by accelerating RUNX2 mRNA degradation via m6A methylation.
item2191	REG00007	M6ATAR00446	Up	M6ADIS0145	.	37356601	"Mechanistically, METTL3 regulated LRP6 expression through post-transcriptional mRNA modification in an m6A-dependent manner, increasing its stability, upregulating VEGFA expression, and promoting angiogenesis in HSV-1-infected HUVECs. Furthermore, METTL3 knockdown or inhibition by STM2457 reduced CNV in vivo."
item2192	REG00024	M6ATAR00916	Up	M6ADIS0291	.	37564203	The m6A reader YTHDF1 attenuates fulminant hepatitis via MFG-E8 translation in an m6A dependent manner.
item2193	REG00005	M6ATAR00917	Up	M6ADIS0059	.	37203239	"Mechanistically, RAB5A was identified as the downstream target of ALKBH5 in CRC development, and ALKBH5 posttranscriptionally activated RAB5A by m6A demethylation, which impeded the YTHDF2-mediated degradation of RAB5A mRNA. In addition, we demonstrated that dysregulation of the ALKBH5-RAB5A axis could affect the tumourigenicity of CRC."
item2194	REG00008	M6ATAR00917	Down	M6ADIS0059	.	37203239	"Mechanistically, RAB5A was identified as the downstream target of ALKBH5 in CRC development, and ALKBH5 posttranscriptionally activated RAB5A by m6A demethylation, which impeded the YTHDF2-mediated degradation of RAB5A mRNA. In addition, we demonstrated that dysregulation of the ALKBH5-RAB5A axis could affect the tumourigenicity of CRC."
item2195	REG00007	M6ATAR00477	.	M6ADIS0029	.	37606168	METTL3-mediated m6A modification of lncRNA SNHG3 promoted the growth and invasion of melanoma cells by regulating the miR-330-5p/CNBP axis.
item2196	REG00006	M6ATAR00393	Up	M6ADIS0115	.	36584783	METTL14 alleviates the development of osteoporosis in ovariectomized mice by upregulating m6A level of SIRT1 mRNA.
item2197	REG00007	M6ATAR00450	Up	M6ADIS0144	.	36546578	"MiR-21-5p inhibited the METTL3-mediated m6A modification and mRNA stability of WIF1, thereby facilitating the proliferation, invasion, and migration of Ect-ESCs."
item2198	REG00001	M6ATAR00918	Down	M6ADIS0368	.	36378581	Fat mass and obesity-associated protein alleviates Abeta1-40 induced retinal pigment epithelial cells degeneration via PKA/CREB signaling pathway.the m6A-mRNA epitranscriptomic microarray suggested that protein kinase A (PKA) was a target of FTO.
item2199	REG00007	M6ATAR00919	Down	M6ADIS0061	.	37998732	This study demonstrates the promise of BANCR as a new diagnostic and therapeutic target for pancreatic cancer and reveals the therapeutic effect that STM2457(METTL3) exerts on pancreatic cancer by down-regulating BANCR m6A modifications.
item2200	REG00007	M6ATAR00675	Up	M6ADIS0091	.	37610605	"Mechanical experiments confirmed that METTL3 m6A dependently increased stability and expression levels of ABHD11-AS1, and elevated ABHD11-AS1 sponged miR-1301-3p to upregulate HIF1AN, resulting in the downregulation of HIF-1alpha. this study firstly reported a novel METTL3/m6A/ ABHD11-AS1/miR-1301-3p/HIF1AN/HIF-1alpha signaling cascade in regulating the progression of cerebral I/R injury, and future work will focus on investigating whether the above genes can be used as biomarkers for the treatment of cerebral I/R injury by performing clinical studies."
item2201	REG00020	M6ATAR00920	Up	M6ADIS0172	.	37625827	RBM15 knockdown suppressed proliferation and inflammation by mediating m6A modification of K17 to reduce K17 stability in IL-17A-induced keratinocytes. Our findings may provide novel idea for improving the treatment of psoriasis.
item2202	REG00009	M6ATAR00921	Down	M6ADIS0110	.	37563688	"m6A modification mediated by WTAP promotes the maturation of pri-miR-92b to miR-92b-5p, thereby enhancing the targeted inhibitory function of miR-92b-5p on TIMP4. Furthermore, we have discovered that WTAP can directly facilitate the degradation of TIMP4 mRNAs in a YTHDF2-dependent manner."
item2203	REG00009	M6ATAR01458	Up	M6ADIS0110	.	37563688	"m6A modification mediated by WTAP promotes the maturation of pri-miR-92b to miR-92b-5p, thereby enhancing the targeted inhibitory function of miR-92b-5p on TIMP4. Furthermore, we have discovered that WTAP can directly facilitate the degradation of TIMP4 mRNAs in a YTHDF2-dependent manner."
item2204	REG00008	M6ATAR01458	Up	M6ADIS0110	.	37563688	"m6A modification mediated by WTAP promotes the maturation of pri-miR-92b to miR-92b-5p, thereby enhancing the targeted inhibitory function of miR-92b-5p on TIMP4. Furthermore, we have discovered that WTAP can directly facilitate the degradation of TIMP4 mRNAs in a YTHDF2-dependent manner."
item2205	REG00008	M6ATAR00420	Down	.	.	37884231	Ythdf2-mediated STK11 mRNA decay supports myogenesis by inhibiting the AMPK/mTOR pathway.
item2206	REG00015	.	.	M6ADIS0006	M6ADRUG0032	36420693	KIAA1429 mediates epithelial mesenchymal transition in sorafenib-resistant hepatocellular carcinoma through m6A methylation modification.
item2207	REG00007	M6ATAR00771	Up	M6ADIS0020	M6ADRUG0133	37481861	"Methyltransferase 3 (Mettl3) catalysed N6-methyladenosine (m6A) methylation of Ldha mRNA. Mettl3 was downregulated in Sertoli cells following exposure to MC-LR, decreasing m6A levels of Ldha."
item2208	REG00008	M6ATAR00922	.	M6ADIS0007	.	37669906	"These findings identified a novel m6A-modified circFUT8 recognized and destabilized by YTHDF2, which competitively interacted with YTHDF2 and miR-186-5p to stabilize FUT8 mRNA to promote malignant progression in LUAD."
item2209	REG00014	M6ATAR00824	Up	M6ADIS0001	.	37156775	RNA N6-methyladenosine reader IGF2BP3 interacts with MYCN and facilitates neuroblastoma cell proliferation.
item2210	REG00007	M6ATAR00923	Up	M6ADIS0068	.	37449729	METTL3-mediated m6A modification of pri-miR-148a-3p affects prostate cancer progression by regulating TXNIP.
item2211	REG00013	M6ATAR00924	Up	M6ADIS0073	.	38102465	m6A reader IGF2BP2 promotes lymphatic metastasis by stabilizing DPP4 in papillary thyroid carcinoma.
item2212	REG00024	M6ATAR00925	Up	M6ADIS0068	.	38042806	RNA N6-methyladenosine-modified-binding protein YTHDF1 promotes prostate cancer progression by regulating androgen function-related gene TRIM68.
item2213	REG00009	M6ATAR00926	Down	M6ADIS0058	.	36849408	WTAP regulates autophagy in colon cancer cells by inhibiting FLNA through N6-methyladenosine.
item2214	REG00007	M6ATAR00141	Up	M6ADIS0250	.	37605570	"ES samples expressed low miR-124-3p and high METTL3, MALAT1 and CDK4. METTL3 elevated MALAT1 expression by m6A modification. MALAT1 enhanced CDK4 expression by competing with miR-124-3p. In ES cells, METTL3 silencing repressed cell migration and invasion by inhibiting MALAT1. In conclusion, METTL3 promotes tumorigenesis of ES through the MALAT1/miR-124-3p/CDK4 axis."
item2215	REG00005	M6ATAR00217	Down	M6ADIS0110	.	37524872	"Downregulation of ALKBH5 expression facilitated MSC senescence by enhancing the stability of CYP1B1 mRNA and inducing mitochondrial dysfunction. In addition, IGF2BP1 was identified as the m6A reader restraining the degradation of m6A-modified CYP1B1 mRNA."
item2216	REG00012	M6ATAR00217	Up	M6ADIS0110	.	37524872	"Downregulation of ALKBH5 expression facilitated MSC senescence by enhancing the stability of CYP1B1 mRNA and inducing mitochondrial dysfunction. In addition, IGF2BP1 was identified as the m6A reader restraining the degradation of m6A-modified CYP1B1 mRNA."
item2217	REG00001	M6ATAR01459	Up	M6ADIS0054	M6ADRUG0152	36343416	m6A demethylase FTO renders radioresistance of nasopharyngeal carcinoma via promoting OTUB1-mediated anti-ferroptosis. FTO inhibitor FB23-2 and the ferroptosis activator erastin altered NPC responsiveness to radiotherapy.
item2218	REG00001	M6ATAR01459	Up	M6ADIS0054	M6ADRUG0157	36343416	m6A demethylase FTO renders radioresistance of nasopharyngeal carcinoma via promoting OTUB1-mediated anti-ferroptosis. FTO inhibitor FB23-2 and the ferroptosis activator erastin altered NPC responsiveness to radiotherapy.
item2219	REG00007	M6ATAR00265	Up	.	.	37400674	Targeted m6A demethylation destabilizes nascent Gata3 mRNA and abolishes the upregulation of GATA3 and ILC2 activation. Our study suggests a lineage-specific requirement of m6A for ILC2 responses.
item2220	REG00009	M6ATAR01460	.	M6ADIS0382	.	37019244	"Mechanistically, WTAP affected the enrichment of H3K9me3 at the CCL2 promoter by regulating the m6A level of SUV39H1 mRNA. The in vivo experiment showed that VEGFA/C/D secretion of macrophages was reduced after WTAP interference. Mechanistically, WTAP regulated the translational efficiency of HIF-1alpha via m6A modification."
item2221	REG00007	M6ATAR01461	Up	M6ADIS0102	.	36947363	"Subsequently, it promotes METTL3 METTL14 complex mediated m6A modification of rip3 mRNA. Meanwhile, the level of rip3 mRNA becomes more stable under the m6A reader of YTHDF3, which increases the protein level of RIP3 and further induces VSMC necroptosis. In addition, cell debris induces inflammatory factors in neighboring VSMCs and recruit monocytes/macrophages to the lesion."
item2222	REG00006	M6ATAR01461	Up	M6ADIS0102	.	36947363	"Subsequently, it promotes METTL3 METTL14 complex mediated m6A modification of rip3 mRNA. Meanwhile, the level of rip3 mRNA becomes more stable under the m6A reader of YTHDF3, which increases the protein level of RIP3 and further induces VSMC necroptosis. In addition, cell debris induces inflammatory factors in neighboring VSMCs and recruit monocytes/macrophages to the lesion."
item2223	REG00025	M6ATAR01461	Up	M6ADIS0102	.	36947363	"Subsequently, it promotes METTL3 METTL14 complex mediated m6A modification of rip3 mRNA. Meanwhile, the level of rip3 mRNA becomes more stable under the m6A reader of YTHDF3, which increases the protein level of RIP3 and further induces VSMC necroptosis. In addition, cell debris induces inflammatory factors in neighboring VSMCs and recruit monocytes/macrophages to the lesion."
item2224	REG00005	M6ATAR01462	Up	M6ADIS0068	.	37493109	"USF1 activates ALKBH5 to stabilize FLII mRNA in an m6A-YTHDF2-dependent manner, thereby repressing glycolysis processes and the progression of PRAD."
item2225	REG00008	M6ATAR01462	Up	M6ADIS0068	.	37493109	"USF1 activates ALKBH5 to stabilize FLII mRNA in an m6A-YTHDF2-dependent manner, thereby repressing glycolysis processes and the progression of PRAD."
item2226	REG00018	M6ATAR01463	Up	M6ADIS0006	.	37735874	METTL5-mediated 18S rRNA m6A modification promotes oncogenic mRNA translation and intrahepatic cholangiocarcinoma progression.
item2227	REG00005	M6ATAR01464	Up	M6ADIS0026	.	37452367	"In terms of its mechanism, ALKBH5 promoted PELI2 expression by removing the m6A modification from PELI2 mRNA and enhancing its stability in a YTHDF2-dependent manner."
item2228	REG00008	M6ATAR01464	Down	M6ADIS0026	.	37452367	"In terms of its mechanism, ALKBH5 promoted PELI2 expression by removing the m6A modification from PELI2 mRNA and enhancing its stability in a YTHDF2-dependent manner."
item2229	REG00001	M6ATAR01465	Up	M6ADIS0091	.	36717587	"Mechanically, circSCMH1 increased the translocation of ubiquitination-modified fat mass and obesity-associated protein (FTO) into nucleus of endothelial cells (ECs), leading to m6A demethylation of phospholipid phosphatase 3 (Plpp3) mRNA and subsequently the increase of Plpp3 expression in ECs. Our data demonstrate that circSCMH1 enhances vascular repair via FTO-regulated m6A methylation after stroke, providing insights into the mechanism of circSCMH1 in promoting stroke recovery."
item2230	REG00004	M6ATAR00258	Up	M6ADIS0067	M6ADRUG0047	38091112	HNRNPA2B1-mediated m6A modification of FOXM1 promotes drug resistance and inhibits ferroptosis in endometrial cancer via regulation of LCN2.
item2231	REG00024	M6ATAR01466	Up	.	.	36693099	The m6A modification in the 5' untranslated region (5'-UTR) of Pgr mRNA enhances PGR protein translation efficiency in a YTHDF1-dependent manner.this study provides evidence that METTL3 is essential for normal P4signaling during embryo implantation via m6A-mediated translation control of Pgr mRNA.
item2232	REG00007	M6ATAR01466	Up	.	.	36693099	The m6A modification in the 5' untranslated region (5'-UTR) of Pgr mRNA enhances PGR protein translation efficiency in a YTHDF1-dependent manner.this study provides evidence that METTL3 is essential for normal P4signaling during embryo implantation via m6A-mediated translation control of Pgr mRNA.
item2233	REG00007	M6ATAR01467	Up	M6ADIS0167	.	37013484	"METTL3 was required for stabilizing Foxp3 mRNA via m6A modification to maintain the Treg differentiation program. METTL3 inhibition contributed to the pathogenesis of SLE by participating in the activation of CD4+T cells and imbalance of effector T-cell differentiation, which could serve as a potential target for therapeutic intervention in SLE."
item2234	REG00008	M6ATAR00927	Up	.	M6ADRUG0148	38152479	"Mechanistically, BHPF-mediated downregulation of YTHDF2 reduced YTHDF2-facilitated translation of m6A-gch1 for cardiomyocyte ferroptosis, and decreased YTHDF2-mediated m6A-sting1 decay for caudal vein plexus (CVP) apoptosis."
item2235	REG00008	M6ATAR00419	Up	.	M6ADRUG0148	38152479	"Mechanistically, BHPF-mediated downregulation of YTHDF2 reduced YTHDF2-facilitated translation of m6A-gch1 for cardiomyocyte ferroptosis, and decreased YTHDF2-mediated m6A-sting1 decay for caudal vein plexus (CVP) apoptosis."
item2236	REG00005	M6ATAR00928	Up	M6ADIS0007	.	37700507	"At the molecular level, ALKBH5 enrichment increased ADIRF mRNA levels and prevented the attenuation of ADIRF mRNA by YTHDC2. The effects of ALKBH5 overexpression could also extend to the inhibition of LUAD cell proliferation and metastasis. This study linked ADIRF with the m6A modifying regulators ALKBH5 and YTHDC2, providing a promising molecular intervention for LUAD and deepening the understanding of LUAD mechanisms."
item2237	REG00023	M6ATAR00928	Down	M6ADIS0007	.	37700507	"At the molecular level, ALKBH5 enrichment increased ADIRF mRNA levels and prevented the attenuation of ADIRF mRNA by YTHDC2. The effects of ALKBH5 overexpression could also extend to the inhibition of LUAD cell proliferation and metastasis. This study linked ADIRF with the m6A modifying regulators ALKBH5 and YTHDC2, providing a promising molecular intervention for LUAD and deepening the understanding of LUAD mechanisms."
item2238	REG00005	M6ATAR00451	.	M6ADIS0018	M6ADRUG0187	37393819	ALKBH5-mediated YAP m6A modification changed in VCD - induced premature ovarian insufficiency.
item2239	REG00007	M6ATAR00427	Up	M6ADIS0232	.	37105375	METTL3 silenced inhibited the ferroptosis development via regulating the TFRC levels in the Intracerebral hemorrhage progression.
item2240	REG00007	M6ATAR00276	Up	M6ADIS0368	.	36945110	METTL3-mediated m6A modification of HMGA2 mRNA promotes subretinal fibrosis and epithelial-mesenchymal transition.
item2241	REG00005	M6ATAR00930	Up	M6ADIS0007	.	37949419	ALKBH5 promotes the development of lung adenocarcinoma by regulating the polarization of M2 macrophages through CDCA4.
item2242	REG00023	M6ATAR00930	Up	M6ADIS0007	.	37949419	ALKBH5 promotes the development of lung adenocarcinoma by regulating the polarization of M2 macrophages through CDCA4.
item2243	REG00012	M6ATAR00931	Up	M6ADIS0066	.	37304234	"LncRNA CACNA1G-AS1 could up-regulate FTH1 expression through IGF2BP1 axis, thus inhibited ferroptosis by regulating ferritinophagy, and finally promoted proliferation and migration in ovarian cancer cells."
item2244	REG00007	M6ATAR00932	Up	M6ADIS0048	.	37222774	m6A methyltransferase METTL3 facilitates multiple myeloma cell growth through the m6A modification of BZW2.
item2245	REG00044	M6ATAR00360	Up	M6ADIS0006	.	37063837	LRPPRC facilitates tumor progression and immune evasion through upregulation of m6A modification of PD-L1 mRNA in hepatocellular carcinoma.
item2246	REG00009	M6ATAR00259	Up	M6ADIS0025	.	38189389	m6A methylase WTAP participates in renal ischemia-reperfusion injury by regulating FOXO1 expression.
item2247	REG00015	M6ATAR01468	Down	M6ADIS0166	.	37721438	VIRMA promotes neuron apoptosis via inducing m6A methylation of STK10 in spinal cord injury animal models.
item2248	REG00020	M6ATAR00894	.	M6ADIS0148	.	36803098	RBM15 suppresses hepatic insulin sensitivity of offspring of gestational diabetes mellitus mice via m6A-mediated regulation of CLDN4.
item2249	REG00017	M6ATAR00360	Down	M6ADIS0059	.	37647025	m6A methyltransferase METTL16 mediates immune evasion of colorectal cancer cells via epigenetically regulating PD-L1 expression.
item2250	REG00006	M6ATAR00933	Up	M6ADIS0166	.	37094938	The METTL14-catalyzed m6A methylation of UBR1 promoted apoptosis and inhibited autophagy in SCI.
item2251	REG00007	M6ATAR00934	Up	M6ADIS0006	.	37658413	METTL3 was upregulated in HCC and closely related to HCC prognosis. And METTL3 induced GBAP1 expression by acting as the m6A writer of GBAP1 and IGF2BP2 worked as its m6A reader.
item2252	REG00013	M6ATAR00934	Up	M6ADIS0006	.	37658413	METTL3 was upregulated in HCC and closely related to HCC prognosis. And METTL3 induced GBAP1 expression by acting as the m6A writer of GBAP1 and IGF2BP2 worked as its m6A reader.
item2253	REG00007	M6ATAR01469	.	M6ADIS0099	.	36583755	"METTL3-mediated NPC1L1 mRNA hypermethylation facilitates AS progression by regulating the MAPK pathway, and NPC1L1 may be a novel target for the treatment of AS."
item2254	REG00007	M6ATAR00935	Up	.	.	38030520	"Remarkably, Mettl3 binds to the Tbx21 transcript and stabilizes it, promoting effector differentiation of CD8+T cells."
item2255	REG00007	M6ATAR00704	Up	M6ADIS0057	.	37999596	Depicting the Profile of METTL3-Mediated lncRNA m6A Modification Variants and Identified SNHG7 as a Prognostic Indicator of MNNG-Induced Gastric Cancer.
item2256	REG00015	M6ATAR00936	Up	M6ADIS0054	.	37028765	"Mechanistically, VIRMA mediated the m6A methylation of E2F7 3'-UTR, then IGF2BP2 bound, and maintained the stability of E2F7 mRNA.E2F7 cooperated with CBFB-recruited RUNX1 in a non-canonical manner to transactivate ITGA2, ITGA5, and NTRK1, strengthening Akt signaling-induced tumor-promoting effect."
item2257	REG00013	M6ATAR00936	Up	M6ADIS0054	.	37028765	"Mechanistically, VIRMA mediated the m6A methylation of E2F7 3'-UTR, then IGF2BP2 bound, and maintained the stability of E2F7 mRNA.E2F7 cooperated with CBFB-recruited RUNX1 in a non-canonical manner to transactivate ITGA2, ITGA5, and NTRK1, strengthening Akt signaling-induced tumor-promoting effect."
item2258	REG00001	M6ATAR00937	Down	M6ADIS0057	.	38082402	"Mechanistically, this work uncovered a crucial suppressive role of FTO in EBVaGC metastasis and invasiveness via an m6A-FOS-IGF2BP1/2-dependent manner, suggesting a promising biomarker panel for GC metastatic prediction and therapy."
item2259	REG00012	M6ATAR00937	Up	M6ADIS0057	.	38082402	"Mechanistically, this work uncovered a crucial suppressive role of FTO in EBVaGC metastasis and invasiveness via an m6A-FOS-IGF2BP1/2-dependent manner, suggesting a promising biomarker panel for GC metastatic prediction and therapy."
item2260	REG00013	M6ATAR00937	Up	M6ADIS0057	.	38082402	"Mechanistically, this work uncovered a crucial suppressive role of FTO in EBVaGC metastasis and invasiveness via an m6A-FOS-IGF2BP1/2-dependent manner, suggesting a promising biomarker panel for GC metastatic prediction and therapy."
item2261	REG00005	M6ATAR00938	Up	.	.	37535403	"Mechanistically, ALKBH5 increased the stability of Lpin2 mRNA and thus limited regenerative growth associated lipid metabolism in dorsal root ganglion neurons."
item2262	REG00009	M6ATAR00939	Down	M6ADIS0046	.	37087529	HIF1alpha-mediated WTAP high expression enhances the malignant behavior of leukemia cells and drives a crosstalk between m6A RNA methylation and histone methylation through monitoring m6A-dependant KDM4B translation.
item2263	REG00007	M6ATAR00940	Down	M6ADIS0164	.	37957139	"Furthermore, the METTL3/YTHDF3-m6A/PTX3 interactions contribute to autophagy maturation in macrophages by modulating STX17 expression."
item2264	REG00025	M6ATAR00940	Down	M6ADIS0164	.	37957139	"Furthermore, the METTL3/YTHDF3-m6A/PTX3 interactions contribute to autophagy maturation in macrophages by modulating STX17 expression."
item2265	REG00005	M6ATAR00941	.	M6ADIS0001	.	37979586	ALKBH5 critically regulated ferroptosis through m6A modulation and YTH N6-methyladenosine RNA binding protein (YTHDF2)-mediated decay of the glutamate-cysteine ligase modifier subunit (GCLM).
item2266	REG00008	M6ATAR00941	.	M6ADIS0001	.	37979586	ALKBH5 critically regulated ferroptosis through m6A modulation and YTH N6-methyladenosine RNA binding protein (YTHDF2)-mediated decay of the glutamate-cysteine ligase modifier subunit (GCLM).
item2267	REG00001	M6ATAR00283	Down	M6ADIS0059	.	37580808	This study revealed the FTO-ALKBH5/IGF2BP2/HK2/FOXO1 axis as a mechanism of aberrant m6A modification and glycolysis regulation in CRC.
item2268	REG00005	M6ATAR00283	Down	M6ADIS0059	.	37580808	This study revealed the FTO-ALKBH5/IGF2BP2/HK2/FOXO1 axis as a mechanism of aberrant m6A modification and glycolysis regulation in CRC.
item2269	REG00013	M6ATAR00283	Up	M6ADIS0059	.	37580808	This study revealed the FTO-ALKBH5/IGF2BP2/HK2/FOXO1 axis as a mechanism of aberrant m6A modification and glycolysis regulation in CRC.
item2270	REG00001	M6ATAR00942	.	M6ADIS0364	.	36823977	FTO suppressed the differentiating ability of hair follicle-derived NCSCs into MCs by m6A modifying Mitf.
item2271	REG00001	M6ATAR00943	Up	M6ADIS0057	M6ADRUG0005	36628934	FTO contributes to the increasing resistance of GC cells to 5-fluorouracil (5-Fu) by upregulating CDKAL1 and inducing mitochondrial fusion.
item2272	REG00007	M6ATAR01470	Down	M6ADIS0070	.	36960869	METTL3 could bind to the m6A sites of RRAS mRNA and suppress the transcriptional activity of RRAS. YTHDF2 could recognize the m6A sites of RRAS and mediate RRAS degradation.Targeting the METTL3/RRAS/YTHDF2 regulatory axis may thus prove to be a promising strategy for the diagnosis and therapy of BCa.
item2273	REG00008	M6ATAR01470	Down	M6ADIS0070	.	36960869	METTL3 could bind to the m6A sites of RRAS mRNA and suppress the transcriptional activity of RRAS. YTHDF2 could recognize the m6A sites of RRAS and mediate RRAS degradation.Targeting the METTL3/RRAS/YTHDF2 regulatory axis may thus prove to be a promising strategy for the diagnosis and therapy of BCa.
item2274	REG00045	.	Up	M6ADIS0068	.	36632223	RNA-binding protein KHSRP recognized both m6A at eRNA and m6Am at 5'-UTR of mRNA to block RNA degradation from exoribonuclease XRN2. Depletion of the MLXIPe/KHSRP/PSMD9 regulatory complex inhibited tumor growth and RT sensitization of bone mPCa xenograft in vitro and in vivo.
item2275	REG00013	M6ATAR00212	Up	M6ADIS0027	.	37816718	IGF2BP2 acts as a m6A modification regulator in laryngeal squamous cell carcinoma through facilitating CDK6 mRNA stabilization.
item2276	REG00007	M6ATAR00944	Up	M6ADIS0061	.	37293163	"METTL3 was upregulated in PC tissues and cells and was associated with malignant tumor progression and poor progression-free survival in PC.Four m6A motifs were identified in Linc00662, which maintained the stability of Linc00662 in an IGF2BP3-coupled manner and were closely associated with the pro-tumor properties of Linc00662 in vitro and in vivo."
item2277	REG00014	M6ATAR00944	Up	M6ADIS0061	.	37293163	"METTL3 was upregulated in PC tissues and cells and was associated with malignant tumor progression and poor progression-free survival in PC.Four m6A motifs were identified in Linc00662, which maintained the stability of Linc00662 in an IGF2BP3-coupled manner and were closely associated with the pro-tumor properties of Linc00662 in vitro and in vivo."
item2278	REG00007	M6ATAR00945	Up	M6ADIS0091	.	37030526	"METTL3 ameliorates rat OLT-stressed IRI by inducing HO-1 in an m6A-dependent manner, highlighting a potential target for IRI in liver transplantation."
item2279	REG00007	M6ATAR00610	Down	M6ADIS0377	.	37405565	"Depletion of METTL3 attenuated IL-17A and CCR5 expression by facilitating SOCS3 mRNA stability in Th17 cells, leading to disrupted Th17 cell differentiation and infiltration, and eventually attenuating the process of EAE."
item2280	REG00001	M6ATAR01471	Down	M6ADIS0185	.	37321527	FTO alleviates cerebral ischemia/reperfusion-induced neuroinflammation by decreasing cGAS mRNA stability in an m6A-dependent manner.
item2281	REG00007	M6ATAR00451	Up	M6ADIS0166	.	36653190	"USP1/UAF1-Stabilized METTL3 Promotes Reactive Astrogliosis and Improves Functional Recovery after Spinal Cord Injury through m6A Modification of YAP1 mRNA.Mechanistically, the YAP1 transcript was identified as a potential target of METTL3 in astrocytes. METTL3 could selectively methylate the 3'-UTR region of the YAP1 transcript, which subsequently maintains its stability in an IGF2BP2-dependent manner."
item2282	REG00013	M6ATAR00451	Up	M6ADIS0166	.	36653190	"USP1/UAF1-Stabilized METTL3 Promotes Reactive Astrogliosis and Improves Functional Recovery after Spinal Cord Injury through m6A Modification of YAP1 mRNA.Mechanistically, the YAP1 transcript was identified as a potential target of METTL3 in astrocytes. METTL3 could selectively methylate the 3'-UTR region of the YAP1 transcript, which subsequently maintains its stability in an IGF2BP2-dependent manner."
item2283	REG00008	M6ATAR00567	Down	M6ADIS0070	M6ADRUG0183	36939388	The m6A Reader YTHDF2 Promotes Bladder Cancer Progression by Suppressing RIG-I-Mediated Immune Response.Recent studies have shown that m6A methyltransferases METTL3 and METTL14 play important roles in urothelial bladder carcinoma (BLCA).
item2284	REG00005	M6ATAR01472	Down	M6ADIS0395	.	37385994	"High glucose suppresses the demethylation modification of Dgkh by ALKBH5, which downregulates Dgkh and leads to tau hyperphosphorylation through activation of PKC-alpha in hippocampal neurons. These findings may indicate a new mechanism and a novel therapeutic target for diabetic cognitive dysfunction."
item2285	REG00007	M6ATAR00946	.	M6ADIS0070	M6ADRUG0047	37108067	This study proposes a novel METTL3/YTHDF1-RPN2-PI3K/AKT/mTOR regulatory axis that affects bladder cancer cell proliferation and cisplatin sensitivity.
item2286	REG00024	M6ATAR00946	.	M6ADIS0070	M6ADRUG0047	37108067	This study proposes a novel METTL3/YTHDF1-RPN2-PI3K/AKT/mTOR regulatory axis that affects bladder cancer cell proliferation and cisplatin sensitivity.
item2287	REG00001	M6ATAR00947	Down	M6ADIS0004	.	36478193	"Silencing of IRF8 Mediated by m6A Modification Promotes the Progression of T-Cell Acute Lymphoblastic Leukemia.The fat mass- and obesity-associated protein (FTO), an m6A demethylase, is responsible for directly binding to m6A sites in 3' untranslated region of IRF8 messenger RNA (mRNA) and inducing mRNA degradation via m6A modification."
item2288	REG00001	M6ATAR00192	Up	M6ADIS0088	.	37737187	FTO-targeted siRNA delivery by MSC-derived exosomes synergistically alleviates dopaminergic neuronal death in Parkinson's disease via m6A-dependent regulation of ATM mRNA .
item2289	REG00007	M6ATAR00117	Up	M6ADIS0059	.	37772373	METTL3 promotes proliferation and migration of colorectal cancer cells by increasing SNHG1 stability.
item2290	REG00007	M6ATAR00189	Up	M6ADIS0051	M6ADRUG0115	37151889	"METTL3 could bind to m6A-modified ATG5 mRNA, which is crucial for autophagosome formation, and inhibit ATG5 mRNA decay on an IGF2BP3 dependent manner, thereby promoting autophagy and the autophagy-associated malignancy of OS. Using a small-molecule inhibitor named Spautin-1 to pharmacologically inhibit USP13 induced METTL3 degradation and exhibited significant therapeutic efficacy both in vitro and in vivo."
item2291	REG00014	M6ATAR00189	Up	M6ADIS0051	M6ADRUG0115	37151889	"METTL3 could bind to m6A-modified ATG5 mRNA, which is crucial for autophagosome formation, and inhibit ATG5 mRNA decay on an IGF2BP3 dependent manner, thereby promoting autophagy and the autophagy-associated malignancy of OS. Using a small-molecule inhibitor named Spautin-1 to pharmacologically inhibit USP13 induced METTL3 degradation and exhibited significant therapeutic efficacy both in vitro and in vivo."
item2292	REG00007	M6ATAR00948	Up	M6ADIS0006	.	36765911	"METTL3 and IGF2BP2 mediated m6A modification stabilized FBXO43, which facilitates the malignant progression of HCC. Mechanistically, FBXO43 exerts its oncogenic role in HCC by promoting ubiquitin-dependent proteasomal degradation of p53 through UBE2C upregulation."
item2293	REG00013	M6ATAR00948	Up	M6ADIS0006	.	36765911	"METTL3 and IGF2BP2 mediated m6A modification stabilized FBXO43, which facilitates the malignant progression of HCC. Mechanistically, FBXO43 exerts its oncogenic role in HCC by promoting ubiquitin-dependent proteasomal degradation of p53 through UBE2C upregulation."
item2294	REG00005	M6ATAR01473	Up	M6ADIS0162	.	37885015	"High-expressed ALKBH5 inhibits the m6A level of PLAC8 mRNA and promotes PLAC8 expression, while PLAC8 overexpression can promote hypoxia-induced invasion and migration of HTR-8/Svneo cells, indicating its potential protective function in PE."
item2295	REG00005	M6ATAR00949	Up	M6ADIS0097	.	37689242	"Mechanistically, ALKBH5 promoted the stability of ErbB4 mRNA and the degradation of ST14 mRNA via m6A demethylation. Fibroblast-specific ErbB4 overexpression ameliorated the impaired fibroblast-to-myofibroblast transformation and poor post-MI repair due to ALKBH5 knockout."
item2296	REG00005	M6ATAR01474	Down	M6ADIS0097	.	37689242	"Mechanistically, ALKBH5 promoted the stability of ErbB4 mRNA and the degradation of ST14 mRNA via m6A demethylation. Fibroblast-specific ErbB4 overexpression ameliorated the impaired fibroblast-to-myofibroblast transformation and poor post-MI repair due to ALKBH5 knockout."
item2297	REG00007	M6ATAR00154	Up	M6ADIS0065	M6ADRUG0022	37243702	"In BC cells and DOX-resistant BC cells, lnc KCNQ1OT1 could be mediated by METTL3 through m6A modification to elevate and stabilize its expression, further inhibiting miR-103a-3p/MDR1 axis to promote DOX resistance, which might provide novel thought to overcome DOX resistance in BC."
item2298	REG00007	M6ATAR00531	Up	M6ADIS0184	.	38043628	METTL3 could modulate FAM83D protein expression through m6A modification to aggravate triple-negative breast cancer progression via the Wnt/beta-catenin pathway.
item2299	REG00006	M6ATAR00381	Up	M6ADIS0055	.	37615536	METTL14 inhibits malignant progression of oral squamous cell carcinoma by targeting the autophagy-related gene RB1CC1 in an m6A-IGF2BP2-dependent manner.
item2300	REG00013	M6ATAR00381	Up	M6ADIS0055	.	37615536	METTL14 inhibits malignant progression of oral squamous cell carcinoma by targeting the autophagy-related gene RB1CC1 in an m6A-IGF2BP2-dependent manner.
item2301	REG00007	M6ATAR00950	Up	M6ADIS0054	.	38018881	Methyltransferase-like 3-mediated m6A modification of miR-1908-5p contributes to nasopharyngeal carcinoma progression by targeting homeodomain-only protein homeobox.
item2302	REG00006	M6ATAR00951	Up	.	.	37951776	METTL14-mediated N6-methyladenosine modification of Col17a1/Itgalpha6/Itgbeta4 governs epidermal homeostasis.
item2303	REG00006	M6ATAR00650	Up	.	.	37951776	METTL14-mediated N6-methyladenosine modification of Col17a1/Itgalpha6/Itgbeta4 governs epidermal homeostasis.
item2304	REG00006	M6ATAR00297	Up	.	.	37951776	METTL14-mediated N6-methyladenosine modification of Col17a1/Itgalpha6/Itgbeta4 governs epidermal homeostasis.
item2305	REG00006	M6ATAR00650	Up	.	.	37951776	METTL14-mediated N6-methyladenosine modification of Col17a1/Itgalpha6/Itgbeta4 governs epidermal homeostasis.
item2306	REG00009	M6ATAR00953	.	M6ADIS0267	.	37516644	IFN-suppressed the susceptibility of HPV infection directly. m6A analysis reveals WTAP is a key m6A writer promoting the m6A modification of IFNE mRNA.IFN-E is an important Type I IFN cytokine involved in the development of genital warts.
item2307	REG00001	M6ATAR00206	Down	M6ADIS0032	.	37154010	"FTO destroys the stability of Cyclin D1 by regulating the abundance of Cyclin D1 m6A, causing cell cycle arrest and inducing cell proliferation, thus inducing the occurrence and development of PVR in PH."
item2308	REG00001	M6ATAR00954	Up	M6ADIS0182	M6ADRUG0152	37492748	"RNA stability assays indicated that GPC4 upregulation was mainly regulated by the downregulation of the m6A ""reader"" YTH domain family protein 3 (YTHDF3). Finally, the FTO inhibitor FB23-2 further exacerbated experimental autoimmune uveitis (EAU) inflammation by promoting the GPC4/TLR4/NF-kappaB signaling axis, and this could be attenuated by the TLR4 inhibitor TAK-242. Collectively, a decreased FTO could facilitate microglial inflammation in EAU, suggesting that the restoration or activation of FTO function may be a potential therapeutic strategy for uveitis."
item2309	REG00025	M6ATAR00954	Down	M6ADIS0182	M6ADRUG0152	37492748	"RNA stability assays indicated that GPC4 upregulation was mainly regulated by the downregulation of the m6A ""reader"" YTH domain family protein 3 (YTHDF3). Finally, the FTO inhibitor FB23-2 further exacerbated experimental autoimmune uveitis (EAU) inflammation by promoting the GPC4/TLR4/NF-kappaB signaling axis, and this could be attenuated by the TLR4 inhibitor TAK-242. Collectively, a decreased FTO could facilitate microglial inflammation in EAU, suggesting that the restoration or activation of FTO function may be a potential therapeutic strategy for uveitis."
item2310	REG00007	M6ATAR01475	Up	.	.	36920907	METTL3 modulation of TLR4 expression is a critical determinant of neutrophil activation in endotoxemia.
item2311	REG00006	M6ATAR00955	Up	M6ADIS0007	.	36873735	"In brief, METTL14 promoted NSCLC development by increasing m6A methylation of PLAGL2 to activate beta-catenin signaling."
item2312	REG00007	M6ATAR00400	Up	M6ADIS0217	M6ADRUG0047	36730541	"METTL3 stimulated the m6A modification of staphylococcal nuclease and Tudor domain-containing protein 1 (SND1) mRNA, recruited YTH m6A RNA binding protein 1 to recognize the m6A site, thereby enhancing its mRNA stability. Rescue experiments demonstrated that METTL3 significantly prohibited NKTCL cell chemotherapy sensitivity to cisplatin (DDP) through regulating SND1 expression."
item2313	REG00024	M6ATAR00400	Up	M6ADIS0217	M6ADRUG0047	36730541	"METTL3 stimulated the m6A modification of staphylococcal nuclease and Tudor domain-containing protein 1 (SND1) mRNA, recruited YTH m6A RNA binding protein 1 to recognize the m6A site, thereby enhancing its mRNA stability. Rescue experiments demonstrated that METTL3 significantly prohibited NKTCL cell chemotherapy sensitivity to cisplatin (DDP) through regulating SND1 expression."
item2314	REG00009	M6ATAR00956	Up	M6ADIS0184	.	37477758	"WTAP Mediates NUPR1 Regulation of LCN2 Through m6A Modification to Influence Ferroptosis, Thereby Promoting Breast Cancer Proliferation, Migration and Invasion."
item2315	REG00013	M6ATAR00022	Up	M6ADIS0056	.	37917979	The m6A reader IGF2BP2 promotes the progression of esophageal squamous cell carcinoma cells by increasing the stability of OCT4 mRNA.
item2316	REG00013	M6ATAR00957	Up	M6ADIS0057	.	37865637	IGF2BP2-meidated m6A modification of CSF2 reprograms MSC to promote gastric cancer progression.
item2317	REG00009	M6ATAR00958	.	M6ADIS0058	.	36855062	Lactoferrin suppresses the progression of colon cancer under hyperglycemia by targeting WTAP/m6A/NT5DC3/HKDC1 axis .
item2318	REG00007	M6ATAR01477	Up	M6ADIS0089	.	36587923	"METTL3 stabilized STUB1 mRNA through the m6A-IGF2BP1-dependent mechanism and naturally promoted STUB1 expression, thereby enhancing autophagic p-Tau clearance in Abeta1-42-treated cells."
item2319	REG00012	M6ATAR01477	Up	M6ADIS0089	.	36587923	"METTL3 stabilized STUB1 mRNA through the m6A-IGF2BP1-dependent mechanism and naturally promoted STUB1 expression, thereby enhancing autophagic p-Tau clearance in Abeta1-42-treated cells."
item2320	REG00006	M6ATAR00959	Down	M6ADIS0017	.	37534933	"METTL14 functioned as a profibrotic gene by suppressing NOVA2 activity in a mechanism dependent on m6A-YTHDF2. Moreover, knocking down METTL14 exacerbated LF, while NOVA2 prevented its development and partly reversed the damage."
item2321	REG00008	M6ATAR00959	Down	M6ADIS0017	.	37534933	"METTL14 functioned as a profibrotic gene by suppressing NOVA2 activity in a mechanism dependent on m6A-YTHDF2. Moreover, knocking down METTL14 exacerbated LF, while NOVA2 prevented its development and partly reversed the damage."
item2322	REG00006	M6ATAR00741	Down	M6ADIS0360	.	35949109	The N6-methyladenosine (m6A) modification of BATF2 mRNA mediated by METTL14 suppressed its expression in TSCC. METTL14/BATF2 axis could serve as a novel promising therapeutic candidate against angiogenesis for TSCC.
item2323	REG00005	M6ATAR00225	Up	M6ADIS0055	.	37257451	"RBM33 is critical for the tumorigenesis of head-neck squamous cell carcinoma (HNSCC). RBM33 promotes autophagy by recruiting ALKBH5 to demethylate and stabilize DDIT4 mRNA, which is responsible for the oncogenic function of RBM33 in HNSCC cells."
item2324	REG00012	M6ATAR00960	Up	M6ADIS0007	.	37841956	"The m6A reader IGF2BP1 manipulates BUB1B expression to affect malignant behaviors, stem cell properties, and immune resistance of non-small-cell lung cancer stem cells."
item2325	REG00007	M6ATAR00961	Up	.	.	37957340	"These results shed light on a CFL1-METTL3-seRNA m6A-YTHDC2/MLL1 axis that plays a role in the epigenetic regulation of local chromatin state and gene expression, which strengthens our knowledge about the functions of super-enhancers and their transcripts."
item2326	REG00023	M6ATAR00961	Up	.	.	37957340	"These results shed light on a CFL1-METTL3-seRNA m6A-YTHDC2/MLL1 axis that plays a role in the epigenetic regulation of local chromatin state and gene expression, which strengthens our knowledge about the functions of super-enhancers and their transcripts."
item2327	REG00007	M6ATAR00962	Up	M6ADIS0055	.	38014887	"Mechanistically, METTL3 was elucidated to mediate the epigenetic upregulation of NTMT1 in HNSC in an m6A-dependent manner, and the overexpression of METTL3 was shown to alleviate the inhibitory impact of downregulated NTMT1 on HNSC proliferation."
item2328	REG00007	M6ATAR00963	Down	M6ADIS0091	.	37249328	"Mechanistically, METTL3 reduced ANXA2 expression in T lymphocytes through m6A modification and inhibited p38MAPK/MMP-9 pathway activation, exerting protective effects against neuronal damage in ischemic stroke."
item2329	REG00005	M6ATAR00964	Down	M6ADIS0008	.	36705046	"ALKBH5 demethylates and destabilizes SIRT3 in an m6A-IGF2BP1-dependent manner, repressing CESC growth, lipid metabolism and tumorigenesis by downregulating ACC1."
item2330	REG00012	M6ATAR00964	Up	M6ADIS0008	.	36705046	"ALKBH5 demethylates and destabilizes SIRT3 in an m6A-IGF2BP1-dependent manner, repressing CESC growth, lipid metabolism and tumorigenesis by downregulating ACC1."
item2331	REG00023	M6ATAR00965	Down	M6ADIS0059	M6ADRUG0005	37778684	LIMK1 m6A-RNA methylation recognized by YTHDC2 induces 5-FU chemoresistance in colorectal cancer via endoplasmic reticulum stress and stress granule formation.
item2332	REG00007	M6ATAR00966	Down	M6ADIS0008	.	37468464	"METTL3/YTHDF2 promoted the degradation of circRNF13 and subsequently affected the stability of CXC motif chemokine ligand 1 (CXCL1), ultimately enhancing the radiosensitivity of CC cells."
item2333	REG00008	M6ATAR00966	Down	M6ADIS0008	.	37468464	"METTL3/YTHDF2 promoted the degradation of circRNF13 and subsequently affected the stability of CXC motif chemokine ligand 1 (CXCL1), ultimately enhancing the radiosensitivity of CC cells."
item2334	REG00007	M6ATAR00967	Up	M6ADIS0061	M6ADRUG0176	38110764	"Celastrol treatment downregulated METTL3 and decreased m6A levels of Claspin and Bcl-2 mRNA, leading to the degradation of Claspin and Bcl-2 mRNA in pancreatic cancer cells. Furthermore, we revealed that celastrol treatment downregulated Claspin and Bcl-2, at least in part, in an m6A-YTHDF3-mediated manner in pancreatic cancer cells."
item2335	REG00007	M6ATAR00196	Up	M6ADIS0061	M6ADRUG0176	38110764	"Celastrol treatment downregulated METTL3 and decreased m6A levels of Claspin and Bcl-2 mRNA, leading to the degradation of Claspin and Bcl-2 mRNA in pancreatic cancer cells. Furthermore, we revealed that celastrol treatment downregulated Claspin and Bcl-2, at least in part, in an m6A-YTHDF3-mediated manner in pancreatic cancer cells."
item2336	REG00025	M6ATAR00967	Up	M6ADIS0061	M6ADRUG0176	38110764	"Celastrol treatment downregulated METTL3 and decreased m6A levels of Claspin and Bcl-2 mRNA, leading to the degradation of Claspin and Bcl-2 mRNA in pancreatic cancer cells. Furthermore, we revealed that celastrol treatment downregulated Claspin and Bcl-2, at least in part, in an m6A-YTHDF3-mediated manner in pancreatic cancer cells."
item2337	REG00025	M6ATAR00196	Up	M6ADIS0061	M6ADRUG0176	38110764	"Celastrol treatment downregulated METTL3 and decreased m6A levels of Claspin and Bcl-2 mRNA, leading to the degradation of Claspin and Bcl-2 mRNA in pancreatic cancer cells. Furthermore, we revealed that celastrol treatment downregulated Claspin and Bcl-2, at least in part, in an m6A-YTHDF3-mediated manner in pancreatic cancer cells."
item2338	REG00014	M6ATAR00274	Up	M6ADIS0390	.	37257765	"IGF2BP3 recognized m6A modification in HIF1A mRNA as an m6A reader, thereby promoting expression of HIF1A by increasing RNA stability. HIF1A activated Rho GTPases (RhoA) and suppressed phosphorylation of YAP via inhibiting LATS1/2, promoting translocation of non-phosphorylated YAP into the nucleus, resulting in fetal liver programme and ultimate hepatic injury in ACLF patients."
item2339	REG00007	M6ATAR01478	Down	.	.	36674918	METTL3 knockdown exacerbated iNOS/NO-mediated mitochondrial dysfunction by promoting a Nos2 mRNA stability in a YTHDF1-dependent manner and further inhibited osteoclast differentiation and increased osteoclast apoptosis in inflammatory conditions.
item2340	REG00024	M6ATAR01478	Down	.	.	36674918	METTL3 knockdown exacerbated iNOS/NO-mediated mitochondrial dysfunction by promoting a Nos2 mRNA stability in a YTHDF1-dependent manner and further inhibited osteoclast differentiation and increased osteoclast apoptosis in inflammatory conditions.
item2341	REG00005	M6ATAR01479	Up	.	.	38114747	"Mechanistically, ALKBH5 erased m6A methylation on the CSF3R mRNA to increase the mRNA stability and protein expression of G-CSFR, consequently upregulating cell surface G-CSFR expression and downstream STAT3 signaling in neutrophils."
item2342	REG00007	M6ATAR00968	.	M6ADIS0282	.	37386028	"Mechanistically, deletion of Mettl3 or Mettl14, another component of the methyltransferase complex, lead to the enhanced expression of inflammatory cytokines. By focusing on one of the most affected mRNAs, namely the one encoding the cytokine IL-13, we find that it is methylated in activated mast cells, and that Mettl3 affects its transcript stability in an enzymatic activity-dependent manner, requiring consensus m6A sites in the Il13 3'-untranslated region."
item2343	REG00007	M6ATAR00968	.	M6ADIS0164	.	37386028	"Mechanistically, deletion of Mettl3 or Mettl14, another component of the methyltransferase complex, lead to the enhanced expression of inflammatory cytokines. By focusing on one of the most affected mRNAs, namely the one encoding the cytokine IL-13, we find that it is methylated in activated mast cells, and that Mettl3 affects its transcript stability in an enzymatic activity-dependent manner, requiring consensus m6A sites in the Il13 3'-untranslated region."
item2344	REG00006	M6ATAR00968	.	M6ADIS0282	.	37386028	"Mechanistically, deletion of Mettl3 or Mettl14, another component of the methyltransferase complex, lead to the enhanced expression of inflammatory cytokines. By focusing on one of the most affected mRNAs, namely the one encoding the cytokine IL-13, we find that it is methylated in activated mast cells, and that Mettl3 affects its transcript stability in an enzymatic activity-dependent manner, requiring consensus m6A sites in the Il13 3'-untranslated region."
item2345	REG00006	M6ATAR00968	.	M6ADIS0164	.	37386028	"Mechanistically, deletion of Mettl3 or Mettl14, another component of the methyltransferase complex, lead to the enhanced expression of inflammatory cytokines. By focusing on one of the most affected mRNAs, namely the one encoding the cytokine IL-13, we find that it is methylated in activated mast cells, and that Mettl3 affects its transcript stability in an enzymatic activity-dependent manner, requiring consensus m6A sites in the Il13 3'-untranslated region."
item2346	REG00006	M6ATAR01480	Up	M6ADIS0007	.	36448247	RNA m6A methyltransferase METTL14 promotes the procession of non-small cell lung cancer by targeted CSF1R.
item2347	REG00014	M6ATAR00969	Up	M6ADIS0046	.	37663284	RNA N6-methyladenosine reader IGF2BP3 promotes acute myeloid leukemia progression by controlling stabilization of EPOR mRNA.
item2348	REG00001	M6ATAR00260	Up	M6ADIS0245	.	36718644	"FTO serves as a tumor suppressor in glioma by suppressing hypoxia-induced malignant behaviors of glioma cells, possibly by promoting the nuclear translocation of FOXO3a and upregulating FOXO3a downstream targets."
item2349	REG00025	M6ATAR00970	Up	M6ADIS0008	.	36380687	YTHDF3 mediates HNF1alpha regulation of cervical cancer radio-resistance by promoting RAD51D translation in an m6A-dependent manner.
item2350	REG00007	M6ATAR00971	Up	M6ADIS0083	M6ADRUG0134	37224383	"Mechanistically, METTL3-catalyzed m6A installation on thermogenic mRNAs, including Kruppel-like factor 9 (Klf9), prevents their degradation. Activation of the METTL3 complex by its chemical ligand methyl piperidine-3-carboxylate promotes WAT beiging, reduces body weight, and corrects metabolic disorders in diet-induced obese mice."
item2351	REG00024	M6ATAR00972	Up	M6ADIS0046	M6ADRUG0113	36634204	The RNA m6A Reader YTHDF1 Is Required for Acute Myeloid Leukemia Progression. Tegaserod blocked the direct binding of YTHDF1 with m6A-modified mRNAs and inhibited YTHDF1-regulated cyclin E2 translation.
item2352	REG00007	M6ATAR00973	Up	.	.	37958523	"METTL3 degradation in hNPCs significantly decreased the enrichment of m6A in SLIT2 mRNA, consequently reducing its expression. This findings reveal a novel functional target (SLIT2) for METTL3 in hNPCs and contribute to a better understanding of m6A-dependent mechanisms in hNPC proliferation."
item2353	REG00005	M6ATAR00635	Down	M6ADIS0057	.	37724907	"YY1 was regulated by ALKBH5 and YTHDF1-mediated m6A modification and served as an autophagy-dependent tumor driver to accelerate cancer progression through ATG4B transactivation, providing an exploitable therapeutic target for GC."
item2354	REG00024	M6ATAR00635	Up	M6ADIS0057	.	37724907	"YY1 was regulated by ALKBH5 and YTHDF1-mediated m6A modification and served as an autophagy-dependent tumor driver to accelerate cancer progression through ATG4B transactivation, providing an exploitable therapeutic target for GC."
item2355	REG00007	M6ATAR00974	Up	M6ADIS0001	.	37614011	"Methyltransferase MELLT3 upregulated m6A modification of CircEPHB4, and YTHDC1 promoted cytoplasmic localization of m6A-modified CircEPHB4. Overexpression of wild-type CircEPHB4 enhanced glioma cells' stemness, metastasis, and proliferation. Cytoplasmic CircEPHB4 increased SOX2 mRNA stability by binding to IGF2BP2, and the effects observed by SOX2 knockdown were reversed by CircEPHB4 in glioma cells."
item2356	REG00022	M6ATAR00974	Up	M6ADIS0001	.	37614011	"Methyltransferase MELLT3 upregulated m6A modification of CircEPHB4, and YTHDC1 promoted cytoplasmic localization of m6A-modified CircEPHB4. Overexpression of wild-type CircEPHB4 enhanced glioma cells' stemness, metastasis, and proliferation. Cytoplasmic CircEPHB4 increased SOX2 mRNA stability by binding to IGF2BP2, and the effects observed by SOX2 knockdown were reversed by CircEPHB4 in glioma cells."
item2357	REG00013	M6ATAR00404	Up	M6ADIS0001	.	37614011	"Methyltransferase MELLT3 upregulated m6A modification of CircEPHB4, and YTHDC1 promoted cytoplasmic localization of m6A-modified CircEPHB4. Overexpression of wild-type CircEPHB4 enhanced glioma cells' stemness, metastasis, and proliferation. Cytoplasmic CircEPHB4 increased SOX2 mRNA stability by binding to IGF2BP2, and the effects observed by SOX2 knockdown were reversed by CircEPHB4 in glioma cells."
item2358	REG00006	M6ATAR00975	Up	M6ADIS0055	.	37017680	METTL14 Promotes Oral Squamous Cell Carcinoma Progression by Regulating the mRNA and m6A Levels of CALD1.
item2359	REG00024	M6ATAR00486	Up	M6ADIS0365	.	36675257	"Hypoxia suppresses osteogenic differentiation and promotes the expression of YTHDF1, which translationally regulates THBS1 in an m6A-dependent manner, potentially counteracting hypoxia-induced osteogenic inhibition through the YTHDF1/THBS1 pathway."
item2360	REG00007	M6ATAR00237	Up	M6ADIS0006	M6ADRUG0108	36898427	"METTL3-m6A axis promotes the translation level of EGFR.targeting METTL3 using specific inhibitor STM2457 improved the sensitivity to lenvatinib in vitro and in vivo, indicating that METTL3 may be a potential therapeutic target to overcome lenvatinib resistance in HCC."
item2361	REG00007	M6ATAR00237	Up	M6ADIS0006	M6ADRUG0138	36898427	"METTL3-m6A axis promotes the translation level of EGFR.targeting METTL3 using specific inhibitor STM2457 improved the sensitivity to lenvatinib in vitro and in vivo, indicating that METTL3 may be a potential therapeutic target to overcome lenvatinib resistance in HCC."
item2362	REG00023	M6ATAR00976	Up	M6ADIS0117	.	36574062	The m6A reader YTHDC2 promotes SIRT3 expression by reducing the stabilization of KDM5B to improve mitochondrial metabolic reprogramming in diabetic peripheral neuropathy.
item2363	REG00008	M6ATAR00977	.	M6ADIS0371	.	37438603	m6A-methylated circGPATCH2L is recognised and endoribonucleolytically cleaved by a YTHDF2-RPL10-RNase P/MRP complex to maintain the physiological state of nucleus pulposus cells.
item2364	REG00005	M6ATAR00978	Up	M6ADIS0061	.	37858219	ALKBH5 enhances lipid metabolism reprogramming by increasing stability of FABP5 to promote pancreatic neuroendocrine neoplasms progression in an m6A-IGF2BP2-dependent manner.
item2365	REG00013	M6ATAR00978	Down	M6ADIS0061	.	37858219	ALKBH5 enhances lipid metabolism reprogramming by increasing stability of FABP5 to promote pancreatic neuroendocrine neoplasms progression in an m6A-IGF2BP2-dependent manner.
item2366	REG00022	M6ATAR00979	Up	M6ADIS0006	.	37400994	"The expression of FAM111A was positively correlated with the m6A level of FAM111A-DT, and the expression of methyltransferase complex, YTHDC1, and KDM3B in HCC tissues. Depletion of FAM111A largely attenuated the roles of m6A-modified FAM111A-DT in HCC. In summary, the m6A-modified FAM111A-DT/YTHDC1/KDM3B/FAM111A regulatory axis promoted HCC growth and represented a candidate therapeutic target for HCC."
item2367	REG00007	M6ATAR00213	.	M6ADIS0065	.	36765397	"METTL3 depletion promotes the proliferation and migration and decreases the drug sensitivity of HR+HER2- BC via regulation of the CDKN1A/EMT and m6A-BAX/caspase-9/-3/-8 signalling pathways, which suggests METTL3 played a tumour-suppressor role and it could be a potential biomarker for predicting the prognosis of patients with HR+HER2- BC."
item2368	REG00007	M6ATAR00140	Up	M6ADIS0007	.	37688756	m6A-mediated lncRNA NEAT1 plays an oncogenic role in non-small cell lung cancer by upregulating the HMGA1 expression through binding miR-361-3p.
item2369	REG00007	M6ATAR00980	Up	M6ADIS0008	M6ADRUG0047	37392859	"METIL3 is believed to enhance the expression of LINC00426 through m6A methylation modification.The LINC00426/miR-200a-3p/ZEB1 axis plays a crucial role in regulating E-cadherin, N-cadherin and vimentin during EMT in CC.Overexpression of LINC00426 in CC cells caused resistance to Cisplatin and Bleomycin, but sensitivity to imatinib."
item2370	REG00007	M6ATAR00980	Up	M6ADIS0008	M6ADRUG0180	37392859	"METIL3 is believed to enhance the expression of LINC00426 through m6A methylation modification.The LINC00426/miR-200a-3p/ZEB1 axis plays a crucial role in regulating E-cadherin, N-cadherin and vimentin during EMT in CC.Overexpression of LINC00426 in CC cells caused resistance to Cisplatin and Bleomycin, but sensitivity to imatinib."
item2371	REG00007	M6ATAR00980	Up	M6ADIS0008	M6ADRUG0107	37392859	"METIL3 is believed to enhance the expression of LINC00426 through m6A methylation modification.The LINC00426/miR-200a-3p/ZEB1 axis plays a crucial role in regulating E-cadherin, N-cadherin and vimentin during EMT in CC.Overexpression of LINC00426 in CC cells caused resistance to Cisplatin and Bleomycin, but sensitivity to imatinib."
item2372	REG00007	M6ATAR00981	Up	M6ADIS0059	.	37370759	METTL3-Modulated circUHRF2 Promotes Colorectal Cancer Stemness and Metastasis through Increasing DDX27 mRNA Stability by Recruiting IGF2BP1.
item2373	REG00012	M6ATAR01481	Up	M6ADIS0059	.	37370759	METTL3-Modulated circUHRF2 Promotes Colorectal Cancer Stemness and Metastasis through Increasing DDX27 mRNA Stability by Recruiting IGF2BP1.
item2374	REG00007	M6ATAR00982	Up	M6ADIS0059	.	37828232	The METTL3/IGF2BP2/STAG3 axis affects CRC progression in an m6A modification-dependent manner. This may guide targeted therapy in CRC patients.
item2375	REG00013	M6ATAR00982	Up	M6ADIS0059	.	37828232	The METTL3/IGF2BP2/STAG3 axis affects CRC progression in an m6A modification-dependent manner. This may guide targeted therapy in CRC patients.
item2376	REG00007	M6ATAR00983	Up	M6ADIS0070	.	37268280	"METTL3/METTL1-mediated dual m6A/m7G RNA modifications enhanced TROP2 translation and promoted BCa development, indicating a novel RNA epigenetic mechanism in BCa."
item2377	REG00007	M6ATAR00460	Up	M6ADIS0007	.	36114749	"METTL3-mediated m6A modification of mRNA inhibited the decay of H2A histone family member X (H2AX) mRNA and enhanced its expression, which led to enhanced DNA damage repair and cell survival."
item2378	REG00006	M6ATAR00984	Up	M6ADIS0183	M6ADRUG0170	38014839	"COP increased TSC1 expression, inhibited the Mitogen-activated protein kinase (MEK) / Extracellular regulated protein kinases (ERK) signaling pathway, and thus inhibited macrophage M1 polarization, whereas COP increased CCAAT Enhancer Binding Protein beta (c/EBPbeta) expression, and thus promoted macrophage M2 polarization. COP also significantly increased the expression of METTL14, which enhanced m6A methylation and ultimately improved the stability of TSC1 mRNA."
item2379	REG00001	M6ATAR00205	Up	M6ADIS0083	.	37666478	"The reduced NADPH attenuates the expression of fat mass and obesity-associated (FTO) protein, a well-known m6A demethylase, to increase the N6-methyladenosine (m6A) levels of Ccna2 and Cdk2 mRNA. Meanwhile, the high m6A levels of Ccna2 and Cdk2 mRNA are recognized by YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), which results in mRNA decay and reduction of their protein expressions. Overall, our data demonstrate that BCAA inhibit obesity and adipogenesis by reducing CDK2 and CCNA2 expression via an NADPH-FTO-m6A coordinated manner in vivo and in vitro, which raises a new perspective on the role of m6A in the BCAA regulation of obesity and adipogenesis."
item2380	REG00008	M6ATAR00205	Down	M6ADIS0083	.	37666478	"The reduced NADPH attenuates the expression of fat mass and obesity-associated (FTO) protein, a well-known m6A demethylase, to increase the N6-methyladenosine (m6A) levels of Ccna2 and Cdk2 mRNA. Meanwhile, the high m6A levels of Ccna2 and Cdk2 mRNA are recognized by YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), which results in mRNA decay and reduction of their protein expressions. Overall, our data demonstrate that BCAA inhibit obesity and adipogenesis by reducing CDK2 and CCNA2 expression via an NADPH-FTO-m6A coordinated manner in vivo and in vitro, which raises a new perspective on the role of m6A in the BCAA regulation of obesity and adipogenesis."
item2381	REG00001	M6ATAR00210	Up	M6ADIS0083	.	37666478	"The reduced NADPH attenuates the expression of fat mass and obesity-associated (FTO) protein, a well-known m6A demethylase, to increase the N6-methyladenosine (m6A) levels of Ccna2 and Cdk2 mRNA. Meanwhile, the high m6A levels of Ccna2 and Cdk2 mRNA are recognized by YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), which results in mRNA decay and reduction of their protein expressions. Overall, our data demonstrate that BCAA inhibit obesity and adipogenesis by reducing CDK2 and CCNA2 expression via an NADPH-FTO-m6A coordinated manner in vivo and in vitro, which raises a new perspective on the role of m6A in the BCAA regulation of obesity and adipogenesis."
item2382	REG00008	M6ATAR00210	Down	M6ADIS0083	.	37666478	"The reduced NADPH attenuates the expression of fat mass and obesity-associated (FTO) protein, a well-known m6A demethylase, to increase the N6-methyladenosine (m6A) levels of Ccna2 and Cdk2 mRNA. Meanwhile, the high m6A levels of Ccna2 and Cdk2 mRNA are recognized by YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), which results in mRNA decay and reduction of their protein expressions. Overall, our data demonstrate that BCAA inhibit obesity and adipogenesis by reducing CDK2 and CCNA2 expression via an NADPH-FTO-m6A coordinated manner in vivo and in vitro, which raises a new perspective on the role of m6A in the BCAA regulation of obesity and adipogenesis."
item2383	REG00007	M6ATAR00148	Down	M6ADIS0375	.	37379961	METTL3 mediated m6A methylation of LncRNA-GAS5 via an YTHDF2-dependent manner.METTL3 boosts mitochondrial fission and induces cardiac fibrosis by enhancing LncRNA GAS5 methylation.
item2384	REG00008	M6ATAR00148	Down	M6ADIS0375	.	37379961	METTL3 mediated m6A methylation of LncRNA-GAS5 via an YTHDF2-dependent manner.METTL3 boosts mitochondrial fission and induces cardiac fibrosis by enhancing LncRNA GAS5 methylation.
item2385	REG00006	M6ATAR00605	Down	M6ADIS0391	.	38047519	METTL14 knockdown inhibited the pyroptosis in the sepsis-induced ALI progression through decreasing the NLRP3 levels dependent on m6A methylation modification.
item2386	REG00007	M6ATAR00326	Up	M6ADIS0245	.	36683086	METTL3 knockdown promotes temozolomide sensitivity of glioma stem cells via decreasing MGMT and APNG mRNA stability.
item2387	REG00007	M6ATAR00158	Up	M6ADIS0245	.	36683086	METTL3 knockdown promotes temozolomide sensitivity of glioma stem cells via decreasing MGMT and APNG mRNA stability.
item2388	REG00022	M6ATAR00985	.	M6ADIS0228	M6ADRUG0169	37821382	"The mTOR inhibitor dactolisib and FAO inhibitor perhexiline exert a synergistic effect on CLL cells. In addition, the biogenesis of circTET2 can be affected by the splicing process and the RBPs RBMX and YTHDC1. CP028, a splicing inhibitor, modulates the expression of circTET2 and shows pronounced inhibitory effects."
item2389	REG00022	M6ATAR00985	.	M6ADIS0228	M6ADRUG0162	37821382	"The mTOR inhibitor dactolisib and FAO inhibitor perhexiline exert a synergistic effect on CLL cells. In addition, the biogenesis of circTET2 can be affected by the splicing process and the RBPs RBMX and YTHDC1. CP028, a splicing inhibitor, modulates the expression of circTET2 and shows pronounced inhibitory effects."
item2390	REG00022	M6ATAR00985	.	M6ADIS0228	M6ADRUG0126	37821382	"The mTOR inhibitor dactolisib and FAO inhibitor perhexiline exert a synergistic effect on CLL cells. In addition, the biogenesis of circTET2 can be affected by the splicing process and the RBPs RBMX and YTHDC1. CP028, a splicing inhibitor, modulates the expression of circTET2 and shows pronounced inhibitory effects."
item2391	REG00027	M6ATAR00985	.	M6ADIS0228	M6ADRUG0169	37821382	"The mTOR inhibitor dactolisib and FAO inhibitor perhexiline exert a synergistic effect on CLL cells. In addition, the biogenesis of circTET2 can be affected by the splicing process and the RBPs RBMX and YTHDC1. CP028, a splicing inhibitor, modulates the expression of circTET2 and shows pronounced inhibitory effects."
item2392	REG00027	M6ATAR00985	.	M6ADIS0228	M6ADRUG0162	37821382	"The mTOR inhibitor dactolisib and FAO inhibitor perhexiline exert a synergistic effect on CLL cells. In addition, the biogenesis of circTET2 can be affected by the splicing process and the RBPs RBMX and YTHDC1. CP028, a splicing inhibitor, modulates the expression of circTET2 and shows pronounced inhibitory effects."
item2393	REG00027	M6ATAR00985	.	M6ADIS0228	M6ADRUG0126	37821382	"The mTOR inhibitor dactolisib and FAO inhibitor perhexiline exert a synergistic effect on CLL cells. In addition, the biogenesis of circTET2 can be affected by the splicing process and the RBPs RBMX and YTHDC1. CP028, a splicing inhibitor, modulates the expression of circTET2 and shows pronounced inhibitory effects."
item2394	REG00007	M6ATAR00986	Up	M6ADIS0048	M6ADRUG0007	36762777	"Metformin attenuates multiple myeloma cell proliferation and encourages apoptosis by suppressing METTL3-mediated m6A methylation of THRAP3, RBM25, and USP4."
item2395	REG00007	M6ATAR00987	Up	M6ADIS0048	M6ADRUG0007	36762777	"Metformin attenuates multiple myeloma cell proliferation and encourages apoptosis by suppressing METTL3-mediated m6A methylation of THRAP3, RBM25, and USP4."
item2396	REG00007	M6ATAR00668	Up	M6ADIS0048	M6ADRUG0007	36762777	"Metformin attenuates multiple myeloma cell proliferation and encourages apoptosis by suppressing METTL3-mediated m6A methylation of THRAP3, RBM25, and USP4."
item2397	REG00015	M6ATAR00988	Up	M6ADIS0184	.	37811616	VIRMA Facilitates Triple-Negative Breast Cancer Progression via Increasing m6A-Dependent KIF15 Expression .
item2398	REG00012	M6ATAR01483	Up	M6ADIS0007	.	37866243	IGF2BP1 enhances the stability of SIK2 mRNA through m6A modification to promote non-small cell lung cancer progression.
item2399	REG00015	.	.	M6ADIS0007	M6ADRUG0030	36493511	KIAA1429 promotes tumorigenesis and gefitinib resistance in lung adenocarcinoma by activating the JNK/ MAPK pathway in an m6A-dependent manner.
item2400	REG00006	M6ATAR00989	Up	M6ADIS0391	M6ADRUG0135	37543013	"LncRNA THRIL, transcriptionally activated by AP-1 and stabilized by METTL14-mediated m6A modification, accelerates LPS-evoked acute injury in alveolar epithelial cells."
item2401	REG00001	M6ATAR00453	Up	M6ADIS0008	.	37306026	FTO promotes the progression of cervical cancer by regulating the N6-methyladenosine modification of ZEB1 and Myc.
item2402	REG00001	M6ATAR00341	Up	M6ADIS0008	.	37306026	FTO promotes the progression of cervical cancer by regulating the N6-methyladenosine modification of ZEB1 and Myc.
item2403	REG00007	M6ATAR00990	Up	M6ADIS0182	.	36753389	METTL3 inhibits autoreactive Th17 cell responses in experimental autoimmune uveitis via stabilizing ASH1L mRNA.
item2404	REG00007	M6ATAR00198	Down	M6ADIS0162	.	36747144	Methyltransferase-like 3 aggravates endoplasmic reticulum stress in preeclampsia by targeting TMBIM6 in YTHDF2-dependent manner .
item2405	REG00008	M6ATAR00198	Down	M6ADIS0162	.	36747144	Methyltransferase-like 3 aggravates endoplasmic reticulum stress in preeclampsia by targeting TMBIM6 in YTHDF2-dependent manner .
item2406	REG00017	M6ATAR00991	Up	M6ADIS0006	M6ADRUG0186	37773181	"Mechanistically, TIALD directly interacts with AURKA and facilitate its degradation through the lysosomal pathway to inhibited EMT and metastasis of HCC. AURKA's specific inhibitor alisertib exerts effective therapeutic effect on liver cancer with low TIALD expression, which might provide a new insight into HCC therapy. Our study uncovers a negative functional loop of METTL16-TIALD-AURKA axis, and identifies a new mechanism for METTL16 mediated m6A-induced decay of TIALD on AURKA signaling in HCC progression, which may provide potential prognostic and therapeutic targets for HCC."
item2407	REG00001	M6ATAR00260	Down	M6ADIS0046	M6ADRUG0165	37402730	FTO knockdown cells exhibit stronger capacity of differentiation towards granules and myeloid lineages after cytosine arabinoside (Ara-C) treatment. FTO-m6A-FOXO3 is the main regulatory axis to affect the chemotherapy resistance of AML cells and FTO is a potential therapeutic target of chemotherapy resistance in AML.
item2408	REG00007	M6ATAR01484	Down	M6ADIS0010	M6ADRUG0156	36860916	"Erianin significantly reduced the expression levels of cellular Ferroptosis protective factors, and upregulated the expression of METTL3 and downregulated that of FTO.Erianin Induces Ferroptosis of Renal Cancer Stem Cells via Promoting ALOX12/ P53 mRNA N6-methyladenosine Modification."
item2409	REG00001	M6ATAR01484	Up	M6ADIS0010	M6ADRUG0156	36860916	"Erianin significantly reduced the expression levels of cellular Ferroptosis protective factors, and upregulated the expression of METTL3 and downregulated that of FTO.Erianin Induces Ferroptosis of Renal Cancer Stem Cells via Promoting ALOX12/ P53 mRNA N6-methyladenosine Modification."
item2410	REG00007	M6ATAR00356	Down	M6ADIS0010	M6ADRUG0156	36860916	"Erianin significantly reduced the expression levels of cellular Ferroptosis protective factors, and upregulated the expression of METTL3 and downregulated that of FTO.Erianin Induces Ferroptosis of Renal Cancer Stem Cells via Promoting ALOX12/ P53 mRNA N6-methyladenosine Modification."
item2411	REG00001	M6ATAR00356	Up	M6ADIS0010	M6ADRUG0156	36860916	"Erianin significantly reduced the expression levels of cellular Ferroptosis protective factors, and upregulated the expression of METTL3 and downregulated that of FTO.Erianin Induces Ferroptosis of Renal Cancer Stem Cells via Promoting ALOX12/ P53 mRNA N6-methyladenosine Modification."
item2412	REG00001	M6ATAR00150	.	M6ADIS0091	.	37676392	Demethylase FTO-Mediated m6A Modification of lncRNA MEG3 Activates Neuronal Pyroptosis via NLRP3 Signaling in Cerebral Ischemic Stroke.
item2413	REG00007	M6ATAR00141	.	M6ADIS0007	.	36608868	"RBM10 recruits METTL3 to induce N6-methyladenosine-MALAT1-dependent modification, inhibiting the invasion and migration of NSCLC."
item2414	REG00001	M6ATAR00992	Down	M6ADIS0080	.	37781923	FTO fuels diabetes-induced vascular endothelial dysfunction associated with inflammation by erasing m6A methylation of TNIP1.
item2415	REG00007	M6ATAR01485	Down	M6ADIS0001	.	35980802	"Specifically, PDGF-PDGFRB signaling upregulates the expression of the m6A methyltransferase METTL3, which then decorates the mitophagy regulator OPTN (optineurin) mRNA with m6A, thereby promoting OPTN mRNA degradation."
item2416	REG00006	M6ATAR00140	Up	M6ADIS0099	.	37078289	"Exercise Mitigates Endothelial Pyroptosis and Atherosclerosis by Downregulating NEAT1 Through N6-Methyladenosine Modifications.exercise induced a significant downregulation of m6A modification and METTL14, which binds to the m6A sites of NEAT1 and promotes NEAT1 expression through subsequent YTHDC1 (YTH domain-containing 1) recognition to promote endothelial pyroptosis."
item2417	REG00006	M6ATAR00140	Up	M6ADIS0386	.	37078289	"Exercise Mitigates Endothelial Pyroptosis and Atherosclerosis by Downregulating NEAT1 Through N6-Methyladenosine Modifications.exercise induced a significant downregulation of m6A modification and METTL14, which binds to the m6A sites of NEAT1 and promotes NEAT1 expression through subsequent YTHDC1 (YTH domain-containing 1) recognition to promote endothelial pyroptosis."
item2418	REG00022	M6ATAR00140	Up	M6ADIS0099	.	37078289	"Exercise Mitigates Endothelial Pyroptosis and Atherosclerosis by Downregulating NEAT1 Through N6-Methyladenosine Modifications.exercise induced a significant downregulation of m6A modification and METTL14, which binds to the m6A sites of NEAT1 and promotes NEAT1 expression through subsequent YTHDC1 (YTH domain-containing 1) recognition to promote endothelial pyroptosis."
item2419	REG00022	M6ATAR00140	Up	M6ADIS0386	.	37078289	"Exercise Mitigates Endothelial Pyroptosis and Atherosclerosis by Downregulating NEAT1 Through N6-Methyladenosine Modifications.exercise induced a significant downregulation of m6A modification and METTL14, which binds to the m6A sites of NEAT1 and promotes NEAT1 expression through subsequent YTHDC1 (YTH domain-containing 1) recognition to promote endothelial pyroptosis."
item2420	REG00006	M6ATAR00993	Up	M6ADIS0059	M6ADRUG0005	36810285	"m6A mRNA methylation initiated by METTL14 inhibits pri-miR-17 mRNA decay via reducing the recognition of YTHDC2 to the ""GGACC"" binding site. The METTL14/miR-17-5p/MFN2 signaling axis may play a critical role in 5-FU chemoresistance in CRC."
item2421	REG00023	M6ATAR00993	Down	M6ADIS0059	M6ADRUG0005	36810285	"m6A mRNA methylation initiated by METTL14 inhibits pri-miR-17 mRNA decay via reducing the recognition of YTHDC2 to the ""GGACC"" binding site. The METTL14/miR-17-5p/MFN2 signaling axis may play a critical role in 5-FU chemoresistance in CRC."
item2422	REG00007	M6ATAR00374	Up	M6ADIS0056	.	37575058	METTL3 facilitated growth and stemness of EC cells via upregulation of PTCH1 expression by enhancing PTCH1 m6A modification.
item2423	REG00007	M6ATAR01486	Up	M6ADIS0001	M6ADRUG0141	36484954	"Fear stress-induced upregulation of METTL3 and FSP1, increased m6A level of glioma tumor tissues, and inhibited ferroptosis in glioma progression, which were reversed by knockdown of METTL3 and FSP1 in vivo. In addition, we found that when iFSP1 (a ferroptosis inducer by targeting inhibition of FSP1) was introduced to glioma cells."
item2424	REG00003	M6ATAR01487	.	M6ADIS0007	.	36175801	"Serum-EVs can deliver HNRNPC to NSCLC cells, wherein HNRNPC recognizes the m6A modification of DLGAP5 mRNA, thus ultimately promoting NSCLC growth and metastasis."
item2425	REG00005	M6ATAR01456	Down	M6ADIS0068	.	36814156	"MiR-141-3p accelerated the malignant progression of PCa through ALKBH5-mediated m6A modification of PRMT6, which might offer a novel insight into the role of miR-141-3p and ALKBH5 in the treatments of PCa patients."
item2426	REG00006	M6ATAR00278	Up	M6ADIS0115	.	36401086	METTL14 plays a protective role against OP by promoting the TCF1/RUNX2 axis.
item2427	REG00006	M6ATAR00994	.	M6ADIS0059	.	37115853	"The rs11245997 A allele facilitated BET1L expression by disrupting miR-140-3p binding. It also reduced BET1L m6A modification, which upregulated BET1L expression levels through a mechanism mediated by the m6A methyltransferases (METTL14 and WTAP) and the m6A demethylase ALKBH5."
item2428	REG00009	M6ATAR00994	.	M6ADIS0059	.	37115853	"The rs11245997 A allele facilitated BET1L expression by disrupting miR-140-3p binding. It also reduced BET1L m6A modification, which upregulated BET1L expression levels through a mechanism mediated by the m6A methyltransferases (METTL14 and WTAP) and the m6A demethylase ALKBH5."
item2429	REG00005	M6ATAR00994	.	M6ADIS0059	.	37115853	"The rs11245997 A allele facilitated BET1L expression by disrupting miR-140-3p binding. It also reduced BET1L m6A modification, which upregulated BET1L expression levels through a mechanism mediated by the m6A methyltransferases (METTL14 and WTAP) and the m6A demethylase ALKBH5."
item2430	REG00046	M6ATAR00995	Up	M6ADIS0061	M6ADRUG0024	37326469	"Mechanistically, GEMIN5 was identified as a novel m6A mediator that specifically bound to m6A-modified FZR1 and recruited the eIF3 translation initiation complex to accelerate FZR1 translation.Increased FZR1 translation induced by m6A modification engenders a gemcitabine-resistant phenotype by inducing a quiescent state and confers a targetable vulnerability to improve treatment response in PDAC."
item2431	REG00008	M6ATAR00996	Up	M6ADIS0142	.	37791304	Loss of YTHDF2 Alters the Expression of m6A-Modified Myzap and Causes Adverse Cardiac Remodeling.
item2432	REG00007	M6ATAR01488	Up	M6ADIS0110	.	38012335	"METTL3 regulated the m6A modification of ACSL4 mRNA, increasing ACSL4 mRNA stability and ACSL4 expression. BMSC-Exos reduced chondrocyte ferroptosis and prevented OA progression via disruption of the METTL3-m6A-ACSL4 axis. BMSC-Exos might exert a chondroprotective effect by attenuating chondrocyte ferroptosis and alleviate OA progression."
item2433	REG00005	M6ATAR00997	Down	M6ADIS0057	M6ADRUG0047	38007439	ALKBH5-mediated CHAC1 depletion promotes malignant progression and decreases cisplatin-induced oxidative stress in gastric cancer.
item2434	REG00026	M6ATAR00709	Down	M6ADIS0073	.	36739231	Overexpressed ZC3H13 suppresses papillary thyroid carcinoma growth through m6A modification-mediated IQGAP1 degradation.
item2435	REG00007	M6ATAR00998	Down	M6ADIS0210	.	37821055	METTL3 and METTL14 regulate IL-6 expression via RNA m6A modification of zinc transporter SLC39A9 and DNA methylation of IL-6 in periodontal ligament cells.
item2436	REG00006	M6ATAR00998	Down	M6ADIS0210	.	37821055	METTL3 and METTL14 regulate IL-6 expression via RNA m6A modification of zinc transporter SLC39A9 and DNA methylation of IL-6 in periodontal ligament cells.
item2437	REG00008	M6ATAR00201	Down	M6ADIS0159	.	37500815	RNA methylation reading protein YTHDF2 relieves myocardial ischemia-reperfusion injury by downregulating BNIP3 via m6A modification.
item2438	REG00005	M6ATAR00999	Up	M6ADIS0162	.	37396548	Decreased expression of m6A demethylase ALKBH5 in decidua contributes to preeclampsia via m6A-CORIN-HuR pathway.
item2439	REG00005	M6ATAR00259	Up	M6ADIS0184	M6ADRUG0022	38104484	"In conclusion, we demonstrated a critical function of ALKBH5-mediated m6A demethylation of FOXO1 mRNA in restoring redox balance, which in turn promoting CSCs characteristics and DOX resistance in TNBC, and suggested that targeting the ALKBH5/FOXO1 axis has therapeutic potential for patients with TNBC refractory to chemotherapy."
item2440	REG00005	M6ATAR01000	Up	M6ADIS0097	.	37966425	"ALKBH5 accelerated MSC senescence through m6A modification-dependent stabilization of the CDKN1C transcript, providing a potential target for MSC rejuvenation. ALKBH5 knockdown rejuvenated AMSCs and enhanced cardiac function when transplanted into the mouse heart following infarction."
item2441	REG00001	M6ATAR01001	Up	M6ADIS0007	M6ADRUG0030	37330168	"FTO m6A demethylase promotes gefitinib resistance in NSCLC patients by upregulating downstream FLRT3, PTGIS, and SIRPA expression, with these three downstream genes serving as strong prognostic indicators."
item2442	REG00001	M6ATAR01002	Up	M6ADIS0007	M6ADRUG0030	37330168	"FTO m6A demethylase promotes gefitinib resistance in NSCLC patients by upregulating downstream FLRT3, PTGIS, and SIRPA expression, with these three downstream genes serving as strong prognostic indicators."
item2443	REG00001	M6ATAR01003	Up	M6ADIS0007	M6ADRUG0030	37330168	"FTO m6A demethylase promotes gefitinib resistance in NSCLC patients by upregulating downstream FLRT3, PTGIS, and SIRPA expression, with these three downstream genes serving as strong prognostic indicators."
item2444	REG00007	M6ATAR00524	Up	M6ADIS0172	.	37355989	"m6A methylation prevents the formation of endogenous double-stranded RNAs and promotes the degradation of Stat1 transcripts, which converge to prevent over-activation of STAT1 signaling and ensuing inhibition of gamma- T17. METTL3-mediated m6A methylation orchestrates mRNA stability and double-stranded RNA (dsRNA) contents to equilibrate gamma- T1 and gamma- T17 cells."
item2445	REG00008	M6ATAR01489	.	M6ADIS0067	.	37030331	"Knockdown of YTH N6-methyladenosine RNA-binding protein F2 (YTHDF2), an m6A reader, ameliorated the reduction in HSPA6 mRNA levels induced by YBX2, indicating the synergistic effects of YBX2 and YTHDF2 on mRNA stability. Therefore, YBX2 regulates RNA stability by interacting with the m6A reader proteins."
item2446	REG00007	M6ATAR01004	.	M6ADIS0061	.	37422970	"METTL3 enhanced the translation of PYGB mRNA in an m6A-YTHDF1-dependent manner.METTL3-mediated m6A modification of PYGB exerted the tumor-promotive effect on PAAD through NF-kappaB signaling, suggesting PYGB is a potential therapeutic target in PAAD."
item2447	REG00024	M6ATAR01004	.	M6ADIS0061	.	37422970	"METTL3 enhanced the translation of PYGB mRNA in an m6A-YTHDF1-dependent manner.METTL3-mediated m6A modification of PYGB exerted the tumor-promotive effect on PAAD through NF-kappaB signaling, suggesting PYGB is a potential therapeutic target in PAAD."
item2448	REG00007	M6ATAR01005	.	M6ADIS0059	.	36348020	METTL3 regulates miR-196b expression via an N6-methyladenosine (m6A)-pri-miR-196b-dependent mechanism and thereby promotes CRC metastasis.
item2449	REG00007	M6ATAR00111	.	M6ADIS0174	.	37678441	"METTL3-mediated m6A modifications were essential for sustaining the stability of microRNA-675, and silencing of METTL3 restrained tumorigenesis of GISTs cells by regulating the microRNA-675/MYPT1 axis."
item2450	REG00025	M6ATAR00237	Up	M6ADIS0006	.	37449789	m6A reader YTHDF3 triggers the progression of hepatocellular carcinoma through the YTHDF3/m6 A-EGFR/STAT3 axis and EMT.
item2451	REG00007	M6ATAR01007	Down	M6ADIS0177	M6ADRUG0119	37907575	"In summary, the aberrant downregulation of C1qA was related to Rituximab resistance in DLBCL cells, and C1qA was found to be regulated by METTL3- and YTHDF2-mediated m6A methylation. Enhancing the response of the complement system via regulation of C1qA might be an effective strategy for inhibiting Rituximab resistance in DLBCL."
item2452	REG00008	M6ATAR01007	Down	M6ADIS0177	M6ADRUG0119	37907575	"In summary, the aberrant downregulation of C1qA was related to Rituximab resistance in DLBCL cells, and C1qA was found to be regulated by METTL3- and YTHDF2-mediated m6A methylation. Enhancing the response of the complement system via regulation of C1qA might be an effective strategy for inhibiting Rituximab resistance in DLBCL."
item2453	REG00007	M6ATAR01008	Up	M6ADIS0066	M6ADRUG0177	37796697	N6-methyladenosine Methyltransferase METTL3 Enhances PTGER2 Expression to Increase Ovarian Cancer Stemness and Chemoresistance.
item2454	REG00007	M6ATAR01008	Up	M6ADIS0066	M6ADRUG0177	37796697	N6-methyladenosine Methyltransferase METTL3 Enhances PTGER2 Expression to Increase Ovarian Cancer Stemness and Chemoresistance.
item2455	REG00015	M6ATAR01490	Up	M6ADIS0065	.	37705505	"Mechanistically, KIAA1429/VIRMA is shown to bind to the m6A-dependent RNA-binding protein insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3), leading to recruitment and stabilization of m6A-modified hyaluronan synthase 2 (HAS2) mRNA. HAS2 mRNA and KIAA1429/VIRMA mRNA levels correlate positively in breast cancer tissues, suggesting that the KIAA1429/VIRMA-IGF2BP3-HAS2 axis promotes breast cancer growth and contributes to poor prognosis."
item2456	REG00015	M6ATAR01490	Up	M6ADIS0065	.	37705505	"Mechanistically, KIAA1429/VIRMA is shown to bind to the m6A-dependent RNA-binding protein insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3), leading to recruitment and stabilization of m6A-modified hyaluronan synthase 2 (HAS2) mRNA. HAS2 mRNA and KIAA1429/VIRMA mRNA levels correlate positively in breast cancer tissues, suggesting that the KIAA1429/VIRMA-IGF2BP3-HAS2 axis promotes breast cancer growth and contributes to poor prognosis."
item2457	REG00014	M6ATAR01490	Up	M6ADIS0065	.	37705505	"Mechanistically, KIAA1429/VIRMA is shown to bind to the m6A-dependent RNA-binding protein insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3), leading to recruitment and stabilization of m6A-modified hyaluronan synthase 2 (HAS2) mRNA. HAS2 mRNA and KIAA1429/VIRMA mRNA levels correlate positively in breast cancer tissues, suggesting that the KIAA1429/VIRMA-IGF2BP3-HAS2 axis promotes breast cancer growth and contributes to poor prognosis."
item2458	REG00006	M6ATAR01009	.	M6ADIS0172	.	38146129	"METTL14, TRIM27, STAT3, p-STAT3 and IL-6 expressions were all found to be increased in clinical skin samples of psoriatic patients. Our results unravelled METTL14/TRIM27/IGF2BP2 signalling axis in keratinocyte cytopathy, which plays a critical role in facilitating the activation of IL-6/STAT3 signalling pathway."
item2459	REG00013	M6ATAR01009	.	M6ADIS0172	.	38146129	"METTL14, TRIM27, STAT3, p-STAT3 and IL-6 expressions were all found to be increased in clinical skin samples of psoriatic patients. Our results unravelled METTL14/TRIM27/IGF2BP2 signalling axis in keratinocyte cytopathy, which plays a critical role in facilitating the activation of IL-6/STAT3 signalling pathway."
item2460	REG00007	M6ATAR00367	Down	M6ADIS0117	.	38013600	METTL3/YTHDF2 m6A axis mediates the progression of diabetic nephropathy through epigenetically suppressing PINK1 and mitophagy.
item2461	REG00008	M6ATAR00367	Down	M6ADIS0117	.	38013600	METTL3/YTHDF2 m6A axis mediates the progression of diabetic nephropathy through epigenetically suppressing PINK1 and mitophagy.
item2462	REG00007	M6ATAR01010	Up	M6ADIS0013	M6ADRUG0116	37179374	Polycystic ovary syndrome (PCOS) is an endocrine and metabolic disorder characterized by chronic low-grade inflammation.Short-chain fatty acid-butyric acid ameliorates granulosa cells inflammation through regulating METTL3-mediated N6-methyladenosine modification of FOSL2 in polycystic ovarian syndrome.
item2463	REG00007	M6ATAR00298	.	M6ADIS0061	.	37659467	Hypoxia promotes immune escape of pancreatic cancer cells by lncRNA NNT-AS1/METTL3-HuR-mediated ITGB1 m6A modification.
item2464	REG00001	M6ATAR00418	Up	M6ADIS0070	.	37538000	FTO promotes proliferation and migration of bladder cancer via enhancing stability of STAT3 mRNA in an m6A-dependent manner .
item2465	REG00007	M6ATAR01491	Up	M6ADIS0089	.	36881554	METTL3 ablation attenuated the m6A modification in DNA methyltransferase 3A (Dnmt3a) mRNAs and consequently impaired YTH N6-methyladenosine RNA binding protein 1 (YTHDF1)-mediated translation of DNMT3A.
item2466	REG00024	M6ATAR01491	Up	M6ADIS0089	.	36881554	METTL3 ablation attenuated the m6A modification in DNA methyltransferase 3A (Dnmt3a) mRNAs and consequently impaired YTH N6-methyladenosine RNA binding protein 1 (YTHDF1)-mediated translation of DNMT3A.
item2467	REG00006	M6ATAR01011	.	M6ADIS0117	.	37428236	METTL14 promotes the development of diabetic kidney disease by regulating m6A modification of TUG1.
item2468	REG00006	M6ATAR01012	.	M6ADIS0059	.	37310898	"METTL14/ALKBH5/IGF2BPs combine to modulate JMJD8 stability in an m6A-dependent manner, which increases glycolysis and accelerates the development of CRC by enhancing the enzymatic activity of PKM2."
item2469	REG00005	M6ATAR01012	.	M6ADIS0059	.	37310898	"METTL14/ALKBH5/IGF2BPs combine to modulate JMJD8 stability in an m6A-dependent manner, which increases glycolysis and accelerates the development of CRC by enhancing the enzymatic activity of PKM2."
item2470	REG00012	M6ATAR01012	.	M6ADIS0059	.	37310898	"METTL14/ALKBH5/IGF2BPs combine to modulate JMJD8 stability in an m6A-dependent manner, which increases glycolysis and accelerates the development of CRC by enhancing the enzymatic activity of PKM2."
item2471	REG00013	M6ATAR01012	.	M6ADIS0059	.	37310898	"METTL14/ALKBH5/IGF2BPs combine to modulate JMJD8 stability in an m6A-dependent manner, which increases glycolysis and accelerates the development of CRC by enhancing the enzymatic activity of PKM2."
item2472	REG00014	M6ATAR01012	.	M6ADIS0059	.	37310898	"METTL14/ALKBH5/IGF2BPs combine to modulate JMJD8 stability in an m6A-dependent manner, which increases glycolysis and accelerates the development of CRC by enhancing the enzymatic activity of PKM2."
item2473	REG00005	M6ATAR01013	.	M6ADIS0048	.	38145297	ALKHB5-demethylated lncRNA SNHG15 promotes myeloma tumorigenicity by increasing chromatin accessibility and recruiting H3K36me3 modifier SETD2.
item2474	REG00024	M6ATAR00258	Up	M6ADIS0032	.	36736607	Pulmonary arterial hypertension (PAH) is a chronic disease characterized by pulmonary vascular remodeling.YTHDF1 silencing inhibits hypoxic PASMC proliferation by regulating Foxm1 translation in an m6A-dependent manner.
item2475	REG00006	M6ATAR01014	Up	M6ADIS0367	.	37741915	METTL14-upregulated miR-6858 triggers cell apoptosis in keratinocytes of oral lichen planus through decreasing GSDMC.
item2476	REG00015	M6ATAR00520	Up	M6ADIS0066	.	37807062	N6-methyladenosine methyltransferase KIAA1429 promoted ovarian cancer aerobic glycolysis and progression through enhancing ENO1 expression.
item2477	REG00004	M6ATAR01015	Down	M6ADIS0006	.	38017546	HnRNPA2B1 promotes the occurrence and progression of hepatocellular carcinoma by downregulating PCK1 mRNA via a m6A RNA methylation manner.
item2478	REG00014	M6ATAR00766	Up	M6ADIS0008	.	38058838	IGF2BP3-mediated regulation of GLS and GLUD1 gene expression promotes treg-induced immune escape in human cervical cancer.
item2479	REG00014	M6ATAR01016	Up	M6ADIS0008	.	38058838	IGF2BP3-mediated regulation of GLS and GLUD1 gene expression promotes treg-induced immune escape in human cervical cancer.
item2480	REG00005	M6ATAR00401	.	M6ADIS0007	.	37246269	"Smoking-Induced M2-TAMs, via circEML4 in EVs, Promote the Progression of NSCLC through ALKBH5-Regulated m6A Modification of SOCS2 in NSCLC Cells."
item2481	REG00005	M6ATAR01017	Down	M6ADIS0073	.	36070054	ALKBH5 inhibits thyroid cancer progression by promoting ferroptosis through TIAM1-Nrf2/HO-1 axis.
item2482	REG00006	M6ATAR01018	Up	M6ADIS0061	.	37215454	METTL14 Facilitates the Metastasis of Pancreatic Carcinoma by Stabilizing LINC00941 in an m6A-IGF2BP2-Dependent Manner.
item2483	REG00013	M6ATAR01018	Up	M6ADIS0061	.	37215454	METTL14 Facilitates the Metastasis of Pancreatic Carcinoma by Stabilizing LINC00941 in an m6A-IGF2BP2-Dependent Manner.
item2484	REG00014	M6ATAR00321	Up	M6ADIS0007	.	37171793	m6A-Dependent Modulation via IGF2BP3/MCM5/Notch Axis Promotes Partial EMT and LUAD Metastasis.
item2485	REG00013	M6ATAR01019	Up	M6ADIS0159	.	37530646	Klf6 aggravates myocardial ischemia/reperfusion injury by activating Acsl4-mediated ferroptosis. Igf2bp2 or Mettl3 knockdown decreased the Klf6 level and inhibited Klf6 mRNA stability.
item2486	REG00007	M6ATAR01019	Up	M6ADIS0159	.	37530646	Klf6 aggravates myocardial ischemia/reperfusion injury by activating Acsl4-mediated ferroptosis. Igf2bp2 or Mettl3 knockdown decreased the Klf6 level and inhibited Klf6 mRNA stability.
item2487	REG00007	M6ATAR00507	Up	M6ADIS0055	.	37498409	METTL3-Mediated Maturation of miR-99a-5p Promotes Cell Migration and Invasion in Oral Squamous Cell Carcinoma by Targeting ZBTB7A.
item2488	REG00005	M6ATAR01492	Down	M6ADIS0091	M6ADRUG0140	36859428	"Inhibition of ALKBH5 promotes the m6A modifications of Ccl28 mRNA, enhancing its stability, and regulating the Treg/inflammatory cell axis. ALKBH5 and this axis is a potential AKI treatment target.The ALKBH5 inhibitor IOX1 exhibits protective effects against I/R-induced AKI."
item2489	REG00007	M6ATAR00097	Up	M6ADIS0162	.	38075198	"Preeclampsia (PE) is a serious pregnancy-specific syndrome. METTL3-mediated lncRNA HOXD-AS1 stability regulates inflammation, and the migration and invasion of trophoblast cells via the miR-135a/ beta-TRCP axis."
item2490	REG00007	M6ATAR01020	Up	M6ADIS0349	.	37976602	"Mechanistically, methyltransferase-like 3 (METTL3) enhanced circMIRLET7BHG expression via m6A methylation, which enhanced ADAM10 mRNA stability via interaction with IGF2BP1,thereby promoting AR by inducing epithelial barrier dysfunction."
item2491	REG00012	M6ATAR01021	Up	M6ADIS0349	.	37976602	"Mechanistically, methyltransferase-like 3 (METTL3) enhanced circMIRLET7BHG expression via m6A methylation, which enhanced ADAM10 mRNA stability via interaction with IGF2BP1,thereby promoting AR by inducing epithelial barrier dysfunction."
item2492	REG00007	M6ATAR00844	Up	M6ADIS0067	.	36721236	"SLERT directly binds to METTL3, increasing the m6A levels of BDNF mRNA; then, the m6A sites were read by IGF2BP1, enhancing BDNF mRNA stability, followed by the activation of BDNF/TRKB signaling, an inducer of EMT."
item2493	REG00012	M6ATAR00844	Up	M6ADIS0067	.	36721236	"SLERT directly binds to METTL3, increasing the m6A levels of BDNF mRNA; then, the m6A sites were read by IGF2BP1, enhancing BDNF mRNA stability, followed by the activation of BDNF/TRKB signaling, an inducer of EMT."
item2494	REG00009	M6ATAR00196	.	M6ADIS0065	.	36333630	NRP1 contributes to stemness and potentiates radioresistance via WTAP-mediated m6A methylation of Bcl-2 mRNA in breast cancer.
item2495	REG00015	M6ATAR01022	Down	M6ADIS0177	.	37076815	"Carbohydrate sulfotransferase 11 (CHST11) was identified as a downstream target of KIAA1429, which mediated m6A modification of CHST11 mRNA and then recruited YTHDF2 for reducing CHST11 stability and expression,highlighting the potential of KIAA1429 as a novel predictive biomarker and therapeutic target for DLBCL progression."
item2496	REG00008	M6ATAR01022	Down	M6ADIS0177	.	37076815	"Carbohydrate sulfotransferase 11 (CHST11) was identified as a downstream target of KIAA1429, which mediated m6A modification of CHST11 mRNA and then recruited YTHDF2 for reducing CHST11 stability and expression,highlighting the potential of KIAA1429 as a novel predictive biomarker and therapeutic target for DLBCL progression."
item2497	REG00015	M6ATAR01023	Up	M6ADIS0054	.	37257820	"Silencing vir-like m6A methyltransferase-associated (VIRMA) and insulin-like growth factor 2 mRNA-binding proteins 1 (IGF2BP1) attenuated the expression level and RNA stability of LINC00839 in an m6A-dependent manner. Taken together, our study unveils a novel oncogenic VIRMA/IGF2BP1-LINC00839-TAF15-AOC1 axis and highlights the significance and prognostic value of LINC00839 expression in NPC carcinogenesis."
item2498	REG00012	M6ATAR01023	Up	M6ADIS0054	.	37257820	"Silencing vir-like m6A methyltransferase-associated (VIRMA) and insulin-like growth factor 2 mRNA-binding proteins 1 (IGF2BP1) attenuated the expression level and RNA stability of LINC00839 in an m6A-dependent manner. Taken together, our study unveils a novel oncogenic VIRMA/IGF2BP1-LINC00839-TAF15-AOC1 axis and highlights the significance and prognostic value of LINC00839 expression in NPC carcinogenesis."
item2499	REG00008	M6ATAR00945	Down	M6ADIS0032	.	36801705	Ythdf2 promotes pulmonary hypertension by suppressing Hmox1-dependent anti-inflammatory and antioxidant function in alveolar macrophages.
item2500	REG00005	M6ATAR01025	Up	M6ADIS0110	.	37752950	ALKBH5-mediated m6A demethylation of HS3ST3B1-IT1 prevents osteoarthritis progression.
item2501	REG00022	M6ATAR01026	.	.	.	36722312	The m6A reader YTHDC1 regulates muscle stem cell proliferation via PI4K-Akt-mTOR signalling.
item2502	REG00007	M6ATAR01493	Down	M6ADIS0057	.	37344779	METTL3 regulates N6-methyladenosine modification of ANGPTL3 mRNA and potentiates malignant progression of stomach adenocarcinoma.
item2503	REG00020	M6ATAR00323	.	M6ADIS0066	M6ADRUG0089	37594126	RBM15-mediating MDR1 mRNA m6A methylation regulated by the TGF/beta signaling pathway in paclitaxel-resistant ovarian cancer.
item2504	REG00008	M6ATAR01028	Down	M6ADIS0197	.	38026444	"YTHDF2 plays an essential role as an inhibitor of inflammation to reduce the release of HMGB1 by inhibiting the IL-6R/JAK2/STAT1 pathway, indicating that YTHDF2 is a novel target for therapeutic interventions in sepsis."
item2505	REG00001	M6ATAR00186	.	M6ADIS0080	M6ADRUG0163	37039556	"NR3C1-enhancement upregulated the RNA demethylase FTO (fat mass and obesity associated) protein in beta-cells, which caused diminished m6A modifications on mRNAs of four core Atg (autophagy related) genes (Atg12, Atg5, Atg16l2, Atg9a) and, hence, hyperactive autophagy and defective insulin output; by contrast, FTO inhibition, achieved by the specific FTO inhibitor Dac51, prevented NR3C1-instigated excessive autophagy activation."
item2506	REG00001	M6ATAR00189	.	M6ADIS0080	M6ADRUG0163	37039556	"NR3C1-enhancement upregulated the RNA demethylase FTO (fat mass and obesity associated) protein in beta-cells, which caused diminished m6A modifications on mRNAs of four core Atg (autophagy related) genes (Atg12, Atg5, Atg16l2, Atg9a) and, hence, hyperactive autophagy and defective insulin output; by contrast, FTO inhibition, achieved by the specific FTO inhibitor Dac51, prevented NR3C1-instigated excessive autophagy activation."
item2507	REG00001	M6ATAR01029	.	M6ADIS0080	M6ADRUG0163	37039556	"NR3C1-enhancement upregulated the RNA demethylase FTO (fat mass and obesity associated) protein in beta-cells, which caused diminished m6A modifications on mRNAs of four core Atg (autophagy related) genes (Atg12, Atg5, Atg16l2, Atg9a) and, hence, hyperactive autophagy and defective insulin output; by contrast, FTO inhibition, achieved by the specific FTO inhibitor Dac51, prevented NR3C1-instigated excessive autophagy activation."
item2508	REG00001	M6ATAR01030	.	M6ADIS0080	M6ADRUG0163	37039556	"NR3C1-enhancement upregulated the RNA demethylase FTO (fat mass and obesity associated) protein in beta-cells, which caused diminished m6A modifications on mRNAs of four core Atg (autophagy related) genes (Atg12, Atg5, Atg16l2, Atg9a) and, hence, hyperactive autophagy and defective insulin output; by contrast, FTO inhibition, achieved by the specific FTO inhibitor Dac51, prevented NR3C1-instigated excessive autophagy activation."
item2509	REG00013	M6ATAR01494	Up	M6ADIS0006	.	37985379	IGF2BP2 promotes glycolysis and hepatocellular carcinoma stemness by stabilizing CDC45 mRNA via m6A modification.
item2510	REG00007	M6ATAR01031	Up	M6ADIS0006	.	37881126	"MiR-935 targeted GJA1 and mediated CCA cell tumor properties by negatively regulating GJA1 expression. METTL3 promoted miR-935 maturation by inducing m6A methylation of pri-miR-935, and its overexpression contributed to CCA cell tumor properties through the regulation of miR-935. METTL3 promoted choriocarcinoma progression by m6A-dependently activating the miR-935/GJA1 pathway."
item2511	REG00007	M6ATAR00274	Up	M6ADIS0391	.	37715457	"Our results indicate the crucial role of NETs in the progression of SI-ALI via NET-activated METTL3 m6A-IGF2BP2-dependent m6A modification of HIF-1alpha, which further contributes to metabolic reprogramming and ferroptosis in alveolar epithelial cells."
item2512	REG00013	M6ATAR00274	Up	M6ADIS0391	.	37715457	"Our results indicate the crucial role of NETs in the progression of SI-ALI via NET-activated METTL3 m6A-IGF2BP2-dependent m6A modification of HIF-1alpha, which further contributes to metabolic reprogramming and ferroptosis in alveolar epithelial cells."
item2513	REG00007	M6ATAR01033	Up	M6ADIS0068	.	37563361	"METTL3 overexpression increased circABCC4 expression via m6A modification in PCa cells.circABCC4 recruited IGF2BP2 protein to CCAR1 mRNA, thereby enhancing CCAR1 mRNA stability and subsequent activation of the Wnt/beta-catenin pathway."
item2514	REG00013	M6ATAR01495	Up	M6ADIS0068	.	37563361	"METTL3 overexpression increased circABCC4 expression via m6A modification in PCa cells.circABCC4 recruited IGF2BP2 protein to CCAR1 mRNA, thereby enhancing CCAR1 mRNA stability and subsequent activation of the Wnt/beta-catenin pathway."
item2515	REG00020	M6ATAR00341	Up	M6ADIS0008	.	37191290	"HPV-E6 can downregulate autophagy, inhibit the degradation of RBM15 protein, induce the accumulation of intracellular RBM15, and increase the m6A modification on c-myc mRNA, resulting in an increase of c-myc protein and a growth promotion for cervical cancer cells."
item2516	REG00007	M6ATAR01034	.	M6ADIS0154	M6ADRUG0127	37958388	"OMT exhibited a dose-dependent inhibitory effect on the volume of IH PPNL-resistant tumors, which was partially dependent on the regulation of m6A methylation transfer enzyme METTL3 and the miR-27a-3p/PPAR-gamma axis, thereby inducing apoptosis."
item2517	REG00007	M6ATAR01034	.	M6ADIS0154	M6ADRUG0124	37958388	"OMT exhibited a dose-dependent inhibitory effect on the volume of IH PPNL-resistant tumors, which was partially dependent on the regulation of m6A methylation transfer enzyme METTL3 and the miR-27a-3p/PPAR-gamma axis, thereby inducing apoptosis."
item2518	REG00017	M6ATAR01035	.	M6ADIS0006	.	38089592	Hypoxia induces hepatocellular carcinoma metastasis via the HIF-1alpha/METTL16/lnc-CSMD1-7/RBFOX2 axis.
item2519	REG00001	M6ATAR01036	Up	M6ADIS0056	.	37858471	These results elucidate the mechanism by which FTO-stabilized LINK-A plays oncogenic roles and identify the FTO/LINK-A/MCM3/HIF-1alpha axis as a promising therapeutic target for ESCC.
item2520	REG00012	M6ATAR00341	Down	M6ADIS0057	.	38115228	Tumor suppressive function of IGF2BP1 in gastric cancer through decreasing MYC.
item2521	REG00007	M6ATAR01496	Up	M6ADIS0057	.	36806557	"METTL3-mediated m6A modification promotes mRNA stability of SUV39H2 in an IGF2BP2 dependent manner, resulting in upregulated mRNA expression of SUV39H2. As a histone methyltransferase, SUV39H2 was verified to increase the phosphorylation level of ATM through transcriptional repression of DUSP6, thereby promoting HRR and ultimately inhibiting GC chemosensitivity to cisplatin."
item2522	REG00013	M6ATAR01496	Up	M6ADIS0057	.	36806557	"METTL3-mediated m6A modification promotes mRNA stability of SUV39H2 in an IGF2BP2 dependent manner, resulting in upregulated mRNA expression of SUV39H2. As a histone methyltransferase, SUV39H2 was verified to increase the phosphorylation level of ATM through transcriptional repression of DUSP6, thereby promoting HRR and ultimately inhibiting GC chemosensitivity to cisplatin."
item2523	REG00007	M6ATAR01497	Up	M6ADIS0099	.	36951060	"METTL3 targeted adenine (39725126 in chromosome 6) on the Braf mRNA. Then, YTHDF1 could bind to m6A-methylated Braf mRNA and promoted its translation.METTL3 (Methyltransferase Like 3)-Dependent N6-Methyladenosine Modification on Braf mRNA Promotes Macrophage Inflammatory Response and Atherosclerosis in Mice."
item2524	REG00024	M6ATAR01497	Up	M6ADIS0099	.	36951060	"METTL3 targeted adenine (39725126 in chromosome 6) on the Braf mRNA. Then, YTHDF1 could bind to m6A-methylated Braf mRNA and promoted its translation.METTL3 (Methyltransferase Like 3)-Dependent N6-Methyladenosine Modification on Braf mRNA Promotes Macrophage Inflammatory Response and Atherosclerosis in Mice."
item2525	REG00006	M6ATAR00373	.	M6ADIS0257	M6ADRUG0067	37730054	"NaAsO2induced hepatic IR and ferroptosis via methyltransferase-like 14 (METTL14) and YTH domain-containing family protein 2 (YTHDF2)-mediated N6-methyladenosine (m6A) of PGC-1alpha mRNA. In conclusion, NaAsO2-mediated PGC-1alpha suppression was m6A methylation-dependent and induced ferroptosis via the PGC-1alpha/NRF1/GSTK1 pathway in hepatic IR. The data might provide insight into potential targets for diabetes prevention and treatment."
item2526	REG00006	M6ATAR00373	.	M6ADIS0257	M6ADRUG0067	37730054	"NaAsO2induced hepatic IR and ferroptosis via methyltransferase-like 14 (METTL14) and YTH domain-containing family protein 2 (YTHDF2)-mediated N6-methyladenosine (m6A) of PGC-1alpha mRNA. In conclusion, NaAsO2-mediated PGC-1alpha suppression was m6A methylation-dependent and induced ferroptosis via the PGC-1alpha/NRF1/GSTK1 pathway in hepatic IR. The data might provide insight into potential targets for diabetes prevention and treatment."
item2527	REG00008	M6ATAR00373	.	M6ADIS0233	M6ADRUG0067	37730054	"NaAsO2induced hepatic IR and ferroptosis via methyltransferase-like 14 (METTL14) and YTH domain-containing family protein 2 (YTHDF2)-mediated N6-methyladenosine (m6A) of PGC-1alpha mRNA. In conclusion, NaAsO2-mediated PGC-1alpha suppression was m6A methylation-dependent and induced ferroptosis via the PGC-1alpha/NRF1/GSTK1 pathway in hepatic IR. The data might provide insight into potential targets for diabetes prevention and treatment."
item2528	REG00008	M6ATAR00373	.	M6ADIS0233	M6ADRUG0067	37730054	"NaAsO2induced hepatic IR and ferroptosis via methyltransferase-like 14 (METTL14) and YTH domain-containing family protein 2 (YTHDF2)-mediated N6-methyladenosine (m6A) of PGC-1alpha mRNA. In conclusion, NaAsO2-mediated PGC-1alpha suppression was m6A methylation-dependent and induced ferroptosis via the PGC-1alpha/NRF1/GSTK1 pathway in hepatic IR. The data might provide insight into potential targets for diabetes prevention and treatment."
item2529	REG00024	M6ATAR01009	Up	M6ADIS0059	M6ADRUG0047	38024865	YTHDF1 recruitment onto m6A-amended TRIM27 was crucial for facilitating the TRIM27 translating process in DDP-resistant CRC cells.
item2530	REG00007	M6ATAR01037	Up	M6ADIS0001	M6ADRUG0010	37427890	Circ TTLL13 Promotes TMZ Resistance in Glioma via Modulating OLR1-Mediated Activation of the Wnt/beta-Catenin Pathway.circTTLL13 stabilizes OLR1 mRNA via recruiting YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) and promotes m6A methylation of OLR1 pre-mRNA through recruiting methyltransferase-like 3 (METTL3).
item2531	REG00024	M6ATAR01037	Up	M6ADIS0001	M6ADRUG0010	37427890	Circ TTLL13 Promotes TMZ Resistance in Glioma via Modulating OLR1-Mediated Activation of the Wnt/beta-Catenin Pathway.circTTLL13 stabilizes OLR1 mRNA via recruiting YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) and promotes m6A methylation of OLR1 pre-mRNA through recruiting methyltransferase-like 3 (METTL3).
item2532	REG00014	M6ATAR01038	Up	M6ADIS0027	M6ADRUG0047	37056932	IGF2BP3 Regulates TMA7-mediated Autophagy and Cisplatin Resistance in Laryngeal Cancer via m6A RNA Methylation.
item2533	REG00001	M6ATAR00223	Up	.	.	36460765	Transient downregulation of YTHDF2 or activation of FTO by using these compounds inhibits CXCR4 decay in CB HSCs and promotes their homing and engraftment. Our results demonstrate a novel regulation strategy to enhance the function of CB HSCs and provide a translational approach to enhance the clinical efficacy of HCT.
item2534	REG00008	M6ATAR00223	Down	.	.	36460765	Transient downregulation of YTHDF2 or activation of FTO by using these compounds inhibits CXCR4 decay in CB HSCs and promotes their homing and engraftment. Our results demonstrate a novel regulation strategy to enhance the function of CB HSCs and provide a translational approach to enhance the clinical efficacy of HCT.
item2535	REG00001	M6ATAR00411	Up	M6ADIS0107	.	36352530	Aberrant elevation of FTO levels promotes liver steatosis by decreasing the m6A methylation and increasing the stability of SREBF1 and ChREBP mRNAs.
item2536	REG00001	M6ATAR01039	Up	M6ADIS0107	.	36352530	Aberrant elevation of FTO levels promotes liver steatosis by decreasing the m6A methylation and increasing the stability of SREBF1 and ChREBP mRNAs.
item2537	REG00009	M6ATAR01040	Up	M6ADIS0008	.	37325054	"PiRNA-17458 is overexpressed in CC tissues and cells, but also shows that piRNA-17458 promotes tumorigenesis of CC in a WTAP-mediated m6A methylation manner."
item2538	REG00006	M6ATAR00466	Up	M6ADIS0008	.	38053376	"TRIM11 mediated by the METTL14-IGF2BP1 axis promotes the AKT pathway to accelerate CC progression by mediating the ubiquitination of PHLPP, which might provide novel therapeutic targets for CC treatment."
item2539	REG00012	M6ATAR00466	Up	M6ADIS0008	.	38053376	"TRIM11 mediated by the METTL14-IGF2BP1 axis promotes the AKT pathway to accelerate CC progression by mediating the ubiquitination of PHLPP, which might provide novel therapeutic targets for CC treatment."
item2540	REG00007	M6ATAR01041	Up	M6ADIS0007	.	37774794	"C-MYC/METTL3/LINC01006 positive feedback loop promotes migration, invasion and proliferation of non-small cell lung cancer."
item2541	REG00007	M6ATAR01042	Down	M6ADIS0359	.	37323630	METTL3 Promotes Osteo/Odontogenic Differentiation of Stem Cells by Inhibiting miR-196b-5p Maturation.
item2542	REG00009	M6ATAR01043	Up	M6ADIS0115	.	36650131	"The WTAP/YTHDC1/miR-181a and miR-181c/SFRP1 axis regulated the differentiation fate of BMSCs, suggesting that it might be a potential therapeutic target for osteoporosis."
item2543	REG00009	M6ATAR01044	Up	M6ADIS0115	.	36650131	"The WTAP/YTHDC1/miR-181a and miR-181c/SFRP1 axis regulated the differentiation fate of BMSCs, suggesting that it might be a potential therapeutic target for osteoporosis."
item2544	REG00022	M6ATAR01043	Up	M6ADIS0115	.	36650131	"The WTAP/YTHDC1/miR-181a and miR-181c/SFRP1 axis regulated the differentiation fate of BMSCs, suggesting that it might be a potential therapeutic target for osteoporosis."
item2545	REG00022	M6ATAR01044	Up	M6ADIS0115	.	36650131	"The WTAP/YTHDC1/miR-181a and miR-181c/SFRP1 axis regulated the differentiation fate of BMSCs, suggesting that it might be a potential therapeutic target for osteoporosis."
item2546	REG00009	M6ATAR00488	Up	M6ADIS0057	.	36030434	"WTAP knockdown inhibited migration of GC cells and decreased TGF-beta expression and stability of mRNA. In addition, WTAP promoted multiple chemotherapy resistance and radiotherapy resistance in GC."
item2547	REG00012	M6ATAR00360	Up	M6ADIS0058	.	37848671	IGF2BP1 targeted PD-L1 to accelerate the immune escape in colon cancer by reducing CD8 + T cells-mediated tumor cytotoxicity in m6A-dependent manner.
item2548	REG00009	M6ATAR01499	Up	M6ADIS0065	.	37856011	"WTAP (Wilms tumor 1-associated protein) bound to EXOSC2 mRNA and increased its m6A methylation, resulting in extending the half-life of EXOSC2 mRNA.EXOSC2 Mediates the Pro-tumor Role of WTAP in Breast Cancer Cells via Activating the Wnt/beta-Catenin Signal."
item2549	REG00006	M6ATAR00619	Up	M6ADIS0072	.	37466203	"HDACis exert anti-cancer effects by orchestrating m6A modification, which unveiling a ""histone-RNA crosstalk"" of the HDAC/METTL14/FAT4 epigenetic cascade in ocular melanoma."
item2550	REG00001	M6ATAR00410	Down	M6ADIS0363	M6ADRUG0178	36685533	This study uncovered a previously unrecognized function of canagliflozin in FTO in the autophagy modulation through the regulation of SQSTM1 mRNA stability in the renal tubular STAT6/PPARalpha/FAO axis and renal fibrosis.
item2551	REG00015	M6ATAR01046	Up	M6ADIS0059	.	36373629	Promotive role of USP29-mediated deubiquitination in malignant proliferation of colorectal cancer cells via the KIAA1429/SOX8 axis.
item2552	REG00023	M6ATAR01047	Up	M6ADIS0234	.	38157933	The m6A reader YTHDC2 maintains visual function and retinal photoreceptor survival through modulating translation of PPEF2 and PDE6B.
item2553	REG00023	M6ATAR01048	Up	M6ADIS0234	.	38157933	The m6A reader YTHDC2 maintains visual function and retinal photoreceptor survival through modulating translation of PPEF2 and PDE6B.
item2554	REG00009	M6ATAR00418	.	M6ADIS0057	.	37983949	"Mechanistically, AGAP2-AS1 bound WT1-associated protein (WTAP) to promote the formation of the WTAP/methyltransferase-like 3 (METTL3)/METTL14 m6A methyltransferase complex. AGAP2-AS1 stabilized signal transducer and activator of transcription 3 (STAT3) mRNA in an m6A-dependent manner and, thus, activated the interleukin 6 (IL6)/STAT3 pathway. Importantly, activation of the AGAP2-AS1/WTAP/STAT3 pathways promoted cell proliferation and migration in GC."
item2555	REG00007	M6ATAR00418	.	M6ADIS0057	.	37983949	"Mechanistically, AGAP2-AS1 bound WT1-associated protein (WTAP) to promote the formation of the WTAP/methyltransferase-like 3 (METTL3)/METTL14 m6A methyltransferase complex. AGAP2-AS1 stabilized signal transducer and activator of transcription 3 (STAT3) mRNA in an m6A-dependent manner and, thus, activated the interleukin 6 (IL6)/STAT3 pathway. Importantly, activation of the AGAP2-AS1/WTAP/STAT3 pathways promoted cell proliferation and migration in GC."
item2556	REG00006	M6ATAR00418	.	M6ADIS0057	.	37983949	"Mechanistically, AGAP2-AS1 bound WT1-associated protein (WTAP) to promote the formation of the WTAP/methyltransferase-like 3 (METTL3)/METTL14 m6A methyltransferase complex. AGAP2-AS1 stabilized signal transducer and activator of transcription 3 (STAT3) mRNA in an m6A-dependent manner and, thus, activated the interleukin 6 (IL6)/STAT3 pathway. Importantly, activation of the AGAP2-AS1/WTAP/STAT3 pathways promoted cell proliferation and migration in GC."
item2557	REG00007	M6ATAR00645	Down	M6ADIS0007	.	37106069	METTL3 promotes the malignancy of non-small cell lung cancer by N6-methyladenosine modifying SFRP2.
item2558	REG00007	M6ATAR01011	Up	M6ADIS0257	.	36653890	N6-Methyladenosine Methyltransferase METTL3 Alleviates Diabetes-Induced Testicular Damage through Modulating TUG1/Clusterin Axis.
item2559	REG00001	M6ATAR01500	.	M6ADIS0061	M6ADRUG0024	37605223	m6A eraser FTO impairs gemcitabine resistance in pancreatic cancer through influencing NEDD4 mRNA stability by regulating the PTEN/PI3K/AKT pathway.
item2560	REG00025	M6ATAR01049	Down	.	.	38205248	YTHDF3 modulates the Cbln1 level by recruiting BTG2 and is implicated in the impaired cognition of prenatal hypoxia offspring.
item2561	REG00007	M6ATAR01050	Up	M6ADIS0006	.	38125436	METTL3/YTHDC1-mediated upregulation of LINC00294 promotes hepatocellular carcinoma progression.LINC00294 promoted the interaction between YTHDC1 and HK2 and GLUT1 mRNA.
item2562	REG00022	M6ATAR01050	Up	M6ADIS0006	.	38125436	METTL3/YTHDC1-mediated upregulation of LINC00294 promotes hepatocellular carcinoma progression.LINC00294 promoted the interaction between YTHDC1 and HK2 and GLUT1 mRNA.
item2563	REG00007	M6ATAR00269	Up	M6ADIS0006	.	38125436	METTL3/YTHDC1-mediated upregulation of LINC00294 promotes hepatocellular carcinoma progression.LINC00294 promoted the interaction between YTHDC1 and HK2 and GLUT1 mRNA.
item2564	REG00008	M6ATAR01501	Down	M6ADIS0384	.	36642058	Suppression of YTHDF2 attenuates autoimmune hepatitis by expansion of myeloid-derived suppressor cells.YTHDF2 directly binds RXRalpha mRNA thus promoting degradation and decreasing gene expression.
item2565	REG00005	M6ATAR01051	Up	M6ADIS0007	.	37884580	"AlkB homolog 5 (ALKBH5) enhanced CALML3-AS1 stability via N6-methyladenosine (m6A) demethylation, whereas m6A reader YTH domain-containing 2 (YTHDC2) destabilized CALML3-AS1.LncRNA CALML3-AS1 modulated by m6A modification induces BTNL9 methylation to drive non-small-cell lung cancer progression."
item2566	REG00023	M6ATAR01051	Down	M6ADIS0007	.	37884580	"AlkB homolog 5 (ALKBH5) enhanced CALML3-AS1 stability via N6-methyladenosine (m6A) demethylation, whereas m6A reader YTH domain-containing 2 (YTHDC2) destabilized CALML3-AS1.LncRNA CALML3-AS1 modulated by m6A modification induces BTNL9 methylation to drive non-small-cell lung cancer progression."
item2567	REG00007	M6ATAR01502	.	M6ADIS0125	.	37952687	Mettl3/Ythdf2 regulate macrophage inflammation and ROS generation by controlling Pyk2 mRNA stability.
item2568	REG00008	M6ATAR01502	.	M6ADIS0125	.	37952687	Mettl3/Ythdf2 regulate macrophage inflammation and ROS generation by controlling Pyk2 mRNA stability.
item2569	REG00005	M6ATAR00736	Down	M6ADIS0091	.	38056583	ALKBH5 protects against stroke by reducing endoplasmic reticulum stress-dependent inflammation injury via the STAT5/PERK/EIF2alpha/CHOP signaling pathway in an m6A-YTHDF1-dependent manner.
item2570	REG00024	M6ATAR00736	Down	M6ADIS0091	.	38056583	ALKBH5 protects against stroke by reducing endoplasmic reticulum stress-dependent inflammation injury via the STAT5/PERK/EIF2alpha/CHOP signaling pathway in an m6A-YTHDF1-dependent manner.
item2571	REG00007	M6ATAR00017	Up	M6ADIS0164	.	37666296	m6A-modified miR-143-3p inhibits epithelial mesenchymal transition in bronchial epithelial cells and extracellular matrix production in lung fibroblasts by targeting Smad3.
item2572	REG00005	M6ATAR01054	Up	M6ADIS0046	.	36899424	RNA demethylase ALKBH5 promotes tumorigenesis of t (8;21) acute myeloid leukemia via ITPA m6A modification.
item2573	REG00017	M6ATAR01503	Up	M6ADIS0228	.	36608679	METTL16 drives leukemogenesis and leukemia stem cell self-renewal by reprogramming BCAA metabolism.METTL16 exerts its oncogenic role by promoting expression of branched-chain amino acid (BCAA) transaminase 1 (BCAT1) and BCAT2 in an m6A-dependent manner and reprogramming BCAA metabolism in AML.
item2574	REG00017	M6ATAR01504	Up	M6ADIS0228	.	36608679	METTL16 drives leukemogenesis and leukemia stem cell self-renewal by reprogramming BCAA metabolism.METTL16 exerts its oncogenic role by promoting expression of branched-chain amino acid (BCAA) transaminase 1 (BCAT1) and BCAT2 in an m6A-dependent manner and reprogramming BCAA metabolism in AML.
item2575	REG00007	M6ATAR00594	Down	M6ADIS0369	.	37355654	"TRF-22 interacted with METTL3 and blocked m6A methylation of Axin1 and Arid1b mRNA transcripts, which led to increased expression of Axin1 and Arid1b.Targeting choroidal vasculopathy via up-regulation of tRNA-derived fragment tRF-22 expression for controlling progression of myopia."
item2576	REG00007	M6ATAR01505	Down	M6ADIS0369	.	37355654	"TRF-22 interacted with METTL3 and blocked m6A methylation of Axin1 and Arid1b mRNA transcripts, which led to increased expression of Axin1 and Arid1b.Targeting choroidal vasculopathy via up-regulation of tRNA-derived fragment tRF-22 expression for controlling progression of myopia."
item2577	REG00007	M6ATAR01055	Up	M6ADIS0006	.	37498069	METTL3 mediated m6A modification of SLC7A11-AS1 to elevate its expression.LncRNA SLC7A11-AS1 promotes the progression of hepatocellular carcinoma by mediating KLF9 ubiquitination.
item2578	REG00009	M6ATAR01056	Up	.	.	36586770	WTAP-mediated m6A modification on circCMTM3 inhibits hepatocellular carcinoma ferroptosis by recruiting IGF2BP1 to increase PARK7 stability.
item2579	REG00012	M6ATAR01506	Up	.	.	36586770	WTAP-mediated m6A modification on circCMTM3 inhibits hepatocellular carcinoma ferroptosis by recruiting IGF2BP1 to increase PARK7 stability.
item2580	REG00009	M6ATAR00446	Up	M6ADIS0059	.	37428639	WTAP activates MAPK signaling through m6A methylation in VEGFA mRNA-mediated by YTHDC1 to promote colorectal cancer development.
item2581	REG00022	M6ATAR00446	Up	M6ADIS0059	.	37428639	WTAP activates MAPK signaling through m6A methylation in VEGFA mRNA-mediated by YTHDC1 to promote colorectal cancer development.
item2582	REG00008	M6ATAR01057	Up	M6ADIS0057	.	36870954	YTHDF2 exerts tumor-suppressor roles in gastric cancer via up-regulating PPP2CA independently of m6A modification.
item2583	REG00001	M6ATAR00348	Up	M6ADIS0091	.	37812019	Ischemic stroke (IS) can cause neuronal cell loss and function defects.Neural stem cell-derived exosomal FTO protects neuron from microglial inflammatory injury by inhibiting microglia NRF2 mRNA m6A modification.
item2584	REG00007	M6ATAR01058	Down	M6ADIS0059	.	38091882	METTL3 mediated m6A methylation of circ_0124554.m6A-modified circ_0124554 promoted CRC progression and radioresistance by inducing LASP1 expression through interaction with miR-1184.
item2585	REG00012	M6ATAR01507	Up	M6ADIS0091	.	37966628	YBX1 enhanced the stability of m6A-modified GPR30 by interacting with IGF2BP1 and thus promoting GPR30 expression.Neural Stem Cell Extracellular Vesicles Carrying YBX1 Inhibited Neuronal Pyroptosis Through Increasing m6A-modified GPR30 Stability and Expression in Ischemic Stroke.
item2586	REG00007	M6ATAR01508	Up	M6ADIS0172	.	37434495	The m6A modification of IL17A mRNA increased the expression of IL-17A (an important pro-inflammatory factor in psoriasis) and promoted psoriasis.
item2587	REG00005	M6ATAR01508	Down	M6ADIS0172	.	37434495	The m6A modification of IL17A mRNA increased the expression of IL-17A (an important pro-inflammatory factor in psoriasis) and promoted psoriasis.
item2588	REG00020	M6ATAR01059	Up	M6ADIS0008	.	37334762	RBM15 m6 A modification-mediated OTUB2 upregulation promotes cervical cancer progression via the AKT/mTOR signaling.
item2589	REG00007	M6ATAR01060	Up	M6ADIS0097	.	37752784	Programmed Release METTL3-14 Inhibitor Microneedle Protects Myocardial Function by Reducing Drp1 m6A Modification-Mediated Mitochondrial Fission.
item2590	REG00006	M6ATAR01060	Up	M6ADIS0097	.	37752784	Programmed Release METTL3-14 Inhibitor Microneedle Protects Myocardial Function by Reducing Drp1 m6A Modification-Mediated Mitochondrial Fission.
item2591	REG00020	M6ATAR01509	Up	M6ADIS0107	.	38150369	RBM15 upregulated RNF5 expression through m6A methylation modification. RNF5 inhibited ROCK1 expression through ubiquitination modification to mitigate NAFLD.
item2592	REG00013	M6ATAR01061	Up	M6ADIS0066	.	37665628	IGF2BP2 promotes ovarian cancer growth and metastasis by upregulating CKAP2L protein expression in an m6A-dependent manner.
item2593	REG00001	M6ATAR01062	Down	M6ADIS0376	.	37409616	"Demethylase knockdown of FTO promoted TXNIP expression, activation of NLRP3 inflammasome and promoted the release of proinflammatory factors in vitro, and the opposite result occurred with demethylase FTO overexpression.the NLRP3 inflammasome was stimulated, leading to the release of proinflammatory factors and facilitating HFMD progression."
item2594	REG00005	M6ATAR00605	Down	M6ADIS0112	.	37244037	ALKBH5-YTHDF2 m6A modification axis inhibits rheumatoid arthritis progression by suppressing NLRP3.
item2595	REG00008	M6ATAR00605	Down	M6ADIS0112	.	37244037	ALKBH5-YTHDF2 m6A modification axis inhibits rheumatoid arthritis progression by suppressing NLRP3.
item2596	REG00007	M6ATAR01063	Up	M6ADIS0066	.	37738681	"METTL3/IGF2BP1-mediated m6A modification maintained circASXL1 stability and upregulated its expression.m6A-modified circASXL1 acts as an oncogene in OC by targeting miR-320d and activating RACGAP1/PI3K/Akt pathway, which provides novel promising biomarkers for OC diagnosis."
item2597	REG00012	M6ATAR01063	Up	M6ADIS0066	.	37738681	"METTL3/IGF2BP1-mediated m6A modification maintained circASXL1 stability and upregulated its expression.m6A-modified circASXL1 acts as an oncogene in OC by targeting miR-320d and activating RACGAP1/PI3K/Akt pathway, which provides novel promising biomarkers for OC diagnosis."
item2598	REG00003	M6ATAR00179	Up	M6ADIS0065	.	37528369	HNRNPC promotes collagen fiber alignment and immune evasion in breast cancer via activation of the VIRMA-mediated TFAP2A/DDR1 axis.
item2599	REG00015	M6ATAR00179	Up	M6ADIS0065	.	37528369	HNRNPC promotes collagen fiber alignment and immune evasion in breast cancer via activation of the VIRMA-mediated TFAP2A/DDR1 axis.
item2600	REG00007	M6ATAR01064	Down	M6ADIS0007	M6ADRUG0108	36932427	"The m6A methyltransferase METTL3 regulates Pink1-Parkin pathway-mediated mitophagy and mitochondrial damage in SCLC cells by targeting DCP2, thereby promoting chemotherapy resistance in patients with SCLC. STM2457, a novel METTL3 inhibitor, can reverse SCLC chemoresistance."
item2601	REG00001	M6ATAR01065	.	M6ADIS0274	M6ADRUG0130	37795601	Prenatal Nicotine Exposure Raises Male Blood Pressure via FTO-Mediated NOX2/ROS Signaling.
item2602	REG00001	M6ATAR01066	Up	M6ADIS0061	.	35879877	"N6 -methyladenosine RNA demethylase FTO regulates extracellular matrix-related genes and promotes pancreatic cancer cell migration and invasion.after knockdown of FTO, the mRNA levels of ADAMTS2, COL12A1, and THBS2 and their m6A modification levels were significantly reduced."
item2603	REG00001	M6ATAR01067	Up	M6ADIS0061	.	35879877	"N6 -methyladenosine RNA demethylase FTO regulates extracellular matrix-related genes and promotes pancreatic cancer cell migration and invasion.after knockdown of FTO, the mRNA levels of ADAMTS2, COL12A1, and THBS2 and their m6A modification levels were significantly reduced."
item2604	REG00001	M6ATAR01068	Up	M6ADIS0061	.	35879877	"N6 -methyladenosine RNA demethylase FTO regulates extracellular matrix-related genes and promotes pancreatic cancer cell migration and invasion.after knockdown of FTO, the mRNA levels of ADAMTS2, COL12A1, and THBS2 and their m6A modification levels were significantly reduced."
item2605	REG00015	M6ATAR00484	.	M6ADIS0006	M6ADRUG0150	37830241	KIAA1429 protects hepatocellular carcinoma cells from ferroptotic cell death with a m6 A-dependent posttranscriptional modification of SLC7A11.Ferroptosis inhibitors ferrostatin-1 (0.5 &mu;M) and liproxstatin-1 (10 &mu;M) blocked KIAA1429 suppression-induced ferroptosis of HCC cells.The regulation SLC7A11 by KIAA1429 was attenuated by global m6A inhibitor cycloleucine (40 &mu;M).
item2606	REG00015	M6ATAR00484	.	M6ADIS0006	M6ADRUG0136	37830241	KIAA1429 protects hepatocellular carcinoma cells from ferroptotic cell death with a m6 A-dependent posttranscriptional modification of SLC7A11.Ferroptosis inhibitors ferrostatin-1 (0.5 &mu;M) and liproxstatin-1 (10 &mu;M) blocked KIAA1429 suppression-induced ferroptosis of HCC cells.The regulation SLC7A11 by KIAA1429 was attenuated by global m6A inhibitor cycloleucine (40 &mu;M).
item2607	REG00015	M6ATAR00484	.	M6ADIS0006	M6ADRUG0166	37830241	KIAA1429 protects hepatocellular carcinoma cells from ferroptotic cell death with a m6 A-dependent posttranscriptional modification of SLC7A11.Ferroptosis inhibitors ferrostatin-1 (0.5 &mu;M) and liproxstatin-1 (10 &mu;M) blocked KIAA1429 suppression-induced ferroptosis of HCC cells.The regulation SLC7A11 by KIAA1429 was attenuated by global m6A inhibitor cycloleucine (40 &mu;M).
item2608	REG00017	M6ATAR01069	Up	M6ADIS0006	.	37817227	The RNA methyltransferase METTL16 enhances cholangiocarcinoma growth through PRDM15-mediated FGFR4 expression.
item2609	REG00024	M6ATAR00375	Up	M6ADIS0091	.	36261761	Silencing of YTHDF1 Attenuates Cerebral Stroke by Inducing PTEN Degradation and Activating the PTEN/AKT/mTOR Pathway.
item2610	REG00005	M6ATAR01070	.	M6ADIS0228	.	37028412	Splice epitranscriptomics and DNA damage repair together: ALKBH5-m6A-SF3B1 regulation in leukemic transformation.
item2611	REG00047	M6ATAR00484	.	M6ADIS0006	M6ADRUG0032	37927237	"SNHG1, interacting with SND1, contributes to sorafenib resistance of liver cancer cells by increasing m6A-mediated SLC7A11 expression and promoting aerobic glycolysis."
item2612	REG00013	M6ATAR00323	Up	M6ADIS0065	M6ADRUG0034	38007504	A1BG-AS1 promotes adriamycin resistance of breast cancer by recruiting IGF2BP2 to upregulate ABCB1 in an m6A-dependent manner.
item2613	REG00007	M6ATAR01071	.	M6ADIS0006	M6ADRUG0108	37420030	"STM2457, a highly potent METTL3 inhibitor, which inhibited METTL3 activity and acted synergistically with gemcitabine, suggests that reprogramming RNA epigenetic modifications may serve as a potential therapeutic strategy.the METTL3/NFAT5 axis was a clinical target for the management of ICC chemoresistance by targeting cancer glycolysis."
item2614	REG00007	M6ATAR01071	.	M6ADIS0006	M6ADRUG0024	37420030	"STM2457, a highly potent METTL3 inhibitor, which inhibited METTL3 activity and acted synergistically with gemcitabine, suggests that reprogramming RNA epigenetic modifications may serve as a potential therapeutic strategy.the METTL3/NFAT5 axis was a clinical target for the management of ICC chemoresistance by targeting cancer glycolysis."
item2615	REG00001	M6ATAR00269	Up	M6ADIS0006	.	37840133	"FTO decreased m6A modification on mRNAs of glycolysis associated genes including GLUT1, PKM2, and c-Myc which alleviated the YTH N6-methyladenosine RNA binding protein 2 (YTHDF2)-mediated mRNA degradation. Therefore, the upregulated expression of FTO-IT1 leaded to overexpression of GLUT1, PKM2, and c-Myc by which enhanced glycolysis of HCC."
item2616	REG00008	M6ATAR00269	Down	M6ADIS0006	.	37840133	"FTO decreased m6A modification on mRNAs of glycolysis associated genes including GLUT1, PKM2, and c-Myc which alleviated the YTH N6-methyladenosine RNA binding protein 2 (YTHDF2)-mediated mRNA degradation. Therefore, the upregulated expression of FTO-IT1 leaded to overexpression of GLUT1, PKM2, and c-Myc by which enhanced glycolysis of HCC."
item2617	REG00001	M6ATAR00312	Up	M6ADIS0006	.	37840133	"FTO decreased m6A modification on mRNAs of glycolysis associated genes including GLUT1, PKM2, and c-Myc which alleviated the YTH N6-methyladenosine RNA binding protein 2 (YTHDF2)-mediated mRNA degradation. Therefore, the upregulated expression of FTO-IT1 leaded to overexpression of GLUT1, PKM2, and c-Myc by which enhanced glycolysis of HCC."
item2618	REG00008	M6ATAR00312	Down	M6ADIS0006	.	37840133	"FTO decreased m6A modification on mRNAs of glycolysis associated genes including GLUT1, PKM2, and c-Myc which alleviated the YTH N6-methyladenosine RNA binding protein 2 (YTHDF2)-mediated mRNA degradation. Therefore, the upregulated expression of FTO-IT1 leaded to overexpression of GLUT1, PKM2, and c-Myc by which enhanced glycolysis of HCC."
item2619	REG00001	M6ATAR00341	Up	M6ADIS0006	.	37840133	"FTO decreased m6A modification on mRNAs of glycolysis associated genes including GLUT1, PKM2, and c-Myc which alleviated the YTH N6-methyladenosine RNA binding protein 2 (YTHDF2)-mediated mRNA degradation. Therefore, the upregulated expression of FTO-IT1 leaded to overexpression of GLUT1, PKM2, and c-Myc by which enhanced glycolysis of HCC."
item2620	REG00008	M6ATAR00341	Down	M6ADIS0006	.	37840133	"FTO decreased m6A modification on mRNAs of glycolysis associated genes including GLUT1, PKM2, and c-Myc which alleviated the YTH N6-methyladenosine RNA binding protein 2 (YTHDF2)-mediated mRNA degradation. Therefore, the upregulated expression of FTO-IT1 leaded to overexpression of GLUT1, PKM2, and c-Myc by which enhanced glycolysis of HCC."
item2621	REG00005	M6ATAR01510	Up	.	.	37742191	Loss of ALKBH5 results in increased RNA methylation and instability of oxoglutarate-dehydrogenase (Ogdh) messenger RNA and reduction of OGDH protein levels.
item2622	REG00006	M6ATAR01414	Up	M6ADIS0115	.	37195267	METTL14 represses osteoclast formation to ameliorate osteoporosis via enhancing GPX4 mRNA stability.
item2623	REG00004	M6ATAR01072	Up	M6ADIS0059	.	36831695	HNRNPA2B1-Mediated MicroRNA-92a Upregulation and Section Acts as a Promising Noninvasive Diagnostic Biomarker in Colorectal Cancer.
item2624	REG00001	M6ATAR01073	Up	M6ADIS0055	.	37655555	FTO is overexpressed in HNSC tumor samples and positively regulates HOXD1 expression in an m6A-dependent manner.Homeobox-D 1 and FTO form a transcriptional-epigenetic feedback loop to promote head and neck cancer proliferation.
item2625	REG00007	M6ATAR00418	Up	M6ADIS0006	.	37231451	"METTL3 could induce the m6A modification of STAT3 mRNA, and then promote the translation of m6A-contained STAT3 mRNA by interacting with the translation initiation machinery.METTL3 and STAT3 form a positive feedback loop to promote cell metastasis in hepatocellular carcinoma."
item2626	REG00007	M6ATAR00341	Up	M6ADIS0177	.	37244946	NCBP1 enhanced proliferation of DLBCL cells via METTL3-mediated m6A modification of c-Myc.
item2627	REG00017	M6ATAR01074	Up	M6ADIS0007	.	36840945	METTL16 promotes translation and lung tumorigenesis by sequestering cytoplasmic eIF4E2.
item2628	REG00012	M6ATAR01414	Up	M6ADIS0065	.	37036576	RUNX1-IT1 favors breast cancer carcinogenesis through regulation of IGF2BP1/GPX4 axis.
item2629	REG00012	M6ATAR01511	Up	M6ADIS0059	.	38009760	"Linc00659 and IGF2BP1 cooperate to promote the stability of the target FZD6 mRNA, thereby facilitating CRC progression, which may represent a potential diagnostic, prognostic and therapeutic target for CRC."
item2630	REG00020	M6ATAR00283	Up	M6ADIS0051	.	36181462	"Circ-CTNNB1 interacted with RBM15 and subsequently promoted the expression of hexokinase 2 (HK2), glucose-6-phosphate isomerase (GPI) and phosphoglycerate kinase 1 (PGK1) through N6-methyladenosine (m6A) modification to facilitate the glycolysis process and activate OS progression."
item2631	REG00020	M6ATAR01512	Up	M6ADIS0051	.	36181462	"Circ-CTNNB1 interacted with RBM15 and subsequently promoted the expression of hexokinase 2 (HK2), glucose-6-phosphate isomerase (GPI) and phosphoglycerate kinase 1 (PGK1) through N6-methyladenosine (m6A) modification to facilitate the glycolysis process and activate OS progression."
item2632	REG00020	M6ATAR01438	Up	M6ADIS0051	.	36181462	"Circ-CTNNB1 interacted with RBM15 and subsequently promoted the expression of hexokinase 2 (HK2), glucose-6-phosphate isomerase (GPI) and phosphoglycerate kinase 1 (PGK1) through N6-methyladenosine (m6A) modification to facilitate the glycolysis process and activate OS progression."
item2633	REG00022	M6ATAR01075	Up	M6ADIS0007	.	37311754	"The nuclear m6A reader YTHDC1 regulated LINC00641 expression by affecting its stability. Downregulation of N6-methyladenosine-modified LINC00641 promotes EMT, but provides a ferroptotic vulnerability in lung cancer."
item2634	REG00005	M6ATAR01070	.	M6ADIS0228	.	36944332	ALKBH5-driven 5' UTR demethylation modulates SF3B1 translation upon oncogenic stress.m6A-driven SF3B1 translation control steers splicing to direct genome integrity and leukemogenesis.
item2635	REG00007	M6ATAR00610	.	M6ADIS0006	M6ADRUG0171	38030810	"METTL3 facilitates stemness properties and tumorigenicity of cancer stem cells in hepatocellular carcinoma through the SOCS3/JAK2/STAT3 signaling pathway.METTL3 depletion suppressed proliferation and stemness in LCSCs, which was restored by SOCS3 knockdown or colivelin treatment."
item2636	REG00008	M6ATAR00274	Down	.	M6ADRUG0172	36739042	YTHDF2 controls hexavalent chromium-induced mitophagy through modulating Hif1alpha and Bnip3 decay via the m6A/mRNA pathway in spermatogonial stem cells/progenitors .
item2637	REG00008	M6ATAR00201	Down	.	M6ADRUG0172	36739042	YTHDF2 controls hexavalent chromium-induced mitophagy through modulating Hif1alpha and Bnip3 decay via the m6A/mRNA pathway in spermatogonial stem cells/progenitors .
item2638	REG00024	M6ATAR00683	Down	.	.	37060562	YTHDF1 LLPS activates IkappaB-NF-kappaB-CCND1 axis by inhibiting IkappaBalpha/beta mRNA translation.
item2639	REG00001	M6ATAR01077	Up	M6ADIS0388	.	37408034	Adolescent idiopathic scoliosis (AIS) is characterized by low lean mass without vertebral deformity.FTO-dependent m6A regulates muscle fiber remodeling in an NFATC1-YTHDF2 dependent manner.
item2640	REG00008	M6ATAR01077	Down	M6ADIS0388	.	37408034	Adolescent idiopathic scoliosis (AIS) is characterized by low lean mass without vertebral deformity.FTO-dependent m6A regulates muscle fiber remodeling in an NFATC1-YTHDF2 dependent manner.
item2641	REG00006	M6ATAR00628	Up	M6ADIS0112	.	36878846	METTL14 promotes fibroblast-like synoviocytes activation via the LASP1/SRC/AKT axis in rheumatoid arthritis.
item2642	REG00013	M6ATAR00097	Up	M6ADIS0015	.	38088496	"PTEN overexpression abolished the inhibition of silenced HAGLR on pyroptosis in HRPE cells. HAGLR, epigenetically modified by IGF2BP2 in an m6A-dependent manner, functioned as a sponge for miR-106b-5p, thereby activating PTEN/Akt signaling cascade to accelerate DR pathology."
item2643	REG00007	M6ATAR01078	Up	M6ADIS0007	.	37156046	"Cigarette smoking, by accelerating the cell cycle, promotes the progression of non-small cell lung cancer through an HIF-1alpha-METTL3-m6A/CDK2AP2 axis."
item2644	REG00006	M6ATAR01079	.	M6ADIS0257	.	37565545	Mettl14 downregulation was observed to attenuate the abnormal differentiation of IECs through modulating Fzd2 m6A modification in DM state.
item2645	REG00007	M6ATAR00579	Down	M6ADIS0038	.	37542992	"N6-methyladenosine (m6A) and MELLT3 assume a role in the development of acute kidney injury (AKI).METTL3 knockdown decreased m6A methylation of MDM2, thus diminishing YTHDF1-mediated MDM2 mRNA stability and translation in LPS-treated HK-2 cells."
item2646	REG00024	M6ATAR00579	Up	M6ADIS0038	.	37542992	"N6-methyladenosine (m6A) and MELLT3 assume a role in the development of acute kidney injury (AKI).METTL3 knockdown decreased m6A methylation of MDM2, thus diminishing YTHDF1-mediated MDM2 mRNA stability and translation in LPS-treated HK-2 cells."
item2647	REG00001	M6ATAR01080	Up	.	.	37698901	The N6-methyladenosine demethylase FTO is required for odontoblast differentiation in vitro and dentine formation in mice by promoting RUNX2 exon 5 inclusion through RBM4.
item2648	REG00017	M6ATAR00828	Up	M6ADIS0059	.	37340443	"METTL16 significantly enhances SOGA1 expression and mRNA stability via binding the ""reader"" protein insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1).METTL16 promotes glycolytic metabolism reprogramming and colorectal cancer progression."
item2649	REG00012	M6ATAR00828	Up	M6ADIS0059	.	37340443	"METTL16 significantly enhances SOGA1 expression and mRNA stability via binding the ""reader"" protein insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1).METTL16 promotes glycolytic metabolism reprogramming and colorectal cancer progression."
item2650	REG00007	M6ATAR01081	.	M6ADIS0381	.	37679886	METTL3-mediated m6 A modification of circPRKAR1B promotes Crohn's colitis by inducing pyroptosis via autophagy inhibition.
item2651	REG00005	M6ATAR01082	.	M6ADIS0001	M6ADRUG0177	37180836	SPP1 is the downstream target gene of the ALKBH5 oncogene. Knocking down SPP1 partially restored the inhibitory effect of ALKBH5 downregulation on neuroblastoma. Downregulation of ALKBH5 can improve the therapeutic efficacy of carboplatin and etoposide in neuroblastoma.
item2652	REG00005	M6ATAR01082	.	M6ADIS0001	M6ADRUG0154	37180836	SPP1 is the downstream target gene of the ALKBH5 oncogene. Knocking down SPP1 partially restored the inhibitory effect of ALKBH5 downregulation on neuroblastoma. Downregulation of ALKBH5 can improve the therapeutic efficacy of carboplatin and etoposide in neuroblastoma.
item2653	REG00006	M6ATAR01077	.	M6ADIS0115	.	37957146	"METTL14 released by exosomes can increase the m6A methylation level of NFATc1 to inhibit osteoclasts, help postmenopausal osteoporosis patients preserve bone mass, and avoid triggering osteonecrosis of the jaw, thus becoming a new bioactive molecule for the treatment of osteoporosis."
item2654	REG00026	M6ATAR01083	Down	M6ADIS0027	.	37536262	ZC3H13 reduced DUOX1-mediated ferroptosis in laryngeal squamous cell carcinoma cells through m6A-dependent modification.
item2655	REG00007	M6ATAR01084	Up	.	.	36639869	The mechanism by which ABRO1 regulates cardiomyocyte proliferation mainly involved METTL3-mediated Psph mRNA methylation and CDK2 phosphorylation.
item2656	REG00014	M6ATAR01085	.	M6ADIS0010	M6ADRUG0093	38073586	"CircRARS synergises with IGF2BP3 to regulate RNA methylation recognition to promote tumour progression in renal cell carcinoma.CAPN15, CD44, HMGA2, TNRC6A and ZMIZ2 were screened to be the target genes regulated by the IGF2BP3/circRARS complex in an m6A-dependent manner.the IGF2BP3/circRARS complex facilitated the lipid accumulation of RCC cells and promoted sunitinib resistance via target genes."
item2657	REG00014	M6ATAR00574	.	M6ADIS0010	M6ADRUG0093	38073586	"CircRARS synergises with IGF2BP3 to regulate RNA methylation recognition to promote tumour progression in renal cell carcinoma.CAPN15, CD44, HMGA2, TNRC6A and ZMIZ2 were screened to be the target genes regulated by the IGF2BP3/circRARS complex in an m6A-dependent manner.the IGF2BP3/circRARS complex facilitated the lipid accumulation of RCC cells and promoted sunitinib resistance via target genes."
item2658	REG00014	M6ATAR00276	.	M6ADIS0010	M6ADRUG0093	38073586	"CircRARS synergises with IGF2BP3 to regulate RNA methylation recognition to promote tumour progression in renal cell carcinoma.CAPN15, CD44, HMGA2, TNRC6A and ZMIZ2 were screened to be the target genes regulated by the IGF2BP3/circRARS complex in an m6A-dependent manner.the IGF2BP3/circRARS complex facilitated the lipid accumulation of RCC cells and promoted sunitinib resistance via target genes."
item2659	REG00014	M6ATAR01086	.	M6ADIS0010	M6ADRUG0093	38073586	"CircRARS synergises with IGF2BP3 to regulate RNA methylation recognition to promote tumour progression in renal cell carcinoma.CAPN15, CD44, HMGA2, TNRC6A and ZMIZ2 were screened to be the target genes regulated by the IGF2BP3/circRARS complex in an m6A-dependent manner.the IGF2BP3/circRARS complex facilitated the lipid accumulation of RCC cells and promoted sunitinib resistance via target genes."
item2660	REG00014	M6ATAR01087	.	M6ADIS0010	M6ADRUG0093	38073586	"CircRARS synergises with IGF2BP3 to regulate RNA methylation recognition to promote tumour progression in renal cell carcinoma.CAPN15, CD44, HMGA2, TNRC6A and ZMIZ2 were screened to be the target genes regulated by the IGF2BP3/circRARS complex in an m6A-dependent manner.the IGF2BP3/circRARS complex facilitated the lipid accumulation of RCC cells and promoted sunitinib resistance via target genes."
item2661	REG00007	M6ATAR01515	Up	M6ADIS0088	.	37735974	"METTL3 promoted m6A modification and IGF2BP2-dependent stability of GLRX mRNA, and NRF1 increased METTL3 expression by binding to METTL3 promoter.NRF1 mitigates motor dysfunction and dopamine neuron degeneration in mice with Parkinson's disease by promoting GLRX m6 A methylation through upregulation of METTL3 transcription."
item2662	REG00013	M6ATAR01515	Up	M6ADIS0088	.	37735974	"METTL3 promoted m6A modification and IGF2BP2-dependent stability of GLRX mRNA, and NRF1 increased METTL3 expression by binding to METTL3 promoter.NRF1 mitigates motor dysfunction and dopamine neuron degeneration in mice with Parkinson's disease by promoting GLRX m6 A methylation through upregulation of METTL3 transcription."
item2663	REG00006	M6ATAR00124	Up	M6ADIS0007	.	37594665	METTL14 drives growth and metastasis of non-small cell lung cancer by regulating pri-miR-93-5p maturation and TXNIP expression.
item2664	REG00005	M6ATAR01089	Up	M6ADIS0001	.	37421841	ALKBH5 induced the upregulation of circPUM1 to accelerate the development of NB through regulating miR-423-5p/PA2G4 axis.
item2665	REG00004	M6ATAR01090	Up	M6ADIS0057	.	37983727	LINC00355 promotes gastric carcinogenesis by scaffolding p300 to activate CDC42 transcription and enhancing HNRNPA2B1 to stabilize CDC42 mRNA dependent on m6A.
item2666	REG00007	M6ATAR01091	Up	M6ADIS0057	.	37256823	"Increased m6A modification of CENPF was mediated by methyltransferase 3, and this modified molecule could be recognized by heterogeneous nuclear ribonucleoprotein A2/B1 (HNRNPA2B1), thereby promoting its mRNA stability.N6-methyladenosine modification of CENPF mRNA facilitates gastric cancer metastasis via regulating FAK nuclear export."
item2667	REG00004	M6ATAR01091	Up	M6ADIS0057	.	37256823	"Increased m6A modification of CENPF was mediated by methyltransferase 3, and this modified molecule could be recognized by heterogeneous nuclear ribonucleoprotein A2/B1 (HNRNPA2B1), thereby promoting its mRNA stability.N6-methyladenosine modification of CENPF mRNA facilitates gastric cancer metastasis via regulating FAK nuclear export."
item2668	REG00001	M6ATAR01092	.	M6ADIS0110	.	36538851	Overexpression of FTO alleviates osteoarthritis by regulating the processing of miR-515-5p and the TLR4/MyD88/NF-kappaB axis.
item2669	REG00005	M6ATAR00443	Up	M6ADIS0107	M6ADRUG0173	37805933	"Chlorogenic acid (CGA) is a naturally occurring plant component with the purpose of alleviating hepatic lipid deposition biological activities.CGA specifically binds to ALKBH5 and inhibits its m6A methylase activity. The inhibition of ALKBH5 activity significantly reduces AXL mRNA stability in liver cells. The AXL downregulation resulted in suppressing ERK signaling pathway activation. Overall, this study demonstrates that CGA can alleviate hepatic steatosis by regulating autophagy through the inhibition of ALKBH5 activity inhibition."
item2670	REG00001	M6ATAR00341	Up	.	M6ADRUG0153	37418628	"We have designed44/ZLD115, a flexible alkaline side-chain-substituted benzoic acid FTO inhibitor derived from FB23.44/ZLD115 treatment noticeably increases m6A abundance on the AML cell RNA, upregulates RARA gene expression, and downregulates MYC gene expression in MOLM13 cells, which are consistent with FTO gene knockdown."
item2671	REG00001	M6ATAR00341	Up	.	M6ADRUG0188	37418628	"We have designed44/ZLD115, a flexible alkaline side-chain-substituted benzoic acid FTO inhibitor derived from FB23.44/ZLD115 treatment noticeably increases m6A abundance on the AML cell RNA, upregulates RARA gene expression, and downregulates MYC gene expression in MOLM13 cells, which are consistent with FTO gene knockdown."
item2672	REG00006	M6ATAR00848	Up	M6ADIS0007	.	37142269	Silencing AC026356.1 significantly inhibited proliferation and migration but increased apoptosis in A549-cisplatin (DDP) cells.METTL14/IGF2BP2-mediated m6A modification and stabilization of the AC026356.1 RNA.
item2673	REG00013	M6ATAR00848	Up	M6ADIS0007	.	37142269	Silencing AC026356.1 significantly inhibited proliferation and migration but increased apoptosis in A549-cisplatin (DDP) cells.METTL14/IGF2BP2-mediated m6A modification and stabilization of the AC026356.1 RNA.
item2674	REG00012	M6ATAR00341	.	M6ADIS0006	M6ADRUG0179	36736530	"IGF2BP1-mediated N6-methyladenosine modification promotes intrahepatic cholangiocarcinoma progression.IGF2BP1 not only regulated the c-Myc/p16 axis to promote iCCA growth and inhibit senescence, but also activated the ZIC2/PAK4/AKT/MMP2 axis to induce tumor metastasis. More importantly, BTYNB, a recently identified IGF2BP1 inhibitor, exerted promising anti-tumor efficacy in a patient-derived xenograft (PDX) model, and IGF2BP1 conditional knockout (cKO) reduced the tumor burden."
item2675	REG00001	M6ATAR01093	Down	M6ADIS0061	.	38001392	FTO Knockdown-Mediated Maturation of miR-383-5p Inhibits Malignant Advancement of Pancreatic Cancer by Targeting ITGA3.m6A-modified miRNA processing was recognized by IGF2BP1.
item2676	REG00012	M6ATAR01093	Up	M6ADIS0061	.	38001392	FTO Knockdown-Mediated Maturation of miR-383-5p Inhibits Malignant Advancement of Pancreatic Cancer by Targeting ITGA3.m6A-modified miRNA processing was recognized by IGF2BP1.
item2677	REG00006	M6ATAR01094	Up	M6ADIS0148	M6ADRUG0151	38044098	Gestational diabetes mellitus (GDM) is an important cause of the increase in incidence rate and mortality of pregnant women and perinatal infants.Fentanyl Promoted the Growth of Placenta Trophoblast Cells through Regulating the METTL14 Mediated CCL5 Levels.
item2678	REG00048	M6ATAR01095	.	M6ADIS0093	.	36648699	LncRNA CRNDE binds hnRNPA1 to facilitate carbon monoxide poisoning-induced delayed encephalopathy via inhibiting UCHL5-mediated SMO deubiquitination.
item2679	REG00007	M6ATAR01096	Up	M6ADIS0067	.	37085864	METTL3 facilitates immunosurveillance by inhibiting YTHDF2-mediated NLRC5 mRNA degradation in endometrial cancer.
item2680	REG00008	M6ATAR01096	Up	M6ADIS0067	.	37085864	METTL3 facilitates immunosurveillance by inhibiting YTHDF2-mediated NLRC5 mRNA degradation in endometrial cancer.
item2681	REG00013	M6ATAR00269	Up	M6ADIS0059	.	37957183	HES1 promotes aerobic glycolysis and cancer progression of colorectal cancer via IGF2BP2-mediated GLUT1 m6A modification.
item2682	REG00002	M6ATAR00755	.	.	.	16109718	.
item2683	REG00009	M6ATAR00205	.	.	.	17088532	.
item2684	REG00002	M6ATAR00393	.	.	.	17317627	.
item2685	REG00027	M6ATAR01097	.	.	.	18445477	.
item2686	REG00027	M6ATAR01098	.	.	.	18445477	.
item2687	REG00012	M6ATAR01099	.	.	.	19029303	.
item2688	REG00012	M6ATAR01100	.	.	.	19029303	.
item2689	REG00012	M6ATAR00452	.	.	.	19029303	.
item2690	REG00012	M6ATAR01101	.	.	.	19029303	.
item2691	REG00012	M6ATAR01102	.	.	.	19029303	.
item2692	REG00012	M6ATAR01103	.	.	.	19029303	.
item2693	REG00012	M6ATAR00295	.	.	.	19029303	.
item2694	REG00012	M6ATAR01104	.	.	.	19029303	.
item2695	REG00012	M6ATAR00241	.	.	.	19029303	.
item2696	REG00012	M6ATAR01105	.	.	.	19029303	.
item2697	REG00012	M6ATAR01106	.	.	.	19029303	.
item2698	REG00012	M6ATAR00226	.	.	.	19029303	.
item2699	REG00012	M6ATAR00288	.	.	.	19029303	.
item2700	REG00012	M6ATAR01107	.	.	.	19029303	.
item2701	REG00012	M6ATAR01108	.	.	.	19029303	.
item2702	REG00012	M6ATAR00341	.	.	.	19029303	.
item2703	REG00002	M6ATAR00658	.	.	.	19270063	.
item2704	REG00002	M6ATAR01109	.	.	.	19322201	.
item2705	REG00002	M6ATAR01110	.	.	.	19322201	.
item2706	REG00002	M6ATAR01111	.	.	.	19322201	.
item2707	REG00002	M6ATAR00768	.	.	.	19322201	.
item2708	REG00002	M6ATAR01112	.	.	.	19322201	.
item2709	REG00002	M6ATAR01113	.	.	.	19322201	.
item2710	REG00002	M6ATAR01114	.	.	.	19322201	.
item2711	REG00002	M6ATAR00379	.	.	.	19322201	.
item2712	REG00002	M6ATAR01115	.	.	.	19322201	.
item2713	REG00002	M6ATAR01116	.	.	.	19322201	.
item2714	REG00002	M6ATAR01117	.	.	.	19322201	.
item2715	REG00002	M6ATAR01118	.	.	.	19322201	.
item2716	REG00002	M6ATAR00499	.	.	.	19322201	.
item2717	REG00002	M6ATAR01119	.	.	.	19322201	.
item2718	REG00002	M6ATAR01120	.	.	.	19322201	.
item2719	REG00002	M6ATAR00447	.	.	.	19322201	.
item2720	REG00029	M6ATAR01121	.	.	.	20473314	.
item2721	REG00003	M6ATAR01121	.	.	.	20473314	.
item2722	REG00004	M6ATAR00196	.	.	.	21642356	.
item2723	REG00004	M6ATAR00195	.	.	.	21642356	.
item2724	REG00004	M6ATAR01122	.	.	.	21642356	.
item2725	REG00004	M6ATAR01123	.	.	.	21642356	.
item2726	REG00012	M6ATAR01124	.	.	.	22151897	.
item2727	REG00012	M6ATAR01125	.	.	.	22279049	.
item2728	REG00012	M6ATAR01126	.	.	.	22279049	.
item2729	REG00012	M6ATAR01127	.	.	.	22279049	.
item2730	REG00012	M6ATAR01128	.	.	.	22279049	.
item2731	REG00012	M6ATAR01129	.	.	.	22279049	.
item2732	REG00012	M6ATAR01130	.	.	.	22279049	.
item2733	REG00012	M6ATAR01131	.	.	.	22279049	.
item2734	REG00012	M6ATAR00574	.	.	.	22279049	.
item2735	REG00012	M6ATAR00341	.	.	.	22279049	.
item2736	REG00012	M6ATAR01124	.	.	.	22279049	.
item2737	REG00012	M6ATAR01132	.	.	.	22279049	.
item2738	REG00012	M6ATAR01133	.	.	.	22279049	.
item2739	REG00012	M6ATAR00375	.	.	.	22279049	.
item2740	REG00003	M6ATAR00132	.	.	.	22907752	.
item2741	REG00004	M6ATAR00206	.	.	.	23495120	.
item2742	REG00004	M6ATAR00208	.	.	.	23495120	.
item2743	REG00004	M6ATAR00696	.	.	.	23495120	.
item2744	REG00004	M6ATAR00214	.	.	.	23495120	.
item2745	REG00004	M6ATAR01134	.	.	.	23495120	.
item2746	REG00004	M6ATAR00887	.	.	.	23495120	.
item2747	REG00004	M6ATAR01135	.	.	.	23495120	.
item2748	REG00004	M6ATAR00344	.	.	.	23495120	.
item2749	REG00004	M6ATAR01136	.	.	.	23495120	.
item2750	REG00004	M6ATAR00022	.	.	.	23495120	.
item2751	REG00004	M6ATAR00399	.	.	.	23495120	.
item2752	REG00004	M6ATAR00677	.	.	.	23495120	.
item2753	REG00004	M6ATAR00404	.	.	.	23495120	.
item2754	REG00004	M6ATAR01138	.	.	.	23495120	.
item2755	REG00004	M6ATAR00518	.	.	.	23495120	.
item2756	REG00012	M6ATAR00341	.	.	.	23677615	.
item2757	REG00012	M6ATAR01131	.	.	.	23677615	.
item2758	REG00012	M6ATAR00315	.	.	.	23677615	.
item2759	REG00012	M6ATAR01140	.	.	.	23728852	.
item2760	REG00012	M6ATAR01141	.	.	.	23728852	.
item2761	REG00022	M6ATAR01142	.	.	.	23765422	.
item2762	REG00022	M6ATAR01466	.	.	.	23765422	.
item2763	REG00001	M6ATAR01143	.	.	.	23867619	.
item2764	REG00001	M6ATAR01144	.	.	.	23867619	.
item2765	REG00048	M6ATAR01145	.	.	.	24001602	.
item2766	REG00008	M6ATAR00705	.	.	.	24284625	.
item2767	REG00008	M6ATAR01146	.	.	.	24284625	.
item2768	REG00008	M6ATAR00814	.	.	.	24284625	.
item2769	REG00012	M6ATAR01147	.	.	.	24395596	.
item2770	REG00012	M6ATAR00341	.	.	.	24395596	.
item2771	REG00001	M6ATAR00418	.	.	.	24410832	.
item2772	REG00014	M6ATAR01124	.	.	.	24457969	.
item2773	REG00014	M6ATAR00574	.	.	.	24457969	.
item2774	REG00002	M6ATAR00223	.	.	.	24692066	.
item2775	REG00012	M6ATAR01148	.	.	.	24704827	.
item2776	REG00002	M6ATAR01149	.	.	.	24729624	.
item2777	REG00012	M6ATAR00341	.	.	.	25670861	.
item2778	REG00012	M6ATAR01147	.	.	.	25670861	.
item2779	REG00012	M6ATAR00375	.	.	.	25670861	.
item2780	REG00012	M6ATAR00574	.	.	.	25670861	.
item2781	REG00001	M6ATAR01150	.	.	.	25723394	.
item2782	REG00001	M6ATAR00125	.	.	.	25723394	.
item2783	REG00001	M6ATAR01151	.	.	.	25723394	.
item2784	REG00012	M6ATAR00341	.	.	.	25889892	.
item2785	REG00024	M6ATAR01152	.	.	.	26046440	.
item2786	REG00024	M6ATAR01153	.	.	.	26046440	.
item2787	REG00024	M6ATAR00239	.	.	.	26046440	.
item2788	REG00024	M6ATAR01146	.	.	.	26046440	.
item2789	REG00024	M6ATAR00814	.	.	.	26046440	.
item2790	REG00012	M6ATAR00497	.	.	.	26160756	.
item2791	REG00013	M6ATAR00497	.	.	.	26160756	.
item2792	REG00014	M6ATAR00497	.	.	.	26160756	.
item2793	REG00014	M6ATAR00323	.	.	.	26327240	.
item2794	REG00014	M6ATAR00472	.	.	.	26327240	.
item2795	REG00014	M6ATAR00689	.	.	.	26327240	.
item2796	REG00014	M6ATAR01499	.	.	.	26522719	.
item2797	REG00014	M6ATAR01155	.	.	.	26522719	.
item2798	REG00014	M6ATAR01156	.	.	.	26522719	.
item2799	REG00001	M6ATAR00279	.	.	.	26593424	.
item2800	REG00012	M6ATAR01157	.	.	.	26852652	.
item2801	REG00014	M6ATAR00212	.	.	.	26974154	.
item2802	REG00014	M6ATAR00341	.	.	.	26974154	.
item2803	REG00007	M6ATAR01158	.	.	.	27117702	.
item2804	REG00007	M6ATAR01107	.	.	.	27117702	.
item2805	REG00007	M6ATAR01153	.	.	.	27117702	.
item2806	REG00007	M6ATAR01491	.	.	.	27117702	.
item2807	REG00007	M6ATAR00237	.	.	.	27117702	.
item2808	REG00007	M6ATAR01159	.	.	.	27117702	.
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item2810	REG00013	M6ATAR00327	.	.	.	27153315	.
item2811	REG00013	M6ATAR00406	.	.	.	27153315	.
item2812	REG00013	M6ATAR01161	.	.	.	27153315	.
item2813	REG00013	M6ATAR00205	.	.	.	27153315	.
item2814	REG00013	M6ATAR01162	.	.	.	27153315	.
item2815	REG00013	M6ATAR01124	.	.	.	27153315	.
item2816	REG00013	M6ATAR01163	.	.	.	27153315	.
item2817	REG00013	M6ATAR01164	.	.	.	27153315	.
item2818	REG00014	M6ATAR01165	.	.	.	27210763	.
item2819	REG00014	M6ATAR00574	.	.	.	27210763	.
item2820	REG00014	M6ATAR01166	.	.	.	27210763	.
item2821	REG00014	M6ATAR01037	.	.	.	27210763	.
item2822	REG00012	M6ATAR00418	.	.	.	27239736	.
item2823	REG00001	M6ATAR01167	.	.	.	27773535	.
item2824	REG00004	M6ATAR00696	.	.	.	28077929	.
item2825	REG00004	M6ATAR00202	.	.	.	28077929	.
item2826	REG00004	M6ATAR00518	.	.	.	28077929	.
item2827	REG00024	M6ATAR00452	.	.	.	28106072	.
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item2829	REG00025	M6ATAR01169	.	.	.	28106072	.
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item2831	REG00025	M6ATAR00452	.	.	.	28106072	.
item2832	REG00025	M6ATAR01168	.	.	.	28106072	.
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item2834	REG00014	M6ATAR01124	.	.	.	28193878	.
item2835	REG00002	M6ATAR01171	.	.	.	28219770	.
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item2838	REG00007	M6ATAR01172	.	.	.	28281539	.
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item2840	REG00001	M6ATAR01172	.	.	.	28281539	.
item2841	REG00025	M6ATAR01172	.	.	.	28281539	.
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item2843	REG00027	M6ATAR01173	.	.	.	28334903	.
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item2849	REG00002	M6ATAR01175	.	.	.	28501005	.
item2850	REG00017	M6ATAR01176	.	.	.	28525753	.
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item2852	REG00012	M6ATAR00330	.	.	.	28677801	.
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item2855	REG00012	M6ATAR00213	.	.	.	28677801	.
item2856	REG00012	M6ATAR00203	.	.	.	28677801	.
item2857	REG00012	M6ATAR01178	.	.	.	28846937	.
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item2859	REG00002	M6ATAR00195	.	.	.	28968471	.
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item2861	REG00022	M6ATAR00416	.	.	.	28984244	.
item2862	REG00022	M6ATAR00750	.	.	.	28984244	.
item2863	REG00022	M6ATAR01179	.	.	.	28984244	.
item2864	REG00017	M6ATAR01180	.	.	.	29051200	.
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item2868	REG00014	M6ATAR01183	.	.	.	29212181	.
item2869	REG00014	M6ATAR00356	.	.	.	29212181	.
item2870	REG00017	M6ATAR01176	.	.	.	29262316	.
item2871	REG00002	M6ATAR01175	.	.	.	29344850	.
item2872	REG00002	M6ATAR01184	.	.	.	29454929	.
item2873	REG00009	M6ATAR00210	.	.	.	29482572	.
item2874	REG00001	M6ATAR00984	.	.	.	29501742	.
item2875	REG00015	M6ATAR00253	.	.	.	29507755	.
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item2884	REG00015	M6ATAR00351	.	.	.	29507755	.
item2885	REG00006	M6ATAR00638	.	.	.	29573145	.
item2886	REG00007	M6ATAR00638	.	.	.	29573145	.
item2887	REG00002	M6ATAR01191	.	.	.	29678826	.
item2888	REG00014	M6ATAR00497	.	.	.	29731738	.
item2889	REG00022	M6ATAR00416	.	.	.	29799838	.
item2890	REG00022	M6ATAR00779	.	.	.	29799838	.
item2891	REG00022	M6ATAR00880	.	.	.	29799838	.
item2892	REG00001	M6ATAR01192	.	.	.	29890211	.
item2893	REG00007	M6ATAR01193	.	.	.	29902206	.
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item2895	REG00007	M6ATAR01194	.	.	.	29902206	.
item2896	REG00008	M6ATAR00280	.	.	.	29902206	.
item2897	REG00008	M6ATAR01127	.	.	.	29902206	.
item2898	REG00008	M6ATAR01194	.	.	.	29902206	.
item2899	REG00002	M6ATAR01195	.	.	.	29931370	.
item2900	REG00002	M6ATAR01196	.	.	.	29931370	.
item2901	REG00002	M6ATAR01197	.	.	.	29931370	.
item2902	REG00002	M6ATAR01198	.	.	.	29931370	.
item2903	REG00002	M6ATAR01107	.	.	.	29931370	.
item2904	REG00002	M6ATAR01199	.	.	.	29931370	.
item2905	REG00002	M6ATAR01200	.	.	.	29931370	.
item2906	REG00007	M6ATAR00253	.	.	.	30038300	.
item2907	REG00002	M6ATAR00197	.	.	.	30081711	.
item2908	REG00007	M6ATAR01201	.	.	.	30218090	.
item2909	REG00007	M6ATAR01202	.	.	.	30218090	.
item2910	REG00007	M6ATAR01203	.	.	.	30218090	.
item2911	REG00006	M6ATAR01201	.	.	.	30218090	.
item2912	REG00006	M6ATAR01202	.	.	.	30218090	.
item2913	REG00006	M6ATAR01203	.	.	.	30218090	.
item2914	REG00009	M6ATAR00448	.	.	.	30218090	.
item2915	REG00009	M6ATAR01187	.	.	.	30218090	.
item2916	REG00009	M6ATAR01201	.	.	.	30218090	.
item2917	REG00009	M6ATAR01202	.	.	.	30218090	.
item2918	REG00009	M6ATAR01203	.	.	.	30218090	.
item2919	REG00015	M6ATAR00253	.	.	.	30218090	.
item2920	REG00015	M6ATAR01187	.	.	.	30218090	.
item2921	REG00015	M6ATAR01201	.	.	.	30218090	.
item2922	REG00015	M6ATAR01202	.	.	.	30218090	.
item2923	REG00015	M6ATAR01203	.	.	.	30218090	.
item2924	REG00015	M6ATAR01204	.	.	.	30218090	.
item2925	REG00015	M6ATAR01205	.	.	.	30218090	.
item2926	REG00015	M6ATAR01206	.	.	.	30218090	.
item2927	REG00009	M6ATAR01204	.	.	.	30218090	.
item2928	REG00009	M6ATAR01205	.	.	.	30218090	.
item2929	REG00009	M6ATAR01206	.	.	.	30218090	.
item2930	REG00022	M6ATAR01203	.	.	.	30218090	.
item2931	REG00022	M6ATAR01204	.	.	.	30218090	.
item2932	REG00022	M6ATAR01205	.	.	.	30218090	.
item2933	REG00022	M6ATAR01206	.	.	.	30218090	.
item2934	REG00007	M6ATAR01207	.	.	.	30232453	.
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item2936	REG00007	M6ATAR01209	.	.	.	30232453	.
item2937	REG00007	M6ATAR00326	.	.	.	30232453	.
item2938	REG00007	M6ATAR00745	.	.	.	30232453	.
item2939	REG00026	M6ATAR00206	.	.	.	30311220	.
item2940	REG00026	M6ATAR00208	.	.	.	30311220	.
item2941	REG00026	M6ATAR01211	.	.	.	30311220	.
item2942	REG00026	M6ATAR00399	.	.	.	30311220	.
item2943	REG00026	M6ATAR01212	.	.	.	30311220	.
item2944	REG00012	M6ATAR00075	.	.	.	30503558	.
item2945	REG00012	M6ATAR01124	.	.	.	30503558	.
item2946	REG00012	M6ATAR00267	.	.	.	30503558	.
item2947	REG00012	M6ATAR00341	.	.	.	30503558	.
item2948	REG00008	M6ATAR01213	.	.	.	30514900	.
item2949	REG00012	M6ATAR01214	.	.	.	30543563	.
item2950	REG00007	M6ATAR00290	.	.	.	30559377	.
item2951	REG00008	M6ATAR00290	.	.	.	30559377	.
item2952	REG00044	M6ATAR00224	.	.	.	30660488	.
item2953	REG00044	M6ATAR00206	.	.	.	30660488	.
item2954	REG00044	M6ATAR00663	.	.	.	30660488	.
item2955	REG00044	M6ATAR00293	.	.	.	30660488	.
item2956	REG00002	M6ATAR01216	.	.	.	30787392	.
item2957	REG00012	M6ATAR01217	.	.	.	30790682	.
item2958	REG00012	M6ATAR00267	.	.	.	30790682	.
item2959	REG00014	M6ATAR01218	.	.	.	30797711	.
item2960	REG00020	M6ATAR01219	.	.	.	31020615	.
item2961	REG00005	M6ATAR00205	.	.	.	31281518	.
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item2963	REG00009	M6ATAR00696	.	.	.	31496724	.
item2964	REG00009	M6ATAR00518	.	.	.	31496724	.
item2965	REG00007	M6ATAR01221	.	.	.	31670863	.
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item2967	REG00008	M6ATAR01222	.	.	.	31815430	.
item2968	REG00008	M6ATAR01223	.	.	.	31815430	.
item2969	REG00008	M6ATAR01224	.	.	.	31815430	.
item2970	REG00008	M6ATAR01225	.	.	.	31815430	.
item2971	REG00008	M6ATAR00295	.	.	.	31815430	.
item2972	REG00008	M6ATAR00320	.	.	.	31815430	.
item2973	REG00008	M6ATAR01226	.	.	.	31815430	.
item2974	REG00008	M6ATAR01227	.	.	.	31815430	.
item2975	REG00013	M6ATAR00175	.	.	.	31852504	.
item2976	REG00002	M6ATAR01228	.	.	.	31886581	.
item2977	REG00002	M6ATAR01229	.	.	.	31886581	.
item2978	REG00007	M6ATAR01230	.	.	.	31896070	.
item2979	REG00002	M6ATAR01231	.	M6ADIS0184	.	31922280	.
item2980	REG00002	M6ATAR00453	.	M6ADIS0184	.	31922280	.
item2981	REG00004	M6ATAR01232	.	.	.	31926942	.
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item2984	REG00017	M6ATAR01234	.	.	.	31940410	.
item2985	REG00017	M6ATAR01235	.	.	.	31940410	.
item2986	REG00017	M6ATAR01176	.	.	.	31940410	.
item2987	REG00017	M6ATAR00141	.	.	.	31940410	.
item2988	REG00017	M6ATAR01236	.	.	.	31940410	.
item2989	REG00017	M6ATAR01237	.	.	.	31940410	.
item2990	REG00017	M6ATAR00274	.	.	.	31940410	.
item2991	REG00017	M6ATAR00341	.	.	.	31940410	.
item2992	REG00017	M6ATAR01238	.	.	.	31940410	.
item2993	REG00017	M6ATAR01477	.	.	.	31940410	.
item2994	REG00017	M6ATAR01126	.	.	.	31940410	.
item2995	REG00005	M6ATAR00258	Up	.	.	31974865	.
item2996	REG00009	M6ATAR00500	.	.	.	31986407	.
item2997	REG00004	M6ATAR01239	.	.	.	32006618	.
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item2999	REG00024	M6ATAR00607	.	.	.	32064749	.
item3000	REG00006	M6ATAR00203	.	.	.	32097728	.
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item3002	REG00012	M6ATAR00195	.	.	.	32123162	.
item3003	REG00012	M6ATAR00196	.	.	.	32123162	.
item3004	REG00012	M6ATAR01123	.	.	.	32123162	.
item3005	REG00012	M6ATAR00210	.	.	.	32123162	.
item3006	REG00012	M6ATAR00205	.	.	.	32123162	.
item3007	REG00007	M6ATAR00446	.	.	.	32148516	.
item3008	REG00007	M6ATAR01242	.	.	.	32148516	.
item3009	REG00007	M6ATAR00488	.	.	.	32148516	.
item3010	REG00007	M6ATAR00957	.	.	.	32148516	.
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item3013	REG00008	M6ATAR01146	.	.	.	32169943	.
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item3016	REG00025	M6ATAR00497	.	.	.	32194978	.
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item3018	REG00004	M6ATAR00228	.	.	.	32246902	.
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item3027	REG00014	M6ATAR01253	.	.	.	32339511	.
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item3029	REG00005	M6ATAR01254	.	.	.	32439916	.
item3030	REG00005	M6ATAR00404	.	.	.	32439916	.
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item3033	REG00014	M6ATAR00574	.	.	.	32560817	.
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item3035	REG00007	M6ATAR01257	.	.	.	32567849	.
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item3037	REG00012	M6ATAR01258	.	M6ADIS0343	.	32583425	.
item3038	REG00001	M6ATAR00341	.	.	.	32655129	.
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item3040	REG00004	M6ATAR01164	.	M6ADIS0059	.	32698890	.
item3041	REG00013	M6ATAR01260	.	M6ADIS0001	.	32713259	.
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item3043	REG00012	M6ATAR00234	.	.	.	32761127	.
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item3054	REG00001	M6ATAR00360	.	.	.	32828292	.
item3055	REG00024	M6ATAR00593	.	M6ADIS0059	.	32838807	.
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item3058	REG00013	M6ATAR00175	.	.	.	32868105	.
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item3061	REG00009	M6ATAR00283	.	M6ADIS0177	.	32967010	.
item3062	REG00012	M6ATAR00496	.	M6ADIS0001	.	32990800	.
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item3068	REG00007	M6ATAR00203	.	.	.	33082869	.
item3069	REG00001	M6ATAR00475	.	M6ADIS0025	.	33157234	.
item3070	REG00002	M6ATAR00212	.	.	.	33219221	.
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item3077	REG00007	M6ATAR00341	.	M6ADIS0007	.	33355622	.
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item3083	REG00024	M6ATAR01119	.	.	.	33526437	.
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item3087	REG00007	M6ATAR00677	.	.	.	33563300	.
item3088	REG00002	M6ATAR00197	.	.	.	33568052	.
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item3092	REG00006	M6ATAR01167	.	.	.	33657363	.
item3093	REG00006	M6ATAR01273	.	.	.	33657363	.
item3094	REG00007	M6ATAR01167	.	.	.	33657363	.
item3095	REG00007	M6ATAR01273	.	.	.	33657363	.
item3096	REG00008	M6ATAR00364	.	M6ADIS0072	.	33726814	.
item3097	REG00008	M6ATAR00356	.	M6ADIS0072	.	33726814	.
item3098	REG00009	M6ATAR01274	.	.	.	33756105	.
item3099	REG00006	M6ATAR00651	.	.	.	33763423	.
item3100	REG00007	M6ATAR01276	.	.	.	33781830	.
item3101	REG00023	M6ATAR01277	.	.	.	33785413	.
item3102	REG00012	M6ATAR00234	.	.	.	33829040	.
item3103	REG00012	M6ATAR01278	.	.	.	33829040	.
item3104	REG00012	M6ATAR01279	.	.	.	33829040	.
item3105	REG00012	M6ATAR01280	.	.	.	33829040	.
item3106	REG00007	M6ATAR01445	.	.	.	33862464	.
item3107	REG00024	M6ATAR01445	.	.	.	33862464	.
item3108	REG00014	M6ATAR01281	.	.	.	33872988	.
item3109	REG00007	M6ATAR00569	.	M6ADIS0057	.	33882457	.
item3110	REG00013	M6ATAR01282	.	.	.	33884031	.
item3111	REG00013	M6ATAR00204	.	.	.	33884031	.
item3112	REG00007	M6ATAR00808	.	.	.	33910374	.
item3113	REG00007	M6ATAR01151	.	.	.	33910374	.
item3114	REG00003	M6ATAR00208	.	.	.	33937074	.
item3115	REG00003	M6ATAR00696	.	.	.	33937074	.
item3116	REG00003	M6ATAR00211	.	.	.	33937074	.
item3117	REG00003	M6ATAR00379	.	.	.	33937074	.
item3118	REG00003	M6ATAR01283	.	.	.	33937074	.
item3119	REG00003	M6ATAR01284	.	.	.	33937074	.
item3120	REG00003	M6ATAR00328	.	.	.	33937074	.
item3121	REG00003	M6ATAR00341	.	.	.	33937074	.
item3122	REG00003	M6ATAR00518	.	.	.	33937074	.
item3123	REG00003	M6ATAR01285	.	.	.	33937074	.
item3124	REG00008	M6ATAR01286	.	.	.	33958724	.
item3125	REG00008	M6ATAR00594	.	.	.	33980824	.
item3126	REG00004	M6ATAR00843	.	.	.	34044823	.
item3127	REG00005	M6ATAR01456	.	.	.	34088896	.
item3128	REG00006	M6ATAR01287	.	.	.	34131102	.
item3129	REG00013	M6ATAR01288	.	.	.	34168980	.
item3130	REG00013	M6ATAR00315	.	.	.	34218464	.
item3131	REG00003	M6ATAR01289	.	.	.	34271104	.
item3132	REG00003	M6ATAR01290	.	.	.	34271104	.
item3133	REG00003	M6ATAR01291	.	.	.	34271104	.
item3134	REG00004	M6ATAR01248	Up	.	.	34277606	.
item3135	REG00004	M6ATAR00993	Up	.	.	34277606	.
item3136	REG00004	M6ATAR01292	Up	.	.	34277606	.
item3137	REG00004	M6ATAR01293	Up	.	.	34277606	.
item3138	REG00004	M6ATAR00124	Up	.	.	34277606	.
item3139	REG00005	M6ATAR00764	.	.	.	34297301	.
item3140	REG00001	M6ATAR00937	.	.	.	34315853	.
item3141	REG00007	M6ATAR00631	.	.	.	34321211	.
item3142	REG00008	M6ATAR01294	.	.	.	34324489	.
item3143	REG00009	M6ATAR01295	.	.	.	34326314	.
item3144	REG00012	M6ATAR01295	.	.	.	34326314	.
item3145	REG00013	M6ATAR01295	.	.	.	34326314	.
item3146	REG00014	M6ATAR01295	.	.	.	34326314	.
item3147	REG00013	M6ATAR00274	.	.	.	34345216	.
item3148	REG00013	M6ATAR01296	.	.	.	34345216	.
item3149	REG00013	M6ATAR01287	.	.	.	34345216	.
item3150	REG00001	M6ATAR01297	.	.	.	34350169	.
item3151	REG00001	M6ATAR01135	.	.	.	34350169	.
item3152	REG00001	M6ATAR00335	.	.	.	34350169	.
item3153	REG00024	M6ATAR01161	.	.	.	34359836	.
item3154	REG00007	M6ATAR01298	.	.	.	34363020	.
item3155	REG00007	M6ATAR00373	.	.	.	34375639	.
item3156	REG00008	M6ATAR00373	.	.	.	34375639	.
item3157	REG00013	M6ATAR00308	.	.	.	34386421	.
item3158	REG00024	M6ATAR00360	.	.	.	34408926	.
item3159	REG00008	M6ATAR00360	.	.	.	34408926	.
item3160	REG00006	M6ATAR00605	.	M6ADIS0168	.	34412584	.
item3161	REG00005	M6ATAR00375	.	.	.	34438274	.
item3162	REG00007	M6ATAR01299	.	.	.	34505967	.
item3163	REG00005	M6ATAR00976	.	.	.	34513291	.
item3164	REG00005	M6ATAR01300	.	.	.	34513291	.
item3165	REG00007	M6ATAR01301	.	.	.	34514103	.
item3166	REG00012	M6ATAR01302	.	.	.	34514861	.
item3167	REG00007	M6ATAR01303	.	.	.	34535671	.
item3168	REG00023	M6ATAR01304	.	.	.	34536357	.
item3169	REG00001	M6ATAR00418	.	.	.	34537236	.
item3170	REG00001	M6ATAR00185	.	.	.	34539907	.
item3171	REG00001	M6ATAR00263	.	.	.	34539907	.
item3172	REG00007	M6ATAR01305	.	.	.	34565019	.
item3173	REG00044	M6ATAR00696	.	.	.	34589577	.
item3174	REG00044	M6ATAR00202	.	.	.	34589577	.
item3175	REG00044	M6ATAR01306	.	.	.	34589577	.
item3176	REG00044	M6ATAR00269	.	.	.	34589577	.
item3177	REG00044	M6ATAR00399	.	.	.	34589577	.
item3178	REG00044	M6ATAR00518	.	.	.	34589577	.
item3179	REG00009	M6ATAR00210	.	M6ADIS0069	.	34595849	.
item3180	REG00009	M6ATAR00211	.	.	.	34595849	.
item3181	REG00009	M6ATAR00212	.	.	.	34595849	.
item3182	REG00009	M6ATAR00206	.	.	.	34595849	.
item3183	REG00013	M6ATAR01263	.	.	.	34630126	.
item3184	REG00013	M6ATAR01147	.	.	.	34630126	.
item3185	REG00005	M6ATAR01307	.	.	.	34631277	.
item3186	REG00001	M6ATAR01308	.	.	.	34632051	.
item3187	REG00007	M6ATAR00301	.	.	.	34645279	.
item3188	REG00002	M6ATAR01309	.	.	.	34645466	.
item3189	REG00002	M6ATAR01475	.	.	.	34645466	.
item3190	REG00007	M6ATAR00200	.	M6ADIS0115	.	34645714	.
item3191	REG00007	M6ATAR00513	.	.	.	34645714	.
item3192	REG00007	M6ATAR01418	.	.	.	34645714	.
item3193	REG00007	M6ATAR01082	.	.	.	34645714	.
item3194	REG00007	M6ATAR01310	.	.	.	34645714	.
item3195	REG00006	M6ATAR00154	.	.	.	34648132	.
item3196	REG00007	M6ATAR01293	.	.	.	34666602	.
item3197	REG00044	M6ATAR00341	.	.	.	34671012	.
item3198	REG00001	M6ATAR00696	.	.	.	34675398	.
item3199	REG00024	M6ATAR01311	.	.	.	34677810	.
item3200	REG00014	M6ATAR00341	.	.	.	34703650	.
item3201	REG00008	M6ATAR00268	.	M6ADIS0059	.	34709763	.
item3202	REG00008	M6ATAR00206	.	.	.	34709763	.
item3203	REG00007	M6ATAR00396	.	.	.	34727293	.
item3204	REG00007	M6ATAR01312	.	.	.	34738869	.
item3205	REG00024	M6ATAR01313	.	.	.	34772913	.
item3206	REG00004	M6ATAR00312	.	.	.	34786210	.
item3207	REG00004	M6ATAR00212	.	.	.	34805798	.
item3208	REG00007	M6ATAR00107	.	.	.	34809621	.
item3209	REG00009	M6ATAR00107	.	.	.	34809621	.
item3210	REG00013	M6ATAR00107	.	.	.	34809621	.
item3211	REG00007	M6ATAR01314	.	.	.	34820430	.
item3212	REG00007	M6ATAR01488	Up	M6ADIS0180	M6ADRUG0108	38852200	These results reveal a histone lactylation-driven mechanism inducing ferroptosis through METTL3-mediated m6A modification. Targeting METTL3 represents a promising therapeutic strategy for patients with sepsis-associated ALI.
item3213	REG00009	M6ATAR00425	.	M6ADIS0125	.	39007267	"We found that WTAP is an NF-kappaB p65-stimulated gene and that its expression is markedly upregulated in response to a variety of inflammatory stimuli and in many inflammatory diseases. Mechanistically, after an increase in its concentration, WTAP spontaneously undergoes phase separation, which facilitates the aggregation of the writer complex to nuclear speckles and the deposition of m6A on transcriptionally active proinflammatory genes. Hence, WTAP enhances the protein synthesis of many m6A-modified proinflammatory transcripts, including IL6ST, IL18R1 and IL15RA, which accelerates inflammatory responses and exacerbates the severity of many inflammatory diseases."
item3214	REG00005	M6ATAR00356	Up	M6ADIS0059	.	39039912	The interplay between CARMN and ALKBH5 promoted tumourigenesis in colorectal cancer patients via the p53/ALKBH5/CARMN/miR-5683 pathway. These findings illuminate the role of m6A methylation in colorectal cancer patients with p53R273H mutation.
item3215	REG00007	M6ATAR00356	.	M6ADIS0198	.	38721764	"The METTL3/METTL14 complex was found to incorporate the m6A modification on PTCHD4mRNA; addition of m6A rendered PTCHD4 mRNA more stable and increased PTCHD4 production. / PTCHD4 mRNA is transcriptionally induced by p53, co-transcriptionally m6A-methylated by METTL3, and post-transcriptionally stabilized by IGF2BP1, which has specific affinity for the m6A-modified PTCHD4 mRNA."
item3216	REG00007	M6ATAR01316	Up	M6ADIS0217	.	38880226	"We demonstrated that METTL3 was highly expressed in NKTCL cells and tissues and indicated poor prognosis. The METTL3 expression was associated with NKTCL survival. Functionally, METTL3 promoted the proliferation capability of NKTCL cells in vitro and in vivo. Furthermore, EBV-miR-BART3-3p was identified as the downstream effector of METTL3, and silencing EBV-miR-BART3-3p inhibited the proliferation of NKTCL. Finally, we confirmed that PLCG2 as a target gene of EBVmiR-BART3-3p by relative assays."
item3217	REG00005	M6ATAR00327	Down	M6ADIS0349	.	39011034	"We identified a MAPK pathway involving Map3k8, Erk2, and Nfkappab1 that may play a role in the disrupted inflammatory response associated with nasal inflammation. /m6A dysregulation mediated by ALKBH5, is likely to contribute to inflammation of the nasal mucosa via the MAPK signaling pathway, suggesting that ALKBH5 is a potential biomarker for AR treatment."
item3218	REG00008	M6ATAR01318	.	M6ADIS0089	.	39424201	"In Alzheimer's disease, YTHDF2 primarily functions by degrading mRNAs of relevant genes, which contributes to neuronal damage and regulates Abeta overexpression and tau phosphorylation."
item3219	REG00008	M6ATAR01319	.	M6ADIS0258	.	39424201	"YTHDF2 plays a key role in maintaining the stability of PVT1, mediated by ALKBH5, while PVT1-induced autophagy protects hippocampal neurons against synaptic plasticity loss and apoptosis, ultimately reducing cognitive deficits associated with diabetes.YTHDF2 may influence cognitive dysfunction in diabetes through several pathways, including the modulation of the PI3K/Akt pathway."
item3220	REG00008	M6ATAR00153	.	M6ADIS0258	.	39424201	"YTHDF2 plays a key role in maintaining the stability of PVT1, mediated by ALKBH5, while PVT1-induced autophagy protects hippocampal neurons against synaptic plasticity loss and apoptosis, ultimately reducing cognitive deficits associated with diabetes.YTHDF2 may influence cognitive dysfunction in diabetes through several pathways, including the modulation of the PI3K/Akt pathway."
item3221	REG00008	M6ATAR00594	.	M6ADIS0088	.	39424201	"YTHDF2 promotes the degradation of AXIN1 mRNA, activating the Wnt/beta-catenin signaling pathway, which inhibits apoptosis in hippocampal neurons."
item3222	REG00008	M6ATAR00381	.	M6ADIS0001	.	39424201	"Research shows that the suppression of FIP200 induces apoptosis in glioblastoma cells and microvascular endothelial cells through increased Pyk2 activity. Specifically, the downregulation of FIP200 promotes apoptosis in these cells, while inhibition of FIP200 mRNA degradation by YTHDF2 suppresses glioblastoma apoptosis .In summary, YTHDF2's regulation of gliomas relies on m6A modification, highlighting the complex interaction between protein and RNA methylation mechanisms."
item3223	REG00008	M6ATAR00136	.	M6ADIS0378	.	39424201	"YTHDF2 has been identified as a direct target of miR-145, and downregulation of miR-145 has been shown to decrease Caspase-9 expression in the hippocampus. This reduction in Caspase-9 levels leads to decreased hippocampal neuronal apoptosis, which positively impacts memory and learning in epileptic rats ."
item3224	REG00030	.	Up	M6ADIS0006	.	38366283	"IGFBP3 is significantly enhanced in normal tissues, while immunohistochemical analysis shows that its expression is lower in tumor tissues, indicating its protective effect in HCC and a good prognosis. Importantly, high IGFBP3 expression is associated with better outcomes in patients receiving immunotherapy.the comprehensive evaluation of m6A modification, immune characteristics, and single-cell analysis in this study not only revealed the TME of HCC but also made significant contributions to the progress of personalized HCC immunotherapy targeting IGFBP3."
item3225	REG00015	M6ATAR01320	Up	M6ADIS0208	.	39256796	"KIAA1429 knockdown abolished the downregulation of TGF-bRII and upregulation of MMP1 in UVR-irradiated human dermal fibroblasts (HDFs). Identified MFAP4 as a target of KIAA1429-mediated m6A modification and KIAA1429 might suppress collagen synthesis through an m6A-MFAP4-mediated process. The increased expression of KIAA1429 hinders collagen synthesis during UVR-induced photoaging, suggesting that KIAA1429 represents a potential candidate for targeted therapy to mitigate UVR-driven photoaging."
item3226	REG00007	M6ATAR00393	.	M6ADIS0014	.	39334185	Silencing METTL3-mediated m6A modifications restored high-glucose-induced autophagy inhibition and prevented premature senescence in LECs. METTL3 induces senescence in DC by destabilizing SIRT1 mRNA in an m6A-YTHDF2-dependent manner. The METTL3-YTHDF2-SIRT1 axis is a key target and potential pathogenic mechanism in DC.
item3227	REG00030	M6ATAR01414	Down	.	.	38429265	We discovered that IGF2BP3 regulated ferroptosis by modulating the protein expression level of GPX4 through direct binding to a specific motif on GPX4 mRNA.shed light on an unrecognized regulatory function of IGF2BP3 in ferroptosis. The identification of a critical m6A site within the GPX4 transcript elucidates the significance of post-transcriptional control in ferroptosis.
item3228	REG00005	M6ATAR01322	Up	M6ADIS0032	.	38821243	"Alkbh5 in modulating the decay of Cyp1a1 mRNA in a manner reliant on m6A under hypoxic conditions and ultimately through the Wnt/beta-catenin signaling pathway, thereby impacting PASMCs proliferation and migration and contributing to the pathological process of pulmonary vascular remodeling in HPH."
item3229	REG00014	M6ATAR00945	.	.	.	38723480	"Arsenic caused a significant increase in SUMOylation of FTO protein, and FTO SUMOylation at lysine (K) 216 site promoted the down-regulation of FTO expression in arsenic target organ lung, and therefore, remarkably elevating the oxidative damage an m6A-dependent pathway by its specific m6A reader insulin-like growth factor-2 mRNA-binding protein-3 (IGF2BP3). Consequently, these findings not only reveal a novel mechanism underlying FTO-mediated oxidative damage from the perspective of m6A, but also imply that regulation of FTO SUMOylation may serve as potential approach for treatment of oxidative damage."
item3230	REG00001	M6ATAR00945	.	.	.	38723480	"Arsenic caused a significant increase in SUMOylation of FTO protein, and FTO SUMOylation at lysine (K) 216 site promoted the down-regulation of FTO expression in arsenic target organ lung, and therefore, remarkably elevating the oxidative damage an m6A-dependent pathway by its specific m6A reader insulin-like growth factor-2 mRNA-binding protein-3 (IGF2BP3). Consequently, these findings not only reveal a novel mechanism underlying FTO-mediated oxidative damage from the perspective of mA, but also imply that regulation of FTO SUMOylation may serve as potential approach for treatment of oxidative damage."
item3231	REG00014	M6ATAR00941	.	.	.	38723480	"Arsenic caused a significant increase in SUMOylation of FTO protein, and FTO SUMOylation at lysine (K) 216 site promoted the down-regulation of FTO expression in arsenic target organ lung, and therefore, remarkably elevating the oxidative damage an m6A-dependent pathway by its specific m6A reader insulin-like growth factor-2 mRNA-binding protein-3 (IGF2BP3). Consequently, these findings not only reveal a novel mechanism underlying FTO-mediated oxidative damage from the perspective of m6A, but also imply that regulation of FTO SUMOylation may serve as potential approach for treatment of oxidative damage."
item3232	REG00001	M6ATAR00941	.	.	.	38723480	"Arsenic caused a significant increase in SUMOylation of FTO protein, and FTO SUMOylation at lysine (K) 216 site promoted the down-regulation of FTO expression in arsenic target organ lung, and therefore, remarkably elevating the oxidative damage an m6A-dependent pathway by its specific m6A reader insulin-like growth factor-2 mRNA-binding protein-3 (IGF2BP3). Consequently, these findings not only reveal a novel mechanism underlying FTO-mediated oxidative damage from the perspective of m6A, but also imply that regulation of FTO SUMOylation may serve as potential approach for treatment of oxidative damage."
item3233	REG00014	M6ATAR00460	.	.	.	38723480	"Arsenic caused a significant increase in SUMOylation of FTO protein, and FTO SUMOylation at lysine (K) 216 site promoted the down-regulation of FTO expression in arsenic target organ lung, and therefore, remarkably elevating the oxidative damage an m6A-dependent pathway by its specific m6A reader insulin-like growth factor-2 mRNA-binding protein-3 (IGF2BP3). Consequently, these findings not only reveal a novel mechanism underlying FTO-mediated oxidative damage from the perspective of m6A, but also imply that regulation of FTO SUMOylation may serve as potential approach for treatment of oxidative damage."
item3234	REG00001	M6ATAR00460	.	.	.	38723480	"Arsenic caused a significant increase in SUMOylation of FTO protein, and FTO SUMOylation at lysine (K) 216 site promoted the down-regulation of FTO expression in arsenic target organ lung, and therefore, remarkably elevating the oxidative damage an m6A-dependent pathway by its specific m6A reader insulin-like growth factor-2 mRNA-binding protein-3 (IGF2BP3). Consequently, these findings not only reveal a novel mechanism underlying FTO-mediated oxidative damage from the perspective of m6A, but also imply that regulation of FTO SUMOylation may serve as potential approach for treatment of oxidative damage."
item3235	REG00007	M6ATAR01324	Down	M6ADIS0148	.	39191355	"Knocking down METTL3 significantly reduced m6A modification of hsa_circ_0072380, indicating that METTL3 regulated changes in m6A modification of hsa_circ_0072380. Our study revealed the important regulatory role of METTL3 and m6A modification of hsa_circ_0072380 in GDM."
item3236	REG00024	M6ATAR01325	.	M6ADIS0056	.	39098703	"YTHDF1 promoted ESCA cell proliferation, migration, and metastasis in vitro and in vivo.YTHDF1 recognized and bound to m6A-modified sites of TINAGL1 mRNA, resulting in enhanced translation of TINAGL1. YTHDF1 facilitates ESCA progression by promoting TINAGL1 translation in an m6A-dependent manner, which offers an attractive therapeutic target for ESCA."
item3237	REG00007	M6ATAR00331	.	.	.	39662354	"The upregulation of m6A levels induced by BPA specifically targets the Map1lc3b mRNA, a pivotal regulator of autophagy, thereby exerting suppressive effects on autophagic processes.m6A 'writer' METTL3 and 'eraser' ALKBH5 play a pivotal role in modulating BPA-induced injury in TM3 Leydig cells. knocking down METTL3 restored LC3B expression and reduced P62 levels, thereby ameliorating the impairment of autophagy caused by BPA, while knocking down ALKBH5 exacerbated the autophagy damage caused by BPA ."
item3238	REG00005	M6ATAR00331	.	.	.	39662354	"The upregulation of m6A levels induced by BPA specifically targets the Map1lc3b mRNA, a pivotal regulator of autophagy, thereby exerting suppressive effects on autophagic processes.m6A 'writer' METTL3 and 'eraser' ALKBH5 play a pivotal role in modulating BPA-induced injury in TM3 Leydig cells. knocking down METTL3 restored LC3B expression and reduced P62 levels, thereby ameliorating the impairment of autophagy caused by BPA, while knocking down ALKBH5 exacerbated the autophagy damage caused by BPA ."
item3239	REG00024	.	.	M6ADIS0222	.	39019337	"In MASLD, damage to the MRC may be regulated by the Mettl3-m6A-YTHDF1 axis, particularly by the role of YTHDF1. Modulation of the Mettl3-m6A-YTHDF1 axis has the potential to improve mitochondrial function, alleviate MASLD symptoms, and decrease the likelihood of disease progression."
item3240	REG00006	M6ATAR00559	.	M6ADIS0055	.	39082352	"The m6A modification of IRS1was increased in OSCC cells. IRS1 were positively regulated by the m6A regulators methyltransferase-like 14 (METTL14) and YTH domain-containing protein 1 (YTHDC1). IRS1 bound to YTHDC1, and YTHDC1 knockdown inhibited the IRS1 nuclear export. The obesity-associated protein (FTO) negatively regulated IRS1, and FTO overexpression reversed the IRS1-induced OSCC tumor growth. Conclusions: m6A methylation-mediated IRS1 regulated EMT in OSCC through p53/Line-1. These findings provide potential therapeutic strategies for managing OSCC."
item3241	REG00005	M6ATAR00446	.	M6ADIS0382	.	39441582	"ALKBH5 knockdown alleviated corneal neovascularization and inflammation and countered IL-6-induced promotion of cell proliferation, migration, and tube formation in HUVECs."
item3242	REG00005	M6ATAR01326	.	M6ADIS0382	.	39441582	"ALKBH5 knockdown alleviated corneal neovascularization and inflammation and countered IL-6-induced promotion of cell proliferation, migration, and tube formation in HUVECs."
item3243	REG00005	M6ATAR00258	.	M6ADIS0382	.	39441582	"ALKBH5 knockdown alleviated corneal neovascularization and inflammation and countered IL-6-induced promotion of cell proliferation, migration, and tube formation in HUVECs."
item3244	REG00024	M6ATAR01327	.	M6ADIS0059	.	39151722	"GID8/Twa1 as a crucial downstream target of YTHDF1. YTHDF1 manipulates GID8 translation efficiency in an m6A-dependent manner, and high expression of GID8 is associated with more aggressive tumor progression and poor overall survival.GID8 is intimately associated with glutamine metabolic demands by maintaining active glutamine uptake and metabolism through the regulation of excitatory amino acid transporter 1 (SLC1A3) and glutaminase (GLS), thereby facilitating the malignant progression of CRC. Inhibition of GID8 attenuated CRC proliferation and metastasis both in vitro and in vivo."
item3245	REG00022	.	Down	M6ADIS0378	M6ADRUG0001	38814536	"m6A methyltransferase METTL14 and recognition protein YTHDC1 were decreased by PTZ stimulation, which might contribute to the reduced m6A level. DG-specific over-expression of METTL14 or YTHDC1 by lentivirus injection could significantly ameliorate seizure-like behaviors and prevent the excessive activation of neuron in epilepsy mice induced by PTZ injection, which might be due to the normalized m6A level."
item3246	REG00006	.	Down	M6ADIS0378	M6ADRUG0001	38814536	"m6A methyltransferase METTL14 and recognition protein YTHDC1 were decreased by PTZ stimulation, which might contribute to the reduced m6A level. DG-specific over-expression of METTL14 or YTHDC1 by lentivirus injection could significantly ameliorate seizure-like behaviors and prevent the excessive activation of neuron in epilepsy mice induced by PTZ injection, which might be due to the normalized m6A level."
item3247	REG00001	M6ATAR01328	.	.	.	38749796	"The cell m6A methylation change lists after repeated UVB irradiation, and revealed that FTO and LPCAT3 play key roles in the m6A methylation pathogenesis of UV-induced skin cell apoptosis. FTO-m6A-LPCAT3 might serve as a novel upstream target for preventing and treating photoaging and UV-induced skin diseases."
item3248	REG00008	.	.	M6ADIS0114	.	38711079	"MiR27a regulates BMSC differentiation through YTHDF2, affecting m6A methylation and promoting osteogenesis. This finding suggests a potential therapeutic target for SNFH."
item3249	REG00007	M6ATAR01329	.	M6ADIS0167	.	39501302	"Upregulated METTL3 promoting IRF4 expression in an m6A-dependent manner, thus causing plasma cell infiltration-mediated kidney damage of SLE. This provides new evidence for the role of m6A in SLE kidney injury."
item3250	REG00007	M6ATAR01330	.	M6ADIS0065	M6ADRUG0089	38582397	The chemotherapeutic drug paclitaxel (PTX) could induce ER stress and increase .the combination of METTL3/METTL14 inhibitors with PTX demonstrated a significant synergistic therapeutic effect in both BC cells and xenograft mice.
item3251	REG00006	M6ATAR01330	.	M6ADIS0065	M6ADRUG0089	38582397	The chemotherapeutic drug paclitaxel (PTX) could induce ER stress and increase .the combination of METTL3/METTL14 inhibitors with PTX demonstrated a significant synergistic therapeutic effect in both BC cells and xenograft mice.
item3252	REG00007	M6ATAR00410	.	M6ADIS0065	M6ADRUG0089	38582397	The chemotherapeutic drug paclitaxel (PTX) could induce ER stress and increase .the combination of METTL3/METTL14 inhibitors with PTX demonstrated a significant synergistic therapeutic effect in both BC cells and xenograft mice.
item3253	REG00006	M6ATAR00410	.	M6ADIS0065	M6ADRUG0089	38582397	The chemotherapeutic drug paclitaxel (PTX) could induce ER stress and increase .the combination of METTL3/METTL14 inhibitors with PTX demonstrated a significant synergistic therapeutic effect in both BC cells and xenograft mice.
item3254	REG00007	M6ATAR01330	.	M6ADIS0065	M6ADRUG0108	38582397	The chemotherapeutic drug paclitaxel (PTX) could induce ER stress and increase .the combination of METTL3/METTL14 inhibitors with PTX demonstrated a significant synergistic therapeutic effect in both BC cells and xenograft mice.
item3255	REG00006	M6ATAR01330	.	M6ADIS0065	M6ADRUG0108	38582397	The chemotherapeutic drug paclitaxel (PTX) could induce ER stress and increase .the combination of METTL3/METTL14 inhibitors with PTX demonstrated a significant synergistic therapeutic effect in both BC cells and xenograft mice.
item3256	REG00007	M6ATAR00410	.	M6ADIS0065	M6ADRUG0108	38582397	The chemotherapeutic drug paclitaxel (PTX) could induce ER stress and increase .the combination of METTL3/METTL14 inhibitors with PTX demonstrated a significant synergistic therapeutic effect in both BC cells and xenograft mice.
item3257	REG00006	M6ATAR00410	.	M6ADIS0065	M6ADRUG0108	38582397	The chemotherapeutic drug paclitaxel (PTX) could induce ER stress and increase .the combination of METTL3/METTL14 inhibitors with PTX demonstrated a significant synergistic therapeutic effect in both BC cells and xenograft mice.
item3258	REG00007	.	.	M6ADIS0112	M6ADRUG0108	39245197	"Overexpression of METTL3 could promote the proliferation, migration, and secretion of IL-6, RANKL of RA-FLSs; inhibition of METTL3 expression could inhibit the abnormal proliferation, migration, invasion, and secretion of IL-6, RANKL, at the same time promoted the apoptosis and secretion of OPG, thus inhibited RA-FLSs tumor-like growth."
item3259	REG00017	.	.	M6ADIS0001	.	39248438	"Gene signatures involved in the m6A-related ferroptosis in gliomas were identified via bioinformatic analyses. NFE2L2 interacted with METTL16 to regulate the immune response in low-grade gliomas, and both molecules may be novel therapeutic targets for gliomas."
item3260	REG00007	M6ATAR00427	.	.	M6ADRUG0022	38631119	"METTL3 promoted mA modification of mRNA, a critical gene governing iron uptake, and enhanced its stability through recognition of the mA reader protein, IGF2BP2. Moreover, pharmacological administration of a highly selective METTL3 inhibitor STM2457 effectively ameliorated DIC in mice. METTL3 plays a cardinal role in the etiology of DIC by regulating cardiac iron metabolism and ferroptosis through mA modification. Inhibition of METTL3 might be a potential therapeutic avenue for DIC."
item3261	REG00007	M6ATAR00427	.	.	M6ADRUG0108	38631119	"METTL3 promoted mA modification of mRNA, a critical gene governing iron uptake, and enhanced its stability through recognition of the mA reader protein, IGF2BP2. Moreover, pharmacological administration of a highly selective METTL3 inhibitor STM2457 effectively ameliorated DIC in mice. METTL3 plays a cardinal role in the etiology of DIC by regulating cardiac iron metabolism and ferroptosis through mA modification. Inhibition of METTL3 might be a potential therapeutic avenue for DIC."
item3262	REG00005	M6ATAR00477	.	M6ADIS0091	.	38996894	"ALKBH5 induced m6A-demethylation in SNHG3, leading to its degradation. Low expression of SNHG3, on the other hand, prevented the formation of the SNHG3-ELAVL1-ZBP1/AIM2 complex, which in turn destabilized ZBP1 and AIM2 mRNA, resulting in the downregulation of these PANoptosis-related genes. ALKBH5 protected against PANoptosis in cerebral I/R injury models through the inhibition of SNHG3.This study sheds light on the intricate molecular mechanisms involved in the pathogenesis of cerebral I/R injury and highlights the potential of m6A-related genes as therapeutic targets in this condition."
item3263	REG00023	M6ATAR01332	.	M6ADIS0007	.	38129673	"YTHDC2 promoted m6A modification-mediated degradation of MRPL12 in LUAD cells, thereby contributing to the inhibition of cancer cell proliferation, invasion and migration. These results showed the anticancer effects of YTHDC2 in LUAD tumorigenesis."
item3264	REG00017	.	.	M6ADIS0224	.	39030605	"Our findings support a molecular model wherein the m6A writer METTL16-mediated alternative splicing and translation efficiency regulation are required to control the mitosis-to-meiosis germ cell fate decision in mice, with implications for understanding meiosis-related male fertility disorders."
item3265	REG00003	M6ATAR01333	.	M6ADIS0065	.	38353359	"HNRNPC was highly expressed in breast cancer, and played a crucial role in cell growth, especially in the luminal subtype. HNRNPC could combine and stabilize WDR77 mRNA. WDR77 successively drove the G1/S phase transition in the cell cycle and promoted cell proliferation. Notably, this regulation axis was closely tied to the m6A modification status of WDR77 mRNA. Overall, a critical regulatory mechanism was identified, as well as promising targets for potential treatment strategies for luminal breast cancer."
item3266	REG00007	M6ATAR00774	.	M6ADIS0161	.	39357736	The dysregulation of METTL3 and the resulting m6A modification of SOCS1 form a crucial epigenetic regulatory loop that promotes the progression of NP. Targeting the METTL3/SOCS1 axis might offer new insights into potential therapeutic strategies for NP.
item3267	REG00001	M6ATAR00189	.	M6ADIS0110	.	39122063	"FTO-EVs-induced suppressing effects on LPS-treated chondrocytes senescence and aging were abolished by Atg5/Atg7 knockdown and BNIP3 overexpression. In conclusion, this study evidenced that BM-MSCs-derived FTO-EVs suppressed cellular senescence and apoptosis, and triggered protective autophagy to suppress OA development through demethylating m6A modifications, and the engineering FTO-EVs could be potentially used to treat OA in clinic."
item3268	REG00001	M6ATAR00190	.	M6ADIS0110	.	39122063	"FTO-EVs-induced suppressing effects on LPS-treated chondrocytes senescence and aging were abolished by Atg5/Atg7 knockdown and BNIP3 overexpression. In conclusion, this study evidenced that BM-MSCs-derived FTO-EVs suppressed cellular senescence and apoptosis, and triggered protective autophagy to suppress OA development through demethylating m6A modifications, and the engineering FTO-EVs could be potentially used to treat OA in clinic."
item3269	REG00001	M6ATAR00201	.	M6ADIS0110	.	39122063	"FTO-EVs-induced suppressing effects on LPS-treated chondrocytes senescence and aging were abolished by Atg5/Atg7 knockdown and BNIP3 overexpression. In conclusion, this study evidenced that BM-MSCs-derived FTO-EVs suppressed cellular senescence and apoptosis, and triggered protective autophagy to suppress OA development through demethylating m6A modifications, and the engineering FTO-EVs could be potentially used to treat OA in clinic."
item3270	REG00008	M6ATAR00189	.	M6ADIS0110	.	39122063	"FTO-EVs-induced suppressing effects on LPS-treated chondrocytes senescence and aging were abolished by Atg5/Atg7 knockdown and BNIP3 overexpression. In conclusion, this study evidenced that BM-MSCs-derived FTO-EVs suppressed cellular senescence and apoptosis, and triggered protective autophagy to suppress OA development through demethylating m6A modifications, and the engineering FTO-EVs could be potentially used to treat OA in clinic."
item3271	REG00008	M6ATAR00190	.	M6ADIS0110	.	39122063	"FTO-EVs-induced suppressing effects on LPS-treated chondrocytes senescence and aging were abolished by Atg5/Atg7 knockdown and BNIP3 overexpression. In conclusion, this study evidenced that BM-MSCs-derived FTO-EVs suppressed cellular senescence and apoptosis, and triggered protective autophagy to suppress OA development through demethylating m6A modifications, and the engineering FTO-EVs could be potentially used to treat OA in clinic."
item3272	REG00008	M6ATAR00201	.	M6ADIS0110	.	39122063	"FTO-EVs-induced suppressing effects on LPS-treated chondrocytes senescence and aging were abolished by Atg5/Atg7 knockdown and BNIP3 overexpression. In conclusion, this study evidenced that BM-MSCs-derived FTO-EVs suppressed cellular senescence and apoptosis, and triggered protective autophagy to suppress OA development through demethylating m6A modifications, and the engineering FTO-EVs could be potentially used to treat OA in clinic."
item3273	REG00007	M6ATAR00189	.	M6ADIS0110	.	39122063	"FTO-EVs-induced suppressing effects on LPS-treated chondrocytes senescence and aging were abolished by Atg5/Atg7 knockdown and BNIP3 overexpression. In conclusion, this study evidenced that BM-MSCs-derived FTO-EVs suppressed cellular senescence and apoptosis, and triggered protective autophagy to suppress OA development through demethylating m6A modifications, and the engineering FTO-EVs could be potentially used to treat OA in clinic."
item3274	REG00007	M6ATAR00190	.	M6ADIS0110	.	39122063	"FTO-EVs-induced suppressing effects on LPS-treated chondrocytes senescence and aging were abolished by Atg5/Atg7 knockdown and BNIP3 overexpression. In conclusion, this study evidenced that BM-MSCs-derived FTO-EVs suppressed cellular senescence and apoptosis, and triggered protective autophagy to suppress OA development through demethylating m6A modifications, and the engineering FTO-EVs could be potentially used to treat OA in clinic."
item3275	REG00007	M6ATAR00201	.	M6ADIS0110	.	39122063	"FTO-EVs-induced suppressing effects on LPS-treated chondrocytes senescence and aging were abolished by Atg5/Atg7 knockdown and BNIP3 overexpression. In conclusion, this study evidenced that BM-MSCs-derived FTO-EVs suppressed cellular senescence and apoptosis, and triggered protective autophagy to suppress OA development through demethylating m6A modifications, and the engineering FTO-EVs could be potentially used to treat OA in clinic."
item3276	REG00007	M6ATAR01334	.	M6ADIS0068	.	38822192	"The silencing of HOXC6 or METTL3 suppresses PCa cell proliferation, invasion, migration, stemness, and glycolysis. Moreover, METTL3-induced HOXC6 m6A modification to stabilize its expression. In addition, the m6A reader IGF2BP2 directly recognized and bound to HOXC6 mRNA, and maintained its stability, and was involved in the regulation of HOXC6 expression by METTL3. Furthermore, IGF2BP2 knockdown impaired PCa cell proliferation, invasion, migration, stemness, and glycolysis by regulating HOXC6. Besides that HOXC6 interacted with the glycoytic enzyme PGK1 in PCa cells. In vivo assays further showed that METTL3 silencing reduced the expression of HOXC6 and PGK1, and impeded PCa growth. METTL3 promoted PCa progression by maintaining HOXC6 expression in an m6A-IGF2BP2-dependent mechanism."
item3277	REG00007	M6ATAR01438	.	M6ADIS0068	.	38822192	"The silencing of HOXC6 or METTL3 suppresses PCa cell proliferation, invasion, migration, stemness, and glycolysis. Moreover, METTL3-induced HOXC6 m6A modification to stabilize its expression. In addition, the m6A reader IGF2BP2 directly recognized and bound to HOXC6 mRNA, and maintained its stability, and was involved in the regulation of HOXC6 expression by METTL3. Furthermore, IGF2BP2 knockdown impaired PCa cell proliferation, invasion, migration, stemness, and glycolysis by regulating HOXC6. Besides that HOXC6 interacted with the glycoytic enzyme PGK1 in PCa cells. In vivo assays further showed that METTL3 silencing reduced the expression of HOXC6 and PGK1, and impeded PCa growth. METTL3 promoted PCa progression by maintaining HOXC6 expression in an m6A-IGF2BP3-dependent mechanism."
item3278	REG00013	M6ATAR01334	.	M6ADIS0068	.	38822192	"The silencing of HOXC6 or METTL3 suppresses PCa cell proliferation, invasion, migration, stemness, and glycolysis. Moreover, METTL3-induced HOXC6 m6A modification to stabilize its expression. In addition, the m6A reader IGF2BP2 directly recognized and bound to HOXC6 mRNA, and maintained its stability, and was involved in the regulation of HOXC6 expression by METTL3. Furthermore, IGF2BP2 knockdown impaired PCa cell proliferation, invasion, migration, stemness, and glycolysis by regulating HOXC6. Besides that HOXC6 interacted with the glycoytic enzyme PGK1 in PCa cells. In vivo assays further showed that METTL3 silencing reduced the expression of HOXC6 and PGK1, and impeded PCa growth. METTL3 promoted PCa progression by maintaining HOXC6 expression in an m6A-IGF2BP4-dependent mechanism."
item3279	REG00007	.	.	M6ADIS0006	M6ADRUG0138	39136667	.
item3280	REG00006	M6ATAR00190	Down	M6ADIS0015	.	39461405	"METTL14 knockdown led to increased ATG7 expression at both mRNA and protein levels, accompanied by reduced m6A methylation of ATG7 mRNA and enhanced mRNA stability. Moreover, silencing of ATG7 counteracted the effects of METTL14 knockdown on endothelial cell functions, emphasizing ATG7 as a downstream target of METTL14-mediated autophagy in HRVECs."
item3281	REG00006	M6ATAR01335	.	M6ADIS0117	.	39151294	"The expression change pattern of DKK3 under DN circumstances is in line with those of METTL14 and WTAP. DKK3's m6A methylation sites were confirmed to be located in the 3'UTR region, which is how METTL14 and WTAP improved DKK3's mRNA stability. Finally, YTHDF1, a m6A reader, was demonstrated to recognize m6A-methylated DKK3 and promote DKK3 expression."
item3282	REG00009	M6ATAR01335	.	M6ADIS0117	.	39151294	"The expression change pattern of DKK3 under DN circumstances is in line with those of METTL14 and WTAP. DKK3's m6A methylation sites were confirmed to be located in the 3'UTR region, which is how METTL14 and WTAP improved DKK3's mRNA stability. Finally, YTHDF1, a m6A reader, was demonstrated to recognize m6A-methylated DKK3 and promote DKK3 expression."
item3283	REG00024	M6ATAR01336	.	M6ADIS0117	.	39151294	"The expression change pattern of DKK3 under DN circumstances is in line with those of METTL14 and WTAP. DKK3's m6A methylation sites were confirmed to be located in the 3'UTR region, which is how METTL14 and WTAP improved DKK3's mRNA stability. Finally, YTHDF1, a m6A reader, was demonstrated to recognize m6A-methylated DKK3 and promote DKK3 expression."
item3284	REG00007	M6ATAR01443	.	M6ADIS0168	.	38853707	"METTL3 stabilized TLR2 mRNA in an IGF2BP1-dependent manner. METTL3 silencing restored specific gut microbiota levels in IDD rats, which was further reversed by administration of Pam3CSK4. These results demonstrate the beneficial effects of METTL3 silencing on NPC senescence and amelioration of IVD injury, involving modulation of TLR2 m6A modification and gut microbiota. These findings support METTL3 silencing as a potential therapeutic target for IDD."
item3285	REG00012	M6ATAR01443	.	M6ADIS0168	.	38853707	"METTL3 stabilized TLR2 mRNA in an IGF2BP1-dependent manner. METTL3 silencing restored specific gut microbiota levels in IDD rats, which was further reversed by administration of Pam3CSK4. These results demonstrate the beneficial effects of METTL3 silencing on NPC senescence and amelioration of IVD injury, involving modulation of TLR2 m6A modification and gut microbiota. These findings support METTL3 silencing as a potential therapeutic target for IDD."
item3286	REG00006	M6ATAR00470	.	M6ADIS0006	M6ADRUG0122	38664644	"The inhibition of HCC development by Regorafenib is attributed to its modulation of m6A expression of CHOP, mediated by METTL14, and the METTL14/CHOP axis enhances the sensitivity of HCC to Regorafenib. These findings provide insights into the treatment of HCC and the issue of drug resistance to Regorafenib."
item3287	REG00007	M6ATAR01337	.	M6ADIS0058	.	38959625	"METTL3 contributes to the malignant progression of COAD cells partly by regulating the stability of CDCA7 mRNA, providing a promising therapeutic target for COAD treatment."
item3288	REG00013	M6ATAR01338	.	M6ADIS0073	.	38289368	"IGF2BP2 was upregulated in THCA and IGF2BP2 expression was positively correlated with immune infiltration in THCA. Additionally, knockdown of IGF2BP2 inhibited the proliferation, invasion, and migration of THCA cells. IGF2BP2 has a contributory effect on the progression of THCA, which is a novel biomarker and a therapeutic target for THCA."
item3289	REG00014	M6ATAR00284	.	M6ADIS0073	.	38289369	"IGF2BP2 was upregulated in THCA and IGF2BP2 expression was positively correlated with immune infiltration in THCA. Additionally, knockdown of IGF2BP2 inhibited the proliferation, invasion, and migration of THCA cells. IGF2BP2 has a contributory effect on the progression of THCA, which is a novel biomarker and a therapeutic target for THCA."
item3290	REG00007	M6ATAR01339	.	M6ADIS0006	M6ADRUG0032	39489921	"We identified three core enzymes in the SSP (PHGDH, PSAT1, and PSPH) as novel targets of METTL3-mediated m6A modification. In these SSP genes, m6A modification recruited m6A reader IGF2BP3 to stabilize their mRNA transcripts, thereby enhancing their mRNA and protein expression in HCC cells. Most importantly, our GLORI-seq data revealed that sorafenib-resistant HCC cells elevated m6A modification in SSP genes to promote protein expression and antioxidant production. STM2457 treatment attenuated the serine synthesis pathway, induced oxidative stress, and sensitized HCC cells to sorafenib and lenvatinib treatments."
item3291	REG00007	M6ATAR01339	.	M6ADIS0006	M6ADRUG0138	39489921	"We identified three core enzymes in the SSP (PHGDH, PSAT1, and PSPH) as novel targets of METTL3-mediated m6A modification. In these SSP genes, m6A modification recruited m6A reader IGF2BP3 to stabilize their mRNA transcripts, thereby enhancing their mRNA and protein expression in HCC cells. Most importantly, our GLORI-seq data revealed that sorafenib-resistant HCC cells elevated m6A modification in SSP genes to promote protein expression and antioxidant production. STM2457 treatment attenuated the serine synthesis pathway, induced oxidative stress, and sensitized HCC cells to sorafenib and lenvatinib treatments."
item3292	REG00007	M6ATAR01339	.	M6ADIS0006	M6ADRUG0108	39489921	"We identified three core enzymes in the SSP (PHGDH, PSAT1, and PSPH) as novel targets of METTL3-mediated m6A modification. In these SSP genes, m6A modification recruited m6A reader IGF2BP3 to stabilize their mRNA transcripts, thereby enhancing their mRNA and protein expression in HCC cells. Most importantly, our GLORI-seq data revealed that sorafenib-resistant HCC cells elevated m6A modification in SSP genes to promote protein expression and antioxidant production. STM2457 treatment attenuated the serine synthesis pathway, induced oxidative stress, and sensitized HCC cells to sorafenib and lenvatinib treatments."
item3293	REG00007	M6ATAR01340	.	M6ADIS0006	M6ADRUG0032	39489921	"We identified three core enzymes in the SSP (PHGDH, PSAT1, and PSPH) as novel targets of METTL3-mediated m6A modification. In these SSP genes, m6A modification recruited m6A reader IGF2BP3 to stabilize their mRNA transcripts, thereby enhancing their mRNA and protein expression in HCC cells. Most importantly, our GLORI-seq data revealed that sorafenib-resistant HCC cells elevated m6A modification in SSP genes to promote protein expression and antioxidant production. STM2457 treatment attenuated the serine synthesis pathway, induced oxidative stress, and sensitized HCC cells to sorafenib and lenvatinib treatments."
item3294	REG00007	M6ATAR01340	.	M6ADIS0006	M6ADRUG0138	39489921	"We identified three core enzymes in the SSP (PHGDH, PSAT1, and PSPH) as novel targets of METTL3-mediated m6A modification. In these SSP genes, m6A modification recruited m6A reader IGF2BP3 to stabilize their mRNA transcripts, thereby enhancing their mRNA and protein expression in HCC cells. Most importantly, our GLORI-seq data revealed that sorafenib-resistant HCC cells elevated m6A modification in SSP genes to promote protein expression and antioxidant production. STM2457 treatment attenuated the serine synthesis pathway, induced oxidative stress, and sensitized HCC cells to sorafenib and lenvatinib treatments."
item3295	REG00007	M6ATAR01340	.	M6ADIS0006	M6ADRUG0108	39489921	"We identified three core enzymes in the SSP (PHGDH, PSAT1, and PSPH) as novel targets of METTL3-mediated m6A modification. In these SSP genes, m6A modification recruited m6A reader IGF2BP3 to stabilize their mRNA transcripts, thereby enhancing their mRNA and protein expression in HCC cells. Most importantly, our GLORI-seq data revealed that sorafenib-resistant HCC cells elevated m6A modification in SSP genes to promote protein expression and antioxidant production. STM2457 treatment attenuated the serine synthesis pathway, induced oxidative stress, and sensitized HCC cells to sorafenib and lenvatinib treatments."
item3296	REG00007	M6ATAR01084	.	M6ADIS0006	M6ADRUG0032	39489921	"We identified three core enzymes in the SSP (PHGDH, PSAT1, and PSPH) as novel targets of METTL3-mediated m6A modification. In these SSP genes, m6A modification recruited m6A reader IGF2BP3 to stabilize their mRNA transcripts, thereby enhancing their mRNA and protein expression in HCC cells. Most importantly, our GLORI-seq data revealed that sorafenib-resistant HCC cells elevated m6A modification in SSP genes to promote protein expression and antioxidant production. STM2457 treatment attenuated the serine synthesis pathway, induced oxidative stress, and sensitized HCC cells to sorafenib and lenvatinib treatments."
item3297	REG00007	M6ATAR01084	.	M6ADIS0006	M6ADRUG0138	39489921	"We identified three core enzymes in the SSP (PHGDH, PSAT1, and PSPH) as novel targets of METTL3-mediated m6A modification. In these SSP genes, m6A modification recruited m6A reader IGF2BP3 to stabilize their mRNA transcripts, thereby enhancing their mRNA and protein expression in HCC cells. Most importantly, our GLORI-seq data revealed that sorafenib-resistant HCC cells elevated m6A modification in SSP genes to promote protein expression and antioxidant production. STM2457 treatment attenuated the serine synthesis pathway, induced oxidative stress, and sensitized HCC cells to sorafenib and lenvatinib treatments."
item3298	REG00007	M6ATAR01084	.	M6ADIS0006	M6ADRUG0108	39489921	"We identified three core enzymes in the SSP (PHGDH, PSAT1, and PSPH) as novel targets of METTL3-mediated m6A modification. In these SSP genes, m6A modification recruited m6A reader IGF2BP3 to stabilize their mRNA transcripts, thereby enhancing their mRNA and protein expression in HCC cells. Most importantly, our GLORI-seq data revealed that sorafenib-resistant HCC cells elevated m6A modification in SSP genes to promote protein expression and antioxidant production. STM2457 treatment attenuated the serine synthesis pathway, induced oxidative stress, and sensitized HCC cells to sorafenib and lenvatinib treatments."
item3299	REG00020	.	.	M6ADIS0061	.	38878830	"Knockdown of RBM15 has the ability to inhibit PC growth and to promote macrophage infiltration and enhance phagocytosis of PC cells by macrophages. In conclusion, m6A modifications play a non-negligible role in the formation of TME diversity and complexity in PC. We reveal that inhibition of RBM15 suppresses PC development and modulates macrophage phagocytosis, and provide a more effective immunotherapeutic strategy for PC."
item3300	REG00015	M6ATAR00268	.	M6ADIS0374	.	38658662	"VIRMA can inhibit cell migration and proliferation by upregulating the expression of GSK3beta, contributing to the onset of HSCR."
item3301	REG00006	M6ATAR01414	.	M6ADIS0110	.	39175261	METTL14 depletion repressed the IL-1beta or erastin-stimulated ECM degradation and ferroptosis in mouse chondrocytes. METTL14 inhibited GPX4 gene through m6A methylation modification. GPX4 knockdown reversed the si-METTL14-mediated protection in IL-1beta-induced chondrocytes.ConclusionMETTL14 depletion inhibits ferroptosis and ECM degradation by suppressing GPX4 mRNA m6A modification in injured chondrocytes.
item3302	REG00001	M6ATAR00931	.	M6ADIS0368	.	39180207	"FTO-mediated N6-methyladenosine (m6A) modification of ferritin heavy chain 1 (FTH1) suppressed its mRNA expression and stability, inhibiting its protein expression. However, overexpression of FTH1 abrogated the effects of FTO and promoted the ferroptosis of neurons. In summary, FTO functions as a protective role in neonatal HIE via inhibiting FTH1 signaling. Thence, targeting may be a promising strategy for FTO neonatal HIE."
item3303	REG00007	.	.	M6ADIS0164	.	38513836	"Through FMT and interference of METTL3, we found that gut microbiota mediated the up-regulation of METTL3 by S. boulardii improved inflammation and oxidative stress in asthmatic mice, and alleviated lung injury. S. boulardii alleviated allergic asthma by restoring gut microbiota and metabolic homeostasis via up-regulation of METTL3 in an m6A-dependent manner."
item3304	REG00015	M6ATAR00258	.	M6ADIS0048	.	39060874	"KIAA1429 mRNA in plasma cells from MM patients was positively linked with to glycolysis-enhancing genes. The levels of glycolysis-enhancing genes, glucose uptake, and lactate production were repressed after KIAA1429 knockdown, along with reduced FOXM1 levels and stability. YTHDF1 recognized KIAA1429-methylated FOXM1 mRNA and raised FOXM1 stability. Knockdown of YTHDF1 curbed aerobic glycolysis and malignant behaviors in MM cells, which was nullified by FOXM1 overexpression."
item3305	REG00024	M6ATAR00258	.	M6ADIS0048	.	39060874	"KIAA1429 mRNA in plasma cells from MM patients was positively linked with to glycolysis-enhancing genes. The levels of glycolysis-enhancing genes, glucose uptake, and lactate production were repressed after KIAA1429 knockdown, along with reduced FOXM1 levels and stability. YTHDF1 recognized KIAA1429-methylated FOXM1 mRNA and raised FOXM1 stability. Knockdown of YTHDF1 curbed aerobic glycolysis and malignant behaviors in MM cells, which was nullified by FOXM2 overexpression."
item3306	REG00007	M6ATAR01345	.	M6ADIS0372	.	39426235	HT-2 toxin induced cartilage ECM degradation by regulating the METTL3-mediated m6A modification of Ctsk. These findings highlight the METTL3/m6A/Ctsk axis as a potential therapeutic target for the treatment of KBD and other cartilage-associated diseases.
item3307	REG00007	.	.	.	.	38554281	"Reader proteins convey m6A effects, and their silencing phenocopies METTL3 depletion. Among the m6A targets, we identified transactive response DNA-binding protein 43 (TDP-43) and discovered that its expression is under epitranscriptomic control. Thus, impaired m6A signaling disrupts MN homeostasis and triggers neurodegeneration conceivably through TDP-43 deregulation."
item3308	REG00006	M6ATAR00610	.	M6ADIS0073	.	39413935	"METTL14-mediated m6A modification of SOCS3 inactivated the janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) pathway, and in the METTL14-overexpressing TC cells, silencing SOCS3-induced upregulation of cell proliferation, EMT and suppression of apoptosis was reversed by JAK2/STAT3 inhibitor AG490 and WP1066. Together, we indicated that METTL14/m6A/SOCS3/JAK2/STAT3 axis play an important role in the progression of TC."
item3309	REG00007	M6ATAR01346	.	M6ADIS0056	.	39708485	"METTL3 was upregulated in tumor tissues and regulated CEP170 expression. RNA-seq upon CEP170 depletion revealed that ASPM was significantly downregulated, indicating its involvement as a downstream target of CEP170 in regulating cell proliferation and mitosis. Our findings provide novel insights into the molecular mechanisms by which CEP170 and m6A modifications regulate esophageal cancer progression, revealing that CEP170 is a potential therapeutic target."
item3310	REG00024	M6ATAR00679	.	M6ADIS0103	.	38768805	"YTHDF1 bound to mA-modified Caveolin 1 (Cav1) mRNA and favored its translation. We further demonstrated that YTHDF1 regulates downstream ERK signaling. Altogether, our findings highlight a novel role for YTHDF1 as a post-transcriptional regulator of caveolar proteins which is necessary for the maintenance of cardiac function."
item3311	REG00007	M6ATAR00141	Up	M6ADIS0051	.	37897586	"METTL3 was upregulated in osteosarcoma tissues and cell lines. Functionally, METTL3 promoted the proliferation and migration of osteosarcoma cells. Moreover, a clear positive correlation was found between METTL3 and MALAT1 expression, and MALAT1 was upregulated in osteosarcoma tissues and cells. Mechanistically, the presence of m6A modification sites in MALAT1 and METTL3-mediated m6A modification increased the stability of MALAT1 in osteosarcoma cells and promoted their proliferation and migration."
item3312	REG00007	M6ATAR00520	Up	M6ADIS0070	.	38823761	"RBM15/METTL3 complex enhances m6A modification and promotes the ENO1 protein translation efficiency through its 359A site by depending on YTHDF1 in BC cells. Our study highlights the significance of RBM15/METTL3 complex-mediated ENO1 mRNA m6A modification in ENO1 expression. It also reveals a novel mechanism by which ENO1 promotes BC progression, thereby suggesting that ENO1 can be a therapeutic target for BC."
item3313	REG00020	M6ATAR00520	Up	M6ADIS0070	.	38823761	"RBM15/METTL3 complex enhances m6A modification and promotes the ENO1 protein translation efficiency through its 359A site by depending on YTHDF1 in BC cells. Our study highlights the significance of RBM15/METTL3 complex-mediated ENO1 mRNA m6A modification in ENO1 expression. It also reveals a novel mechanism by which ENO1 promotes BC progression, thereby suggesting that ENO1 can be a therapeutic target for BC."
item3314	REG00024	M6ATAR00520	.	M6ADIS0070	.	38823761	"RBM15/METTL3 complex enhances m6A modification and promotes the ENO1 protein translation efficiency through its 359A site by depending on YTHDF1 in BC cells. Our study highlights the significance of RBM15/METTL3 complex-mediated ENO1 mRNA m6A modification in ENO1 expression. It also reveals a novel mechanism by which ENO1 promotes BC progression, thereby suggesting that ENO1 can be a therapeutic target for BC."
item3315	REG00009	M6ATAR00431	.	M6ADIS0168	.	38345407	"In vitro and in vivo inhibition of WTAP expression or TIMP3 overexpression significantly increased stress resistance in the nucleus pulposus, thereby alleviating IDD. Our results show that abnormal stress disrupts IVD matrix stability through WTAP/YTHDF2-dependent TIMP3 m6A modification."
item3316	REG00008	M6ATAR00431	.	M6ADIS0168	.	38345407	"In vitro and in vivo inhibition of WTAP expression or TIMP3 overexpression significantly increased stress resistance in the nucleus pulposus, thereby alleviating IDD. Our results show that abnormal stress disrupts IVD matrix stability through WTAP/YTHDF2-dependent TIMP3 m6A modification."
item3317	REG00007	M6ATAR01200	.	M6ADIS0008	.	39424828	"The METTL3-NEK2 axis promoted CC progression by activating the Wnt/beta-catenin pathway and inhibiting the apoptosis pathway. In conclusion, METTL3 facilitated the malignant progression of CC and contributed to the formation of the METTL3-NEK2 regulatory axis in an m6A-dependent manner, which represented a potential target for CC therapy."
item3318	REG00050	.	.	M6ADIS0055	.	39244024	Our study identifies RBFOX2 as a critical player in OSCC pathogenesis and opens avenues for novel therapeutic strategies targeting the m6A regulatory machinery in this malignancy.
item3319	REG00007	M6ATAR01347	.	M6ADIS0006	M6ADRUG0147	39234824	"TGF-beta can promote the liquid phase separation of METTL3, which further leads to the reduction of mRNA stability of ITIH1.r-ITIH1 can play a synergistic role in targeting HCC with TGF-beta inhibitor. The downstream ITIH1 regulatory mechanism of TGF-beta and m6A modification is revealed, and ITIH1 can be translational as a potential target for HCC."
item3320	REG00006	M6ATAR01414	.	M6ADIS0007	.	38993012	The METTL14/GPX4 axis promotes NSCLC progression by inhibiting cell ferroptosis through the recognition of m6A modification mediated by IGF2BP1.
item3321	REG00013	M6ATAR01414	.	M6ADIS0007	.	38993012	The METTL14/GPX4 axis promotes NSCLC progression by inhibiting cell ferroptosis through the recognition of m6A modification mediated by IGF2BP1.
item3322	REG00006	M6ATAR00049	.	M6ADIS0361	.	39332090	"Taken together, this study establishes the involvement of m6A in SA and identified a novel SA signaling pathway. These results reveal the underlying molecular mechanisms of trophoblast cell dysfunction induced by m6A modification and provide new strategies to identify and mitigate SA."
item3323	REG00017	M6ATAR01349	.	M6ADIS0061	.	39434688	"The METTL16-MROH8-TBP-CAPN2 pathway offers potential therapeutic targets for pancreatic cancer treatment, highlighting the significance of m6A modifications in tumor regulation. Further clinical validation is needed to confirm these findings in human patients."
item3324	REG00023	M6ATAR01349	.	M6ADIS0061	.	39434688	"The METTL16-MROH8-TBP-CAPN2 pathway offers potential therapeutic targets for pancreatic cancer treatment, highlighting the significance of m6A modifications in tumor regulation. Further clinical validation is needed to confirm these findings in human patients."
item3325	REG00007	M6ATAR01350	.	M6ADIS0073	.	39623910	"METTL3 was notably reduced in PTC samples and was positively correlated with hsa_circ_0136959. Mechanistically, METTL3 enhanced hsa_circ_0136959 expression through m6A modification. Our results demonstrate that METTL3-mediated m6A modification elevated hsa_circ_0136959 expression and subsequently restricted the tumor characteristics of PTC by accelerating ferroptosis."
item3326	REG00021	M6ATAR01263	Down	M6ADIS0068	.	39361104	"Mechanical analysis showed that RBM15B facilitated m6A modification of PCNA mRNA, leading to increasing m6A methylation. YTHDF1 bound to these m6A sites on PCNA mRNA, thus stabilizing it. Furthermore, PCNA overexpression mitigated the effects of RBM15B knockdown on PC cell proliferation. In conclusion, RBM15B promotes PC cell proliferation by enhancing the stability of PCNA mRNA through YTHDF1-mediated m6A modification."
item3327	REG00024	M6ATAR01263	Down	M6ADIS0068	.	39361104	"Mechanical analysis showed that RBM15B facilitated m6A modification of PCNA mRNA, leading to increasing m6A methylation. YTHDF1 bound to these m6A sites on PCNA mRNA, thus stabilizing it. Furthermore, PCNA overexpression mitigated the effects of RBM15B knockdown on PC cell proliferation. In conclusion, RBM15B promotes PC cell proliferation by enhancing the stability of PCNA mRNA through YTHDF1-mediated m6A modification."
item3328	REG00006	M6ATAR01352	.	M6ADIS0115	.	39737912	"METTL14 promotes GLUT3 expression via YTHDF1, leading to the modulation of various parameters in the H2O2-induced model. Similar positive effects of METTL14 on osteogenesis were observed in an ovariectomized mouse osteoporosis model. DISCUSSION METTL14 could serve as a potential therapeutic approach for enhancing osteoporosis treatment."
item3329	REG00024	M6ATAR01352	.	M6ADIS0115	.	39737912	"METTL14 promotes GLUT3 expression via YTHDF1, leading to the modulation of various parameters in the H2O2-induced model. Similar positive effects of METTL14 on osteogenesis were observed in an ovariectomized mouse osteoporosis model. DISCUSSION METTL14 could serve as a potential therapeutic approach for enhancing osteoporosis treatment."
item3330	REG00009	M6ATAR00827	.	M6ADIS0057	.	37477820	"WTAP silencing reversed the cancer-promoting role of FAM83H-AS1 overexpression in GC cell migration, proliferation, and invasion. Our results suggest that WTAP-mediated FAM83H-AS1 promotes GC development via m6A modification. Our findings provide new biomarkers for GC diagnosis and targeted therapy."
item3331	REG00020	M6ATAR01353	Up	M6ADIS0008	.	38429603	"Decorin (DCN) downregulated in CC was a direct substrate of RBM15 m6A methylation, and RBM15 knockdown could enhance DCN expression in CC cells. The anti-tumor effects of RBM15 knockdown could be abolished by DCN silencing. Overall, RBM15 knockdown lowered the tumorigenesis of CC both in vitro and in vivo, and it does so via mediating m6A modification of DCN mRNA in CC cells."
item3332	REG00004	M6ATAR01100	Up	M6ADIS0057	.	38887155	"Cytoplasm-anchored hnRNPA2B1 coordinated PABPC1 to stabilize its relationship with cap-binding eIF4F complex, which facilitated the translation of CIP2A, DLAT and GPX1 independent of m6A modification. In summary, hnRNPA2B1 facilitates the non-m6A translation of epigenetic mRNAs in GC progression by interacting with PABPC1-eIF4F complex and predicts poor prognosis for patients with GC."
item3333	REG00015	M6ATAR01355	.	M6ADIS0007	.	38848293	This study showed that KIAA1429 enhanced LINC01106 m6A modification to promote LUAD development. These results may lead to a better understanding of the mechanism of KIAA1429-m6A-LINC01106 in LUAD and offer a valuable therapeutic target for LUAD.
item3334	REG00001	M6ATAR01356	Down	M6ADIS0161	.	39023405	"FTO silencing leads to increased m6A methylation of Grp177 through a YTHDF2-dependent mechanism, resulting in decreased Grp177 stability and ultimately reducing NP in rats by OS suppression."
item3335	REG00008	M6ATAR01356	Down	M6ADIS0161	.	39023405	"FTO silencing leads to increased m6A methylation of Grp177 through a YTHDF2-dependent mechanism, resulting in decreased Grp177 stability and ultimately reducing NP in rats by OS suppression."
item3336	REG00026	M6ATAR01357	.	M6ADIS0008	.	39476847	ZC3H13-mediated m6A modification of hsa_circ_0081723 promotes CC progression by modulating AMPK/p53 pathway. Our findings may contribute to the understanding of the molecular mechanisms underlying CC and offer potential therapeutic targets for clinical treatment.
item3337	REG00014	M6ATAR00222	.	M6ADIS0117	.	38904026	"METTL3 promotes kidney fibrosis by stimulating the m6A modification of beta-catenin mRNA, leading to its stabilization and its downstream profibrotic genes expression. Our findings suggest that targeting METTL3/IGF2BP3/beta-catenin pathway may be a novel strategy for the treatment of fibrotic CKD."
item3338	REG00007	M6ATAR00222	.	M6ADIS0117	.	38904026	"METTL3 promotes kidney fibrosis by stimulating the m6A modification of beta-catenin mRNA, leading to its stabilization and its downstream profibrotic genes expression. Our findings suggest that targeting METTL3/IGF2BP3/beta-catenin pathway may be a novel strategy for the treatment of fibrotic CKD."
item3339	REG00021	.	.	M6ADIS0265	.	39167728	"Three key MRREs in HUVECs and FMC84 mouse cardiomyocytes were reduced in the OGD group. Through hypoxia, smoking might reduce the expression levels of RBM15B, YTHDC2, and ZC3H13 in smokers with CAD. Our findings provide an important theoretical basis for the treatment of smokers with CAD."
item3340	REG00023	.	.	M6ADIS0265	.	39167728	"Three key MRREs in HUVECs and FMC84 mouse cardiomyocytes were reduced in the OGD group. Through hypoxia, smoking might reduce the expression levels of RBM15B, YTHDC2, and ZC3H13 in smokers with CAD. Our findings provide an important theoretical basis for the treatment of smokers with CAD."
item3341	REG00006	M6ATAR01359	.	M6ADIS0115	M6ADRUG0143	38906316	"METTL14 knockdown overturned the promotive effects of ICA on P4HB m6A level and BMSC osteogenic differentiation. To sum up, ICA elevated the METTL14-mediated m6A modification of P4HB to facilitate BMSC osteogenic differentiation."
item3342	REG00006	M6ATAR01245	.	M6ADIS0091	.	39622391	"METTL14 enhanced PAX6 mRNA m6A modification to promote YTHDF2 binding to PAX6 mRNA and its degradation. PAX6 bound to TREM2 promoter and facilitated its transcription and expression. In conclusion, METTL14-mediated m6A modification aggravates ischemic stroke by promoting microglial M1 polarization via YTHDF2/PAX6/TREM2 axis."
item3343	REG00008	M6ATAR01245	.	M6ADIS0091	.	39622391	"METTL14 enhanced PAX6 mRNA m6A modification to promote YTHDF2 binding to PAX6 mRNA and its degradation. PAX6 bound to TREM2 promoter and facilitated its transcription and expression. In conclusion, METTL14-mediated m6A modification aggravates ischemic stroke by promoting microglial M1 polarization via YTHDF2/PAX6/TREM2 axis."
item3344	REG00009	M6ATAR01431	.	M6ADIS0206	.	38866113	"Trophoblast-specific knockout mice of Wtap, a critical component of methyltransferase complex, and demonstrated that Wtap was essential for trophoblast proliferation, placentation and perinatal growth. Further in vitro experiments which includes cell viability assays and series molecular binding assays demonstrated that WTAP-m6A-IGF2BP3 axis regulated the RNA stability ."
item3345	REG00014	M6ATAR01431	.	M6ADIS0206	.	38866113	"Trophoblast-specific knockout mice of Wtap, a critical component of methyltransferase complex, and demonstrated that Wtap was essential for trophoblast proliferation, placentation and perinatal growth. Further in vitro experiments which includes cell viability assays and series molecular binding assays demonstrated that WTAP-m6A-IGF2BP3 axis regulated the RNA stability ."
item3346	REG00009	M6ATAR00446	.	M6ADIS0206	.	38866113	"Trophoblast-specific knockout mice of Wtap, a critical component of methyltransferase complex, and demonstrated that Wtap was essential for trophoblast proliferation, placentation and perinatal growth. Further in vitro experiments which includes cell viability assays and series molecular binding assays demonstrated that WTAP-m6A-IGF2BP3 axis regulated the RNA stability ."
item3347	REG00014	M6ATAR00446	.	M6ADIS0206	.	38866113	"Trophoblast-specific knockout mice of Wtap, a critical component of methyltransferase complex, and demonstrated that Wtap was essential for trophoblast proliferation, placentation and perinatal growth. Further in vitro experiments which includes cell viability assays and series molecular binding assays demonstrated that WTAP-m6A-IGF2BP3 axis regulated the RNA stability ."
item3348	REG00007	M6ATAR01414	.	M6ADIS0013	.	39261364	"METTL3 knockdown promoted GPX4 expression in DHEA-induced granulosa cells by m6A modification and restrained DHEA-induced fibrosis, lipid peroxidation and ferroptosis in granulosa cells via elevating GPX4. METTL3 silence inhibited ovarian fibrosis in PCOS, which was mediated through suppressing ferroptosis by upregulating GPX4 in m6A-dependent manner."
item3349	REG00001	M6ATAR01360	.	M6ADIS0112	.	39025373	"FTO promotes the inflammatory response, migration, and invasion of RA FLS through m6A-IGF2BP1-dependent ADAMST15 axis, indicating that FTO may act as a novel potential therapeutic target in RA."
item3350	REG00012	M6ATAR01360	.	M6ADIS0112	.	39025373	"FTO promotes the inflammatory response, migration, and invasion of RA FLS through m6A-IGF2BP1-dependent ADAMST15 axis, indicating that FTO may act as a novel potential therapeutic target in RA."
item3351	REG00007	M6ATAR01361	.	M6ADIS0359	.	38825638	"The m6A level and odonto/osteoblastic differentiation capacity were affected by the overexpression or inhibition of METTL3. Overall, the METTL3/pre-miR-665/DLX3 pathway might provide a new target for SCAP-based tooth root/maxillofacial bone tissue regeneration."
item3352	REG00024	M6ATAR01361	.	M6ADIS0359	.	38825638	"The m6A level and odonto/osteoblastic differentiation capacity were affected by the overexpression or inhibition of METTL3. Overall, the METTL3/pre-miR-665/DLX3 pathway might provide a new target for SCAP-based tooth root/maxillofacial bone tissue regeneration."
item3353	REG00007	M6ATAR01362	.	M6ADIS0359	.	38825638	"The m6A level and odonto/osteoblastic differentiation capacity were affected by the overexpression or inhibition of METTL3. Overall, the METTL3/pre-miR-665/DLX3 pathway might provide a new target for SCAP-based tooth root/maxillofacial bone tissue regeneration."
item3354	REG00024	M6ATAR01362	.	M6ADIS0359	.	38825638	"The m6A level and odonto/osteoblastic differentiation capacity were affected by the overexpression or inhibition of METTL3. Overall, the METTL3/pre-miR-665/DLX3 pathway might provide a new target for SCAP-based tooth root/maxillofacial bone tissue regeneration."
item3355	REG00007	M6ATAR01437	Down	M6ADIS0232	.	38408556	"Silencing of METTL3 inhibited hemin-induced HT-22 cell pyroptosis by suppressing m6A methylation of NEK7, which was recognized by IGF2BP2. These findings are envisaged to identify a novel therapeutic strategy for ICH."
item3356	REG00013	M6ATAR01437	Down	M6ADIS0232	.	38408556	"Silencing of METTL3 inhibited hemin-induced HT-22 cell pyroptosis by suppressing m6A methylation of NEK7, which was recognized by IGF2BP2. These findings are envisaged to identify a novel therapeutic strategy for ICH."
item3357	REG00006	M6ATAR01363	.	M6ADIS0117	.	39080055	"Exosomal METTL14 derived from M1 macrophages promoted HG-induced apoptosis, inflammation and oxidative stress in GECs by mediating PAQR3 m6A modification."
item3358	REG00001	.	.	M6ADIS0091	.	38945353	"The expression levels of m6A regulators FTO and YTHDC1 were notably decreased in the neutrophils following ischemic stroke, and FTOexpression was negatively correlated with neutrophil counts and neutrophil-to-lymphocyte ratio (NLR).Moreover, the expression levels of major m6A regulators Mettl3, Fto, Ythdf1, and Ythdf3 were obviously declined in the brain and leukocytes of post-stroke mouse models."
item3359	REG00022	.	.	M6ADIS0091	.	38945353	"The expression levels of m6A regulators FTO and YTHDC1 were notably decreased in the neutrophils following ischemic stroke, and FTOexpression was negatively correlated with neutrophil counts and neutrophil-to-lymphocyte ratio (NLR).Moreover, the expression levels of major m6A regulators Mettl3, Fto, Ythdf1, and Ythdf3 were obviously declined in the brain and leukocytes of post-stroke mouse models."
item3360	REG00007	.	.	M6ADIS0091	.	38945353	"The expression levels of m6A regulators FTO and YTHDC1 were notably decreased in the neutrophils following ischemic stroke, and FTOexpression was negatively correlated with neutrophil counts and neutrophil-to-lymphocyte ratio (NLR).Moreover, the expression levels of major m6A regulators Mettl3, Fto, Ythdf1, and Ythdf3 were obviously declined in the brain and leukocytes of post-stroke mouse models."
item3361	REG00024	.	.	M6ADIS0091	.	38945353	"The expression levels of m6A regulators FTO and YTHDC1 were notably decreased in the neutrophils following ischemic stroke, and FTOexpression was negatively correlated with neutrophil counts and neutrophil-to-lymphocyte ratio (NLR).Moreover, the expression levels of major m6A regulators Mettl3, Fto, Ythdf1, and Ythdf3 were obviously declined in the brain and leukocytes of post-stroke mouse models."
item3362	REG00025	.	.	M6ADIS0091	.	38945353	"The expression levels of m6A regulators FTO and YTHDC1 were notably decreased in the neutrophils following ischemic stroke, and FTOexpression was negatively correlated with neutrophil counts and neutrophil-to-lymphocyte ratio (NLR).Moreover, the expression levels of major m6A regulators Mettl3, Fto, Ythdf1, and Ythdf3 were obviously declined in the brain and leukocytes of post-stroke mouse models."
item3363	REG00024	M6ATAR01364	.	M6ADIS0008	.	39557826	"Our results revealed an oncogenic role played by YTHDF1 in cervical cancer through m6A/MCT1-dependent manner. In conclusion, these findings unveil the immune escape-promoting effect of YTHDF1 in cervical cancer by boosting the lactate accumulation, which might illuminate a novel target for more precise immunotherapy."
item3364	REG00007	M6ATAR00513	.	M6ADIS0223	.	36705430	"METTL3 in BMSCs osteogenic differentiation via the IGF2BP1/m6A/RUNX2 signaling axis of m6A-dependent manner, providing a potential therapeutic target for maxillofacial bone defects treatment."
item3365	REG00012	M6ATAR00513	.	M6ADIS0223	.	36705430	"METTL3 in BMSCs osteogenic differentiation via the IGF2BP1/m6A/RUNX2 signaling axis of m6A-dependent manner, providing a potential therapeutic target for maxillofacial bone defects treatment."
item3366	REG00001	M6ATAR01365	.	M6ADIS0008	.	39692250	"The Merip-seq and Merip-qPCR evoked that relative PIK3R3 m6A level was significantly increased after FTO knockdown, which effected the activation of FoxO pathway. After knocking down FTO, upregulation of PIK3R3 can restore the malignancy of cervical cancer."
item3367	REG00007	M6ATAR01366	.	M6ADIS0155	.	39259386	"HucMSC-Ex promoted the binding of METTL3 to the Slc37a2 mRNA complex, and enhanced the binding of Slc37a2 to YTHDF1 to upregulate the intracellular expression of Slc37a2, thereby attenuating the pro-inflammatory function of macrophage. This study confirms the modulatory role of hucMSC-Ex on the m6A modification of macrophages in IBD, providing a new scientific basis for the treatment of IBD with hucMSC-Ex."
item3368	REG00024	M6ATAR01366	.	M6ADIS0155	.	39259386	"HucMSC-Ex promoted the binding of METTL3 to the Slc37a2 mRNA complex, and enhanced the binding of Slc37a2 to YTHDF1 to upregulate the intracellular expression of Slc37a2, thereby attenuating the pro-inflammatory function of macrophage. This study confirms the modulatory role of hucMSC-Ex on the m6A modification of macrophages in IBD, providing a new scientific basis for the treatment of IBD with hucMSC-Ex."
item3369	REG00007	M6ATAR00396	.	M6ADIS0006	M6ADRUG0190	39326134	"Len resistance in HCC is related to the increased m6A level and the high expression of METTL3. Reserpine, a small-molecule regulator of m6A, reverses Lenvatinib-resistant phenotypes, including proliferation, migration and anti-apoptosis, in vitro and in vivo by targeting SMAD3 and down-regulating the m6A level in HCC."
item3370	REG00007	M6ATAR00396	.	M6ADIS0006	M6ADRUG0138	39326134	"Len resistance in HCC is related to the increased m6A level and the high expression of METTL3. Reserpine, a small-molecule regulator of m6A, reverses Lenvatinib-resistant phenotypes, including proliferation, migration and anti-apoptosis, in vitro and in vivo by targeting SMAD3 and down-regulating the m6A level in HCC."
item3371	REG00006	M6ATAR01367	Up	M6ADIS0099	.	39588760	METTL14-mediated m6A modification upregulated circARHGAP12 and ASPH to aggravate overload-induced lipid peroxidative damage and facilitate AS progression.
item3372	REG00006	M6ATAR01368	Up	M6ADIS0099	.	39588760	METTL14-mediated m6A modification upregulated circARHGAP12 and ASPH to aggravate overload-induced lipid peroxidative damage and facilitate AS progression.
item3373	REG00023	M6ATAR01369	.	.	.	38793659	"YTHDC1 abrogates RSV infection by reducing the expression of RSV entry receptor CX3C motif chemokine receptor 1 (CX3CR1) on the cell surface of lung epithelial cells. Altogether, these data reveal a novel role for m6A methylation and YTHDC1 in the viral entry of RSV. These findings may contribute to the development of novel treatment options to control RSV infection."
item3374	REG00007	M6ATAR01370	.	M6ADIS0065	.	39218290	"STAT5B facilitated METTL3-induced tumor formation by increasing CCND1 expression in an orthotopic mouse model. In clinical context, a positive correlation was observed between p-STAT5B and METTL3 expression in high-grade breast tumors. This study elucidates a novel mechanism that underlies the specificity of m6A modification in breast cancer cells, thereby underscoring its potential therapeutic value."
item3375	REG00008	M6ATAR01371	.	M6ADIS0385	.	39432207	"YTHDF2 can alter Cav1.2 protein expression in an m6A-independent manner, thereby facilitating the onset of AF. Our study suggests that YTHDF2 may be a potential intervention target for AF."
item3376	REG00014	M6ATAR00832	.	M6ADIS0389	.	39247830	"IGF2BP3 is the most significantly up-regulated m6A regulator in AEG tumors versus paired normal adjacent tissues from the expression profile of m6A regulators in a large cohort of AEG patients. In conclusion, our study highlights the role of post-transcriptional regulation in modulating AEG tumor progression and elucidates the functional importance of the m6A/IGF2BP3/CDC25A axis in AEG cells."
item3377	REG00001	M6ATAR01373	Down	M6ADIS0066	.	38615731	"FTO overexpression significantly decreased m6A modification in the 3' and 5' untranslated regions of KREMEN2mRNA and downregulated its expression. In addition, we found that FTO-mediated m6A modification of KREMEN2 mRNA was recognized and stabilized by the m6A reader IGF2BP1 rather than by IGF2BP2 or IGF2BP3. This study highlights the m6A modification of KREMEN2 and extends the importance of RNA epigenetics in HGSOC."
item3378	REG00012	M6ATAR01373	Down	M6ADIS0066	.	38615731	"FTO overexpression significantly decreased m6A modification in the 3' and 5' untranslated regions of KREMEN2mRNA and downregulated its expression. In addition, we found that FTO-mediated m6A modification of KREMEN2 mRNA was recognized and stabilized by the m6A reader IGF2BP1 rather than by IGF2BP2 or IGF2BP3. This study highlights the m6A modification of KREMEN2 and extends the importance of RNA epigenetics in HGSOC."
item3379	REG00001	M6ATAR00201	Up	M6ADIS0197	.	39308045	"FTO interacted with BNIP3 transcripts and regulated their expression in an m6A-dependent manner. Following FTO silencing, BNIP3 transcripts with elevated m6A modification levels in their coding regions were bound by YTHDF2 (YT521-B homology m6A RNA-binding protein 2), leading to mRNA destabilization and decreased BNIP3 protein levels. These findings highlight the importance of FTO-dependent cardiac m6A methylation in regulating mitophagy and enhance our understanding of this critical interplay, which is essential for developing therapeutic strategies to protect cardiac mitochondrial function, alleviate cardiac dysfunction, and improve survival during sepsis."
item3380	REG00008	M6ATAR00201	.	M6ADIS0197	.	39308045	"FTO interacted with BNIP3 transcripts and regulated their expression in an m6A-dependent manner. Following FTO silencing, BNIP3 transcripts with elevated m6A modification levels in their coding regions were bound by YTHDF2 (YT521-B homology m6A RNA-binding protein 2), leading to mRNA destabilization and decreased BNIP3 protein levels. These findings highlight the importance of FTO-dependent cardiac m6A methylation in regulating mitophagy and enhance our understanding of this critical interplay, which is essential for developing therapeutic strategies to protect cardiac mitochondrial function, alleviate cardiac dysfunction, and improve survival during sepsis."
item3381	REG00006	M6ATAR00388	.	M6ADIS0058	.	37592151	"METTL14 overexpression substantially augmented the m6A modification of SCD1 mRNA and diminished the SCD1 mRNA level. In addition, we revealed that YTHDF2 was the m6A reader to recognize METTL14 m6A-modified SCD1 mRNA and abolish its stability. Finally, we also validated that METTL14 might impede the tumorigenic process of CC through SCD1 mediated Wnt/beta-catenin signaling. Taken together, this study presented that METTL14 performed as a potential therapeutic target in CC with important implications for the prognosis amelioration of CC patients."
item3382	REG00008	M6ATAR00388	.	M6ADIS0058	.	37592151	"METTL14 overexpression substantially augmented the m6A modification of SCD1 mRNA and diminished the SCD1 mRNA level. In addition, we revealed that YTHDF2 was the m6A reader to recognize METTL14 m6A-modified SCD1 mRNA and abolish its stability. Finally, we also validated that METTL14 might impede the tumorigenic process of CC through SCD1 mediated Wnt/beta-catenin signaling. Taken together, this study presented that METTL14 performed as a potential therapeutic target in CC with important implications for the prognosis amelioration of CC patients."
item3383	REG00007	M6ATAR00303	.	M6ADIS0006	.	39515695	"METTL3 directly modulates the stability of AK3, thereby promoting its expression via m6A modification. This finding is pivotal as it underscores the regulatory role that METTL3 plays in AK3 RNA expression, facilitated through the m6A modification pathway."
item3384	REG00007	M6ATAR00303	.	M6ADIS0006	.	39515695	"METTL3 directly modulates the stability of AK3, thereby promoting its expression via m6A modification. This finding is pivotal as it underscores the regulatory role that METTL3 plays in AK3 RNA expression, facilitated through the m6A modification pathway."
item3385	REG00006	M6ATAR01374	.	M6ADIS0219	.	39054337	"METTL14 facilitated the m6A modification of SETBP1 mRNA by formation of METTL3-METTL14 complex, leading to increased stabilization of SETBP1 mRNA and subsequent activation of the PI3K-AKT signaling pathway. Overall, this study elucidated the involvement of the METTL14/m6A/SETBP1/PI3K-AKT signaling axis in MDS, highlighting the therapeutic potential of targeting METTL3-METTL14 complex-mediated m6A modification for MDS therapy."
item3386	REG00007	M6ATAR01374	.	M6ADIS0219	.	39054337	"METTL14 facilitated the m6A modification of SETBP1 mRNA by formation of METTL3-METTL14 complex, leading to increased stabilization of SETBP1 mRNA and subsequent activation of the PI3K-AKT signaling pathway. Overall, this study elucidated the involvement of the METTL14/m6A/SETBP1/PI3K-AKT signaling axis in MDS, highlighting the therapeutic potential of targeting METTL3-METTL14 complex-mediated m6A modification for MDS therapy."
item3387	REG00009	M6ATAR00365	.	M6ADIS0091	.	39687949	"WTAP knockdown confers cerebral protection by shifting the microglial phenotype from M1 to M2, primarily by reducing PTGS2 mRNA stability in an m6A-dependent manner."
item3388	REG00007	M6ATAR01375	.	M6ADIS0057	.	37733183	"MiR-181-5p/KLHL5 could promote the proliferation, migration, and invasion of gastric cancer by activating m6A process through regulating METTL3."
item3389	REG00026	.	.	M6ADIS0142	.	39284557	"The silence of ZC3H13 increased the proliferation and ferroptosis-related protein expression, decreased apoptosis and ROS accumulation, as well as maybe by regulating Pnn and Rbm25 expression."
item3390	REG00007	M6ATAR01376	Down	M6ADIS0006	.	39608479	"METTL3 aggravates ICC cell proliferation, invasion, and migration by promoting the degradation of NDFIP1 mRNA in a YTHDF2-dependent manner."
item3391	REG00025	M6ATAR01376	.	M6ADIS0006	.	39608479	"METTL3 aggravates ICC cell proliferation, invasion, and migration by promoting the degradation of NDFIP1 mRNA in a YTHDF2-dependent manner."
item3392	REG00009	M6ATAR01377	.	M6ADIS0110	.	39639339	"IL-1beta-induced WTAP enhances CA12 mRNA stability depending on m6A modification, thus promoting chondrocyte apoptosis, inflammatory response, OxS, and ECM degradation, providing evidence to support the possibility of WTAP and CA12 as potential targets for OA treatment."
item3393	REG00001	M6ATAR00150	.	M6ADIS0361	.	38245815	"FTO protein regulates the MEG3-TGF-beta signalling pathway, thereby suppressing trophoblast invasion and proliferation in URSA trophoblast cells. These findings provide new insights for the treatment of URSA."
item3394	REG00022	M6ATAR00150	.	M6ADIS0361	.	38245815	"FTO protein regulates the MEG3-TGF-beta signalling pathway, thereby suppressing trophoblast invasion and proliferation in URSA trophoblast cells. These findings provide new insights for the treatment of URSA."
item3395	REG00007	M6ATAR01378	.	M6ADIS0068	.	39367907	"Leveraging the 3D structural protein-protein interaction between METTL3 and METTL14, we successfully develop two potential METTL3 peptide inhibitors (RM3 and RSM3) that effectively suppress cancer cell proliferation in vitro and tumor growth in vivo. Collectively, our study reveals a novel METTL3/m6A/RRBP1 axis in enhancing aggressive traits of PCa, which can be therapeutically targeted by small-peptide METTL3 antagonists."
item3396	REG00006	M6ATAR01379	.	M6ADIS0068	.	39322401	"METTL14 was upstream of TRHDE-AS1 to induce m6A modification of TRHDE-AS1 in PC cells. Collectively, our results show that propofol prevents PC progression by upregulating TRHDE-AS1 expression and METTL14 is involved in the m6A modification of TRHDE-AS1. These findings suggest that TRHDE-AS1 may be a potential therapeutic target for the improvement of propofol's therapeutic effect."
item3397	REG00020	M6ATAR01380	Down	M6ADIS0059	.	39403943	RBM15 regulated E2F2 in an m6A modification-dependent manner thereby boosting malignant cellular processes in CRC. The RBM15/E2F2 axis may be a novel target for CRC therapy.
item3398	REG00007	M6ATAR01381	Up	M6ADIS0006	M6ADRUG0032	38486042	m6A modification level of SREBF2-AS1 was also increased in HCC and positively correlated with poor prognosis of HCC patients. METTL3 and METTL14-induced m6A modification upregulated SREBF2-AS1 expression through increasing SREBF2-AS1 transcript stability.
item3399	REG00006	M6ATAR01381	Up	M6ADIS0006	M6ADRUG0032	38486042	m6A modification level of SREBF2-AS1 was also increased in HCC and positively correlated with poor prognosis of HCC patients. METTL3 and METTL14-induced m6A modification upregulated SREBF2-AS1 expression through increasing SREBF2-AS1 transcript stability.
item3400	REG00007	M6ATAR00945	Down	M6ADIS0394	.	39075530	"METTL3 downregulation appears to repress ferroptosis by stabilizing HMOX1 mRNA, thereby potentially elucidating the mechanism through which MB-exos inhibit ferroptosis in ESCs. We identified YTHDF2 as a critical m6A reader protein that contributes to HMOX1 mRNA degradation."
item3401	REG00008	M6ATAR00945	Down	M6ADIS0394	.	39075530	"METTL3 downregulation appears to repress ferroptosis by stabilizing HMOX1 mRNA, thereby potentially elucidating the mechanism through which MB-exos inhibit ferroptosis in ESCs. We identified YTHDF2 as a critical m6A reader protein that contributes to HMOX1 mRNA degradation."
item3402	REG00014	M6ATAR01383	.	M6ADIS0397	.	39088948	Our study revealed that PM exposure increased the expression of histone deacetylase 9 (HDAC9) in human bronchial epithelial cells and mouse airway epithelium through the METTL3/m6A methylation/IGF2BP3 pathway.
item3403	REG00007	M6ATAR01383	.	M6ADIS0397	.	39088948	Our study revealed that PM exposure increased the expression of histone deacetylase 9 (HDAC9) in human bronchial epithelial cells and mouse airway epithelium through the METTL3/m6A methylation/IGF2BP3 pathway.
item3404	REG00014	M6ATAR00388	.	M6ADIS0008	.	38355626	"Mechanistically, IGF2BP3 regulated SCD mRNA m6A modifications via IGF2BP3-METTL14 complex, thereby enhanced CC proliferation, metastasis, and lipid metabolism."
item3405	REG00006	M6ATAR00388	.	M6ADIS0008	.	38355626	"Mechanistically, IGF2BP3 regulated SCD mRNA m6A modifications via IGF2BP3-METTL14 complex, thereby enhanced CC proliferation, metastasis, and lipid metabolism."
item3406	REG00001	M6ATAR00427	.	.	.	38996995	"Mechanistically, FTO could significantly down-regulate the m6A modification level of TfRc and SLC7A11 mRNA through MeRIP experiment. RIP experiments showed that YTHDF1 can bind to TfRc mRNA and promote its translation while YTHDF2 could bind to SLC7A11 mRNA and reduce its mRNA stability. FTO plays a key role in BPF induced male reproductive toxicity through YTHDF1-TfRc axis and YTHDF2-SLC7A11 axis and may provide new ideas and methods for the prevention and treatment of male reproductive diseases associated with environmental pollutants."
item3407	REG00024	M6ATAR00427	.	.	.	38996995	"Mechanistically, FTO could significantly down-regulate the m6A modification level of TfRc and SLC7A11 mRNA through MeRIP experiment. RIP experiments showed that YTHDF1 can bind to TfRc mRNA and promote its translation while YTHDF2 could bind to SLC7A11 mRNA and reduce its mRNA stability. FTO plays a key role in BPF induced male reproductive toxicity through YTHDF1-TfRc axis and YTHDF2-SLC7A11 axis and may provide new ideas and methods for the prevention and treatment of male reproductive diseases associated with environmental pollutants."
item3408	REG00001	M6ATAR00484	.	.	.	38996995	"Mechanistically, FTO could significantly down-regulate the m6A modification level of TfRc and SLC7A11 mRNA through MeRIP experiment. RIP experiments showed that YTHDF1 can bind to TfRc mRNA and promote its translation while YTHDF2 could bind to SLC7A11 mRNA and reduce its mRNA stability. FTO plays a key role in BPF induced male reproductive toxicity through YTHDF1-TfRc axis and YTHDF2-SLC7A11 axis and may provide new ideas and methods for the prevention and treatment of male reproductive diseases associated with environmental pollutants."
item3409	REG00008	M6ATAR00484	.	.	.	38996995	"Mechanistically, FTO could significantly down-regulate the m6A modification level of TfRc and SLC7A11 mRNA through MeRIP experiment. RIP experiments showed that YTHDF1 can bind to TfRc mRNA and promote its translation while YTHDF2 could bind to SLC7A11 mRNA and reduce its mRNA stability. FTO plays a key role in BPF induced male reproductive toxicity through YTHDF1-TfRc axis and YTHDF2-SLC7A11 axis and may provide new ideas and methods for the prevention and treatment of male reproductive diseases associated with environmental pollutants."
item3410	REG00012	M6ATAR01385	.	M6ADIS0066	M6ADRUG0149	39390256	"N-acetyltransferase 10 (NAT10) is notably upregulated in ovarian cancer (OC), correlating with poor patient prognosis. IGF2BP1 enhances the translation of NAT10 mRNA in an m6A-dependent manner in OC cells. NAT10 drives tumorigenesis by mediating N4-acetylcytidine (ac4C) modification of ACOT7 mRNA, thereby augmenting its stability and translation. This NAT10-ACOT7 axis modulates fatty acid metabolism in cancer cells and promotes tumor progression by suppressing ferroptosis. ."
item3411	REG00008	M6ATAR01386	.	M6ADIS0112	.	38388473	"CircFTO facilitates the formation of methyltransferases complex to suppress SRY-related high-mobility group box 9 (SOX9) expression with assistance from YTH domain family 2 (YTHDF2) through an m6A-dependent mechanism. Furthermore, inhibition of circFTO improved symptoms of RA in vivo.Remarkably, the biotinylated antisense of circFTO successfully captured METTL14, while the METTL14 antibody also effectively captured circFTO. circFTO also was found to colocalize with METTL14 protein in chondrocytes. These findings strongly support the interaction between circFTO and the WTAP/METTL3/METTL14 complex.Collectively, our findings suggest a potential role for circFTO in facilitating the formation of WTAP/METTL3/METTL14 complex and enhancing overall m6A modification levels within chondrocytes."
item3412	REG00007	M6ATAR01386	.	M6ADIS0112	.	38388473	"CircFTO facilitates the formation of methyltransferases complex to suppress SRY-related high-mobility group box 9 (SOX9) expression with assistance from YTH domain family 2 (YTHDF2) through an m6A-dependent mechanism. Furthermore, inhibition of circFTO improved symptoms of RA in vivo.Remarkably, the biotinylated antisense of circFTO successfully captured METTL14, while the METTL14 antibody also effectively captured circFTO. circFTO also was found to colocalize with METTL14 protein in chondrocytes. These findings strongly support the interaction between circFTO and the WTAP/METTL3/METTL14 complex.Collectively, our findings suggest a potential role for circFTO in facilitating the formation of WTAP/METTL3/METTL14 complex and enhancing overall m6A modification levels within chondrocytes."
item3413	REG00009	M6ATAR01386	.	M6ADIS0112	.	38388473	"CircFTO facilitates the formation of methyltransferases complex to suppress SRY-related high-mobility group box 9 (SOX9) expression with assistance from YTH domain family 2 (YTHDF2) through an m6A-dependent mechanism. Furthermore, inhibition of circFTO improved symptoms of RA in vivo.Remarkably, the biotinylated antisense of circFTO successfully captured METTL14, while the METTL14 antibody also effectively captured circFTO. circFTO also was found to colocalize with METTL14 protein in chondrocytes. These findings strongly support the interaction between circFTO and the WTAP/METTL3/METTL14 complex.Collectively, our findings suggest a potential role for circFTO in facilitating the formation of WTAP/METTL3/METTL14 complex and enhancing overall m6A modification levels within chondrocytes."
item3414	REG00006	M6ATAR01386	.	M6ADIS0112	.	38388473	"CircFTO facilitates the formation of methyltransferases complex to suppress SRY-related high-mobility group box 9 (SOX9) expression with assistance from YTH domain family 2 (YTHDF2) through an m6A-dependent mechanism. Furthermore, inhibition of circFTO improved symptoms of RA in vivo.Remarkably, the biotinylated antisense of circFTO successfully captured METTL14, while the METTL14 antibody also effectively captured circFTO. circFTO also was found to colocalize with METTL14 protein in chondrocytes. These findings strongly support the interaction between circFTO and the WTAP/METTL3/METTL14 complex.Collectively, our findings suggest a potential role for circFTO in facilitating the formation of WTAP/METTL3/METTL14 complex and enhancing overall m6A modification levels within chondrocytes."
item3415	REG00051	M6ATAR01199	.	M6ADIS0194	.	39387242	"These results indicate that the METTL3-FXR1 axis enhances the expression and stability of MAD2L1 mRNA in an m6A-dependent manner.m6A mRNA Modification is Required for the FXR1-Dependent, KIFC1-Mediated Expression of MAD2L1."
item3416	REG00009	M6ATAR01387	.	M6ADIS0378	.	39173889	"Mechanistically, TRPML1 activation allows more Ca2+ to permeate from the lysosome into the cytoplasm, resulting in the dephosphorylation of TFEB and its nuclear translocation. This process further enhances autophagy initiation and lysosomal biogenesis. Additionally, the expression of TRPML1 is positively regulated by WTAP-mediated m6A modification."
item3417	REG00012	.	.	M6ADIS0370	.	38453794	"In summary, further research into the roles of NUDT21 and IGF2BP1 would be valuable for understanding MDD prognosis. The identified RNA modification-related gene signatures and pathways provide insights into MDD molecular etiology and potential diagnostic biomarkers."
item3418	REG00025	M6ATAR01389	.	M6ADIS0073	.	38744201	"The YTHDF3-regulated P4HA2 acts as an oncogenic factor, regulating glycolysis in PTC through the Hippo signaling pathway. This suggests that P4HA2 holds potential as a promising diagnostic marker and therapeutic target for patients with PTC."
item3419	REG00007	M6ATAR00473	.	M6ADIS0055	M6ADRUG0110	38744201	"METTL3 was upregulated in OSCC cells and was inhibited post-verbascoside treatment. Overexpressing METTL3 promoted the cellular processes. Moreover, miR-31-5p was upregulated in OSCC cells, where METTL3 facilitated the processing of miR-31-5p in an N6-methyladenosine (m6A)-dependent manner. The HIPK2 served as miR-31-5p target, where overexpressing miR-31-5p or HIPK2 knockdown reversed the suppression of verbascoside-induced biological behaviors."
item3420	REG00007	M6ATAR01390	.	M6ADIS0056	M6ADRUG0175	38570607	"ESCC cells readily harness exogenous methionine to generate S-adenosyl-methionine (SAM), thus promoting cell proliferation. Mechanistically, methionine augments METTL3-mediated RNA m6A methylation through SAM and revises gene expression. Integrative omics analysis highlights the potent influence of methionine/SAM on NR4A2 expression in a tumor-specific manner, mediated by the IGF2BP2-dependent stabilization of methylated NR4A2 mRNA. We demonstrate that NR4A2 facilitates ESCC growth and negatively impacts patient survival."
item3421	REG00013	M6ATAR00069	.	M6ADIS0057	.	39080693	"Both in vitro and in vivo experiments revealed that circRHBDD1 upregulated the expression of PD-L1 and impeded the infiltration of CD8 T cells. Further, we found that circRHBDD1 binds to IGF2BP2, disrupting the interaction between E3 ligase TRIM25 and IGF2BP2, and ultimately inhibiting IGF2BP2 ubiquitination and degradation. Intriguingly, IGF2BP2 enhances PD-L1 mRNA stability through m+6A modification, Additionally, we developed Poly (lactide-co-glycolic acid) (PLGA)-Polyethylene glycol (PEG)-based nanoparticles loaded with circRHBDD1 siRNA. In vivo experiments validated that the combination of PLGA-PEG(si-circRHBDD1) and anti-PD-1 offers a safe and efficacious nano-drug regimen for cancer."
item3422	REG00007	M6ATAR01392	.	M6ADIS0001	M6ADRUG0010	39580518	"GNAO1 overexpression downregulated HES1 expression, which reinforced neuronal differentiation. In addition, knockdown of METTL3, a key writer of the N6-methyladenosine (m6A), enhanced GNAO1 mRNA stability."
item3423	REG00025	M6ATAR01393	.	M6ADIS0010	.	38811341	"RNA binding proteins (RBPs) can promote tumor progression and immune evasion. However, research on RBPs, particularly m6A reader YTHDF3, in ccRCC development and immune evasion is limited. In this study, we found that YTHDF3 level was downregulated in ccRCC and was an independent prognostic biomarker for ccRCC. Decreased YTHDF3 expression was correlated with the malignancy, immune evasion, and poor response to anti-programmed death ligand 1 (PD-L1)/CTLA-4 in ccRCC. YTHDF3 overexpression restrained ccRCC cell malignancy, PD-L1 expression, CD8+ T cell infiltration and activities in vivo, indicating its inhibitory role in ccRCC development and immune evasion. Mechanistically, YTHDF3 WT was found to have phase separation characteristics and suppress ccRCC malignancy and immune evasion. Whereas YTHDF3 mutant, which disrupted phase separation, abolished its function. YTHDF3 enhanced the degradation of its target mRNA HSPA13 by phase separation and recruiting DDX6, resulting in the downregulation of the downstream immune checkpoint PD-L1. HSPA13 overexpression restored ccRCC malignancy and immune evasion suppressed by YTHDF3 overexpression. In all, our results identify a new model of YTHDF3 in regulating ccRCC progression and immune evasion through phase separation."
item3424	REG00006	M6ATAR00847	.	M6ADIS0056	.	38291241	"To further verify the influence of NNMT, IGF2BP1 and METTL14 on the RNA stability of E-cadherin, we treated Eca-109 cells with the transcription inhibitor actinomycin D after knockdown of NNMT, IGF2BP1 and METTL14. Indeed, we found that knockdown of NNMT increased the half-life of E-cadherin mRNA, whereas knockdown of IGF2BP1 promoted mRNA degradation of E-cadherin (Fig. 7j). Conversely, the half-life of E-cadherin transcripts was significantly decreased after silencing METTL14 (Fig. 7k). These results indicated that the m6A modification of E-cadherin mRNA could be recognized and bound by IGF2BP1. Moreover, RIP assay further confirmed that the IGF2BP1 protein could directly bind to E-cadherin mRNA. The binding abundance of IGF2BP1 on E-cadherin mRNA increased significantly after silencing NNMT but inhibited by METTL14 knockdown (Fig. 7I). Taken together, these results showed that abnormal histone modification and m6A modification mediated inhibition of E-cadherin expression to promote metastasis of ESCC through NNMT-mediated regulation of EMT (Fig. 7m).Therefore, these data suggest that METTL14 can post-transcriptionally regulate E-cadherin expression in an m6A modification-dependent manner."
item3425	REG00012	M6ATAR00696	.	M6ADIS0056	.	38291241	"To further verify the influence of NNMT, IGF2BP1 and METTL14 on the RNA stability of E-cadherin, we treated Eca-109 cells with the transcription inhibitor actinomycin D after knockdown of NNMT, IGF2BP1 and METTL14. Indeed, we found that knockdown of NNMT increased the half-life of E-cadherin mRNA, whereas knockdown of IGF2BP1 promoted mRNA degradation of E-cadherin (Fig. 7j). Conversely, the half-life of E-cadherin transcripts was significantly decreased after silencing METTL14 (Fig. 7k). These results indicated that the m6A modification of E-cadherin mRNA could be recognized and bound by IGF2BP1. Moreover, RIP assay further confirmed that the IGF2BP1 protein could directly bind to E-cadherin mRNA. The binding abundance of IGF2BP1 on E-cadherin mRNA increased significantly after silencing NNMT but inhibited by METTL14 knockdown (Fig. 7I). Taken together, these results showed that abnormal histone modification and m6A modification mediated inhibition of E-cadherin expression to promote metastasis of ESCC through NNMT-mediated regulation of EMT (Fig. 7m).Therefore, these data suggest that METTL14 can post-transcriptionally regulate E-cadherin expression in an m6A modification-dependent manner."
item3426	REG00006	M6ATAR00696	.	M6ADIS0056	.	38291241	"To further verify the influence of NNMT, IGF2BP1 and METTL14 on the RNA stability of E-cadherin, we treated Eca-109 cells with the transcription inhibitor actinomycin D after knockdown of NNMT, IGF2BP1 and METTL14. Indeed, we found that knockdown of NNMT increased the half-life of E-cadherin mRNA, whereas knockdown of IGF2BP1 promoted mRNA degradation of E-cadherin (Fig. 7j). Conversely, the half-life of E-cadherin transcripts was significantly decreased after silencing METTL14 (Fig. 7k). These results indicated that the m6A modification of E-cadherin mRNA could be recognized and bound by IGF2BP1. Moreover, RIP assay further confirmed that the IGF2BP1 protein could directly bind to E-cadherin mRNA. The binding abundance of IGF2BP1 on E-cadherin mRNA increased significantly after silencing NNMT but inhibited by METTL14 knockdown (Fig. 7I). Taken together, these results showed that abnormal histone modification and m6A modification mediated inhibition of E-cadherin expression to promote metastasis of ESCC through NNMT-mediated regulation of EMT (Fig. 7m).Therefore, these data suggest that METTL14 can post-transcriptionally regulate E-cadherin expression in an m6A modification-dependent manner."
item3427	REG00009	M6ATAR01394	.	M6ADIS0200	.	39289355	"Notably, the mRNA levels of several m6A modification related proteins, such as METTL3, WTAP, METTL14 and ALKBH5, were not affected at 24 h after SARS-CoV-2 infection (Supplementary Fig. 2d-g). Taken together, above data indicated that SARS-CoV-2 infection altered the m6A modifications in cells, which correlated with the decreased of ACTN4 expression.Further experiments demonstrated that depletion of WTAP reduced levels of m6A modifications on ACTN4 mRNAs (Fig. 2b, c), whereas overexpressed WTAP was capable to target ACTN4 mRNA for binding and increased levels of m6A modified ACTN4 transcripts (Fig. 2d-f). In contrast, knockdown of METTL3 or METTL14 only did not exert discernible effects on ACTN4 expression (Supplementary Fig. 3a-h). However, similar with WTAP depletion, knocking down METTL3 and METTL14 in the same cells decreased both m6A modifications and mRNA levels of ACTN4 (Supplementary Fig. 4a-c). Additionally, without affecting levels of ACTN4 mRNA, its expression was enhanced by depletion of ALKBH5, but was decreased by exogenous ALKBH5 (Supplementary Fig. 3i-l). While, FTO was found not to regulate ACTN4 expression (Supplementary Fig. 3m-p). To sum up, these data revealed that the m6A modification levels of ACTN4 mRNA determine its expression by affecting mRNA stability and translation efficiency."
item3428	REG00007	M6ATAR01394	.	M6ADIS0200	.	39289355	"Notably, the mRNA levels of several m6A modification related proteins, such as METTL3, WTAP, METTL14 and ALKBH5, were not affected at 24 h after SARS-CoV-2 infection (Supplementary Fig. 2d-g). Taken together, above data indicated that SARS-CoV-2 infection altered the m6A modifications in cells, which correlated with the decreased of ACTN4 expression.Further experiments demonstrated that depletion of WTAP reduced levels of m6A modifications on ACTN4 mRNAs (Fig. 2b, c), whereas overexpressed WTAP was capable to target ACTN4 mRNA for binding and increased levels of m6A modified ACTN4 transcripts (Fig. 2d-f). In contrast, knockdown of METTL3 or METTL14 only did not exert discernible effects on ACTN4 expression (Supplementary Fig. 3a-h). However, similar with WTAP depletion, knocking down METTL3 and METTL14 in the same cells decreased both m6A modifications and mRNA levels of ACTN4 (Supplementary Fig. 4a-c). Additionally, without affecting levels of ACTN4 mRNA, its expression was enhanced by depletion of ALKBH5, but was decreased by exogenous ALKBH5 (Supplementary Fig. 3i-l). While, FTO was found not to regulate ACTN4 expression (Supplementary Fig. 3m-p). To sum up, these data revealed that the m6A modification levels of ACTN4 mRNA determine its expression by affecting mRNA stability and translation efficiency."
item3429	REG00005	M6ATAR01394	.	M6ADIS0200	.	39289355	"Notably, the mRNA levels of several m6A modification related proteins, such as METTL3, WTAP, METTL14 and ALKBH5, were not affected at 24 h after SARS-CoV-2 infection (Supplementary Fig. 2d-g). Taken together, above data indicated that SARS-CoV-2 infection altered the m6A modifications in cells, which correlated with the decreased of ACTN4 expression.Further experiments demonstrated that depletion of WTAP reduced levels of m6A modifications on ACTN4 mRNAs (Fig. 2b, c), whereas overexpressed WTAP was capable to target ACTN4 mRNA for binding and increased levels of m6A modified ACTN4 transcripts (Fig. 2d-f). In contrast, knockdown of METTL3 or METTL14 only did not exert discernible effects on ACTN4 expression (Supplementary Fig. 3a-h). However, similar with WTAP depletion, knocking down METTL3 and METTL14 in the same cells decreased both m6A modifications and mRNA levels of ACTN4 (Supplementary Fig. 4a-c). Additionally, without affecting levels of ACTN4 mRNA, its expression was enhanced by depletion of ALKBH5, but was decreased by exogenous ALKBH5 (Supplementary Fig. 3i-l). While, FTO was found not to regulate ACTN4 expression (Supplementary Fig. 3m-p). To sum up, these data revealed that the m6A modification levels of ACTN4 mRNA determine its expression by affecting mRNA stability and translation efficiency."
item3430	REG00006	M6ATAR01394	.	M6ADIS0200	.	39289355	"Notably, the mRNA levels of several m6A modification related proteins, such as METTL3, WTAP, METTL14 and ALKBH5, were not affected at 24 h after SARS-CoV-2 infection (Supplementary Fig. 2d-g). Taken together, above data indicated that SARS-CoV-2 infection altered the m6A modifications in cells, which correlated with the decreased of ACTN4 expression.Further experiments demonstrated that depletion of WTAP reduced levels of m6A modifications on ACTN4 mRNAs (Fig. 2b, c), whereas overexpressed WTAP was capable to target ACTN4 mRNA for binding and increased levels of m6A modified ACTN4 transcripts (Fig. 2d-f). In contrast, knockdown of METTL3 or METTL14 only did not exert discernible effects on ACTN4 expression (Supplementary Fig. 3a-h). However, similar with WTAP depletion, knocking down METTL3 and METTL14 in the same cells decreased both m6A modifications and mRNA levels of ACTN4 (Supplementary Fig. 4a-c). Additionally, without affecting levels of ACTN4 mRNA, its expression was enhanced by depletion of ALKBH5, but was decreased by exogenous ALKBH5 (Supplementary Fig. 3i-l). While, FTO was found not to regulate ACTN4 expression (Supplementary Fig. 3m-p). To sum up, these data revealed that the m6A modification levels of ACTN4 mRNA determine its expression by affecting mRNA stability and translation efficiency."
item3431	REG00013	M6ATAR01395	.	M6ADIS0007	.	39022816	"Bioinformatics and RIP and RNA pull-down assessed association of circDHTKD1 with upstream molecule Eukaryotic initiation factor 4A-III (EIF4A3) or downstream molecule phosphofructokinase-1 liver type (PFKL) and insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) in NSCLC cells.CircDHTKD1 exerts a promoting influence on NSCLC glucose metabolism through PFKL upregulation. RIP and RNA pull-down showed that circDHTKD1 could bind to IGF2BP, PFKL could bind to IGF2BP2, and circDHTKD1 promoted the binding of PFKL to IGF2BP2. In addition, RT-qPCR showed that IGF2BP2 knockdown promoted PFKL mRNA degradation, suggesting that IGF2BP2 stabilized PFKL in NSCLC cells. We innovatively validate that EIF4A3-triggered circDHTKD1 upregulation facilitates NSCLC glycolysis through recruiting m6A reader IGF2BP2 to stabilize PFKL, which may provide a new direction for seeking targeted therapy plans of NSCLC."
item3432	REG00007	M6ATAR01396	.	M6ADIS0141	.	38232538	"Furthermore, ApoC3 activated the expression of SYK, which in turn induced NLRP3 inflammasome-regulated pyroptosis in the ALI model. METTL3 was found to mediate the m6A mRNA expression of ApoC3."
item3433	REG00014	.	.	M6ADIS0065	.	37861451	"IGF2BP3 may serve as a novel predictive biomarker and a potential therapeutic target for breast cancer brain metastasis, which warrants further investigation."
item3434	REG00007	M6ATAR01397	.	M6ADIS0185	M6ADRUG0044	39702325	"Abnormal methyltransferase like protein 3 (METTL3) expression in CIRI enhanced m6A modification and promoted Nek6 expression level. This study confirmed that Nek6 regulates autophagy and alleviates CIRI through the mTOR signaling pathway, ."
item3435	.	M6ATAR01398	.	M6ADIS0059	.	39341990	CircAURKA stability was regulated by m6A methylation modification.
item3436	REG00013	M6ATAR01399	.	.	.	38787118	"To explore substrates targeted by RNA m6A methylation regulators, the writers RBM15, RBM15B, WTAP, and readers IGF2BP2, FMR1, HNRNPA2B1, and YTHDF2 were selected, along with genes related to the Wnt signaling pathway, regulation of the cell cycle, cellular response to DNA damage, and tight junction. The results indicated that IGF2BP2 and FMR1 were extensively involved in regulating the majority of genes within these four terms ."
item3437	REG00029	M6ATAR01500	.	.	.	38787118	"To explore substrates targeted by RNA m6A methylation regulators, the writers RBM15, RBM15B, WTAP, and readers IGF2BP2, FMR1, HNRNPA2B1, and YTHDF2 were selected, along with genes related to the Wnt signaling pathway, regulation of the cell cycle, cellular response to DNA damage, and tight junction. The results indicated that IGF2BP2 and FMR1 were extensively involved in regulating the majority of genes within these four terms ."
item3438	REG00012	M6ATAR01400	.	M6ADIS0006	.	39617786	"Mechanistically, reduced VIM-AS1 expression stabilized EPHA3 mRNA by enhancing the binding of IGF2BP1 to EPHA3 mRNA, leading to increased expression of EPHA3 mRNA and the promotion of HCC progression.These findings suggest that the downregulation of VIM-AS1 due to hypermethylation at cg02746869 increased EPHA3 mRNA expression via a m6A-dependent mechanism to increase HCC aggressiveness."
item3439	REG00007	M6ATAR01401	.	.	.	39559922	"Nanopore RNA sequencing, RIP assay, IP-MS, MeRIP-qPCR, PAR-CLIP and luciferase reporter experiments showed that Hnrnpa1 induced Mettl3 post-transcriptional splicing to inhibit m6A-dependent Pbx1 and E2F1 degradation, thereby increasing Runx1, Ccne1, Cdk2 and Ccnb2 expression to promote CM DACCA."
item3440	REG00007	M6ATAR00234	.	.	.	39559922	"Nanopore RNA sequencing, RIP assay, IP-MS, MeRIP-qPCR, PAR-CLIP and luciferase reporter experiments showed that Hnrnpa1 induced Mettl3 post-transcriptional splicing to inhibit m6A-dependent Pbx1 and E2F1 degradation, thereby increasing Runx1, Ccne1, Cdk2 and Ccnb2 expression to promote CM DACCA."
item3441	REG00001	M6ATAR00353	.	M6ADIS0112	.	38243394	"FTO overexpression inhibited RA by inhibiting the expression of NSUN2, up-regulating the level of SFRP1 protein, and blocking the Wnt/bate-catenin signaling pathway. NSUN2 overexpression interfered with the inhibitory effects of FTO on the Wnt/beta-catenin signaling pathway and RA pathology, which further verified that FTO inhibited RA through the NSUN2/SFRP1/Wnt/beta-catenin signal axis."
item3442	REG00007	M6ATAR00411	.	M6ADIS0038	.	39680752	"Moreover, cisplatin-induced methyltransferase-like 3 (METTL3)-mediated m6A modification enhances SREBP1c mRNA stability, thereby upregulating its expression. Notably, both depletion of SREBP1c and renal tubule-specific overexpression of YME1L1 markedly ameliorate cisplatin-induced AKI and its transition to CKD. Taken together, these findings suggest that METTL3-mediated SREBP1c upregulation contributes to AKI and its progression to CKD through disrupting mitochondrial energy metabolism via transcriptionally suppressing YME1L1."
item3443	REG00007	M6ATAR01402	.	M6ADIS0038	.	39680752	"Moreover, cisplatin-induced methyltransferase-like 3 (METTL3)-mediated m6A modification enhances SREBP1c mRNA stability, thereby upregulating its expression. Notably, both depletion of SREBP1c and renal tubule-specific overexpression of YME1L1 markedly ameliorate cisplatin-induced AKI and its transition to CKD. Taken together, these findings suggest that METTL3-mediated SREBP1c upregulation contributes to AKI and its progression to CKD through disrupting mitochondrial energy metabolism via transcriptionally suppressing YME1L1."
item3444	REG00008	M6ATAR01403	.	M6ADIS0376	.	38516932	"Mechanically, FMDV VP1 promotes autophagy during virus infection and interacts with and degrades YTHDF2 (YTH N6-methyladenosine RNA binding protein F2) in an AKT-MTOR-dependent autophagy pathway, resulting in an increase in GTPBP4 mRNA and protein levels. Increased GTPBP4 inhibits IRF3 binding to the Ifnb/Ifn-beta promoter, suppressing FMDV-induced type I interferon production."
item3445	REG00008	M6ATAR00296	.	M6ADIS0376	.	38516932	"Mechanically, FMDV VP1 promotes autophagy during virus infection and interacts with and degrades YTHDF2 (YTH N6-methyladenosine RNA binding protein F2) in an AKT-MTOR-dependent autophagy pathway, resulting in an increase in GTPBP4 mRNA and protein levels. Increased GTPBP4 inhibits IRF3 binding to the Ifnb/Ifn-beta promoter, suppressing FMDV-induced type I interferon production."
item3446	REG00005	M6ATAR01404	.	M6ADIS0183	.	39060657	"ALKBH5 inhibited SMARCA5 expression via m6A modification, while RNF180 reduced ALKBH5 expression via ubiquitination. Our findings indicate that RNF180 aggravated the colon inflammation and Th17/Treg cell imbalance in UC mice by regulating the ALKBH5/SMARCA5 axis."
item3447	REG00006	M6ATAR00152	.	M6ADIS0177	.	38426786	"Because methylation regulates XIST expression, the differences in m6A-related genes expressed between the high and low XIST expression groups were analyzed (Supplementary Table S4 and Figure S1). The expression of METTL14 in the low XIST expression group was notably increased compared with that in the high XIST expression group (P = 0.03276), which indicated that METTL14 participated in XIST m6A-methylation."
item3448	REG00007	M6ATAR01405	.	M6ADIS0055	.	38355684	"Mechanistically, we illustrated that SALL4 is a direct downstream transcriptional regulation target of METTL3, the transcription activation of SALL4 promotes the nuclear transport of bate-catenin and the expression of downstream target genes after radiation therapy, there by activates the Wnt/beta-catenin pathway, effectively enhancing the CSCs phenotype and causing radioresistance. Herein, this study indicates that the METTL3/SALL4 axis promotes the CSCs phenotype and resistance to radiation in OSCC via the Wnt/beta-catenin signaling pathway, and provides a potential therapeutic target to eliminate radioresistant OSCC."
item3449	REG00024	M6ATAR00414	.	M6ADIS0057	.	39024555	"Acetylated SRSF2 directly bound to the pre-mRNA of the m6A reader YTHDF1, resulting in enhanced YTHDF1 exon 4 skipping and upregulation of a short YTHDF1 transcript that could stimulate gastric cancer cell proliferation and migration. Furthermore, YTHDF1 exon 4 skipping correlated with NAT10 and SRSF2 expression and was associated with a more aggressive phenotype in samples of patients with gastric cancer. Together, this study uncovers the role of NAT10 liquid-liquid phase separation in modulating YTHDF1 splicing through SRSF2 acetylation to drive gastric cancer progression, providing insights into the oncogenic mechanism of NAT10."
item3450	REG00013	M6ATAR01407	.	M6ADIS0065	.	39496940	"Mechanistically, RPPH1 protects IGF2BP2 from ubiquitination-induced degradation, stabilizes N6-methyladenosine (m6A)-modified FGFR2 mRNA, and activates the PI3K/AKT pathway."
item3451	REG00007	M6ATAR01408	.	M6ADIS0107	.	39146936	"Mechanistically, RPN11 deubiquitinates and stabilizes METTL3 to enhance the m6A modification and expression of acyl-coenzyme A (CoA) synthetase short-chain family member 3 (ACSS3), which generates propionyl-CoA to upregulate lipid metabolism genes via histone propionylation. The RPN11-METTL3-ACSS3-histone propionylation pathway is activated in the livers of patients with NAFLD."
item3452	REG00007	M6ATAR01409	.	M6ADIS0001	M6ADRUG0111	38332508	"MRNA levels of AhR and SRF were stabilized by decreased METTL3 and YTHDF2. YKL-40 and Kyn secreted from tumor cells and infiltrating M2 macrophages cooperated to enhance tumor cell migration and inhibit CTL immunity. In xenografts, tumors expressing YKL-40 displayed the elevated KP metabolism and macrophage infiltration, but decreased CTLs."
item3453	REG00008	M6ATAR01409	.	M6ADIS0001	M6ADRUG0111	38332508	"MRNA levels of AhR and SRF were stabilized by decreased METTL3 and YTHDF2. YKL-40 and Kyn secreted from tumor cells and infiltrating M2 macrophages cooperated to enhance tumor cell migration and inhibit CTL immunity. In xenografts, tumors expressing YKL-40 displayed the elevated KP metabolism and macrophage infiltration, but decreased CTLs."
item3454	REG00007	M6ATAR00461	.	M6ADIS0001	M6ADRUG0111	38332508	"MRNA levels of AhR and SRF were stabilized by decreased METTL3 and YTHDF2. YKL-40 and Kyn secreted from tumor cells and infiltrating M2 macrophages cooperated to enhance tumor cell migration and inhibit CTL immunity. In xenografts, tumors expressing YKL-40 displayed the elevated KP metabolism and macrophage infiltration, but decreased CTLs."
item3455	REG00008	M6ATAR00461	.	M6ADIS0001	M6ADRUG0111	38332508	"MRNA levels of AhR and SRF were stabilized by decreased METTL3 and YTHDF2. YKL-40 and Kyn secreted from tumor cells and infiltrating M2 macrophages cooperated to enhance tumor cell migration and inhibit CTL immunity. In xenografts, tumors expressing YKL-40 displayed the elevated KP metabolism and macrophage infiltration, but decreased CTLs."
item3456	REG00008	M6ATAR00419	.	M6ADIS0376	.	39641410	"Mechanistically, 2B inhibited the mRNA of STING by recruiting YTH m6A RNA-binding protein 2 (YTHDF2) to bind to STING mRNA, repressing the generation of FMDV-induced type-I interferon and facilitating virus replication."
item3457	REG00012	M6ATAR00360	.	M6ADIS0057	.	38929036	TRIM29 interacted with IGF2BP1 and induced its ubiquitination at Lys440 and Lys450 site by K48-mediated linkage for protein degradation. IGF2BP1 promoted PD-L1 mRNA stability and expression in a 3'UTR and m6A-dependent manner.
item3458	REG00001	M6ATAR01488	.	M6ADIS0375	.	38834654	"Mechanistically, acyl-CoA synthetase long chain family 4 (ACSL4) and transferrin receptor protein 1 (TFRC), two key positive contributors to ferroptosis, are FTO targets. For ameliorative effect, FTO requires the inhibition of Acsl4 and Tfrc mRNA stability in a m6A-dependent manner. Furthermore, we demonstrate nicotinamide mononucleotide can upregulate FTO demethylase activity, suppressing ferroptosis and decreasing older HIRI."
item3459	REG00001	M6ATAR00427	.	M6ADIS0375	.	38834654	"Mechanistically, acyl-CoA synthetase long chain family 4 (ACSL4) and transferrin receptor protein 1 (TFRC), two key positive contributors to ferroptosis, are FTO targets. For ameliorative effect, FTO requires the inhibition of Acsl4 and Tfrc mRNA stability in a m6A-dependent manner. Furthermore, we demonstrate nicotinamide mononucleotide can upregulate FTO demethylase activity, suppressing ferroptosis and decreasing older HIRI."
item3460	REG00001	M6ATAR00023	.	M6ADIS0251	.	38041494	"It is demonstrated that substrate stiffening can activate mTORC1 and elevate mTOR level through integrins and GSK3beta-FTO mediated mRNA m6 A modification, promoting anabolic metabolism. Inhibition of this axis upon ECM detachment enhances autophagy, which in turn conveys resilience of tumor cells to anoikis, as it is demonstrated in human breast ductal carcinoma in situ (DCIS) and mice malignant ascites."
item3461	REG00008	M6ATAR00503	.	M6ADIS0119	.	38161229	"LXRalpha mature mRNA could undergo m6A-mediated mRNA decay via the interaction with m6A ""reader"" YTH N6-methyladenosine RNA binding protein F2 (YTHDF2). We then examined if Dock5 regulates LXRalpha in podocytes through the YTHDF2-mediated m6A pathway. RNA immunoprecipitation analysis showed that the YTHDF2 protein could bind to LXRalpha mRNAs (Figure S8A, Supporting Information). YTHDF2 knockdown increased LXRalpha protein and mRNA levels without affecting its pre-mRNA (Figure 6C), and inhibited the decay rate of LXRalpha mRNAs, which was detected when treating podocytes with transcription inhibitor actinomycin D ."
item3462	REG00003	M6ATAR01412	.	M6ADIS0007	.	39102940	"We then aimed to investigate whether TBUR1 can promote hnRNPC binding to GRB2 mRNA. To test it, we conducted a RIP assay using an anti-hnRNPC antibody in TBUR1-depleted A549 cells. As expected, the knockdown of TBUR1 resulted in reduced binding of hnRNPC to GRB2 mRNA (Fig. 6L). Taken together, these results provide evidence that TBUR1 regulates the abundance of GRB2 mRNA by facilitating the binding of hnRNPC to GRB2 mRNA in a m6A-dependent manner."
item3463	REG00007	M6ATAR01413	.	M6ADIS0007	.	38372068	"Moreover, the decrease in METTL3-mediated N6-methyladenosine modification of TRIB3 results in a substantial elevation of its expression levels in LUAD cells. Collectively, our research unveils a novel discovery that TRIB3 enhances the growth and invasion of LUAD cells by interacting with LATS1 and inhibiting the Hippo signaling pathway."
item3464	REG00007	M6ATAR00402	Up	.	M6ADRUG0108	38142659	"During arsenic-induced cell transformation, METTL3-upregulated m6A on the mRNAs of SOD1, SOD2, CAT, TXN, and GPX1 promoted the mRNA translation and protein expressions of these antioxidant enzymes by increasing YTHDF1-mediated mRNA stability. Meanwhile, FTO-downregulated m6A on PRDX5 mRNA increased PRDX5 translation and expression by reducing YTHDF2-mediated mRNA decay."
item3466	REG00024	M6ATAR00402	Up	.	.	38142659	"During arsenic-induced cell transformation, METTL3-upregulated m6A on the mRNAs of SOD1, SOD2, CAT, TXN, and GPX1 promoted the mRNA translation and protein expressions of these antioxidant enzymes by increasing YTHDF1-mediated mRNA stability. Meanwhile, FTO-downregulated m6A on PRDX5 mRNA increased PRDX5 translation and expression by reducing YTHDF6-mediated mRNA decay."
item3466	REG00024	M6ATAR01834	Down	.	.	37060562	YTHDF1 LLPS activates IkappaB-NF-kappaB-CCND1 axis by inhibiting IkappaBalpha/beta mRNA translation.
item3467	REG00007	M6ATAR00763	.	.	.	29304330	"Both the presence and extent of A-to-I sites in m6A-negative RNA transcripts suggest a negative correlation between m6A and A-to-I. Suppression of m6A-catalyzing enzymes results in global A-to-I RNA editing changes. Further depletion of m6A modification increases the association of m6A-depleted transcripts with adenosine deaminase acting on RNA (ADAR) enzymes, resulting in upregulated A-to-I editing on the same m6A-depleted transcripts."
item3468	REG00007	M6ATAR01518	.	.	.	29304330	"Both the presence and extent of A-to-I sites in m6A-negative RNA transcripts suggest a negative correlation between m6A and A-to-I. Suppression of m6A-catalyzing enzymes results in global A-to-I RNA editing changes. Further depletion of m6A modification increases the association of m6A-depleted transcripts with adenosine deaminase acting on RNA (ADAR) enzymes, resulting in upregulated A-to-I editing on the same m6A-depleted transcripts."
item3469	REG00007	M6ATAR01519	.	.	.	29304330	"Both the presence and extent of A-to-I sites in m6A-negative RNA transcripts suggest a negative correlation between m6A and A-to-I. Suppression of m6A-catalyzing enzymes results in global A-to-I RNA editing changes. Further depletion of m6A modification increases the association of m6A-depleted transcripts with adenosine deaminase acting on RNA (ADAR) enzymes, resulting in upregulated A-to-I editing on the same m6A-depleted transcripts."
item3470	REG00007	M6ATAR01520	.	.	.	29304330	"Both the presence and extent of A-to-I sites in m6A-negative RNA transcripts suggest a negative correlation between m6A and A-to-I. Suppression of m6A-catalyzing enzymes results in global A-to-I RNA editing changes. Further depletion of m6A modification increases the association of m6A-depleted transcripts with adenosine deaminase acting on RNA (ADAR) enzymes, resulting in upregulated A-to-I editing on the same m6A-depleted transcripts."
item3471	REG00007	M6ATAR01521	.	.	.	29304330	"Both the presence and extent of A-to-I sites in m6A-negative RNA transcripts suggest a negative correlation between m6A and A-to-I. Suppression of m6A-catalyzing enzymes results in global A-to-I RNA editing changes. Further depletion of m6A modification increases the association of m6A-depleted transcripts with adenosine deaminase acting on RNA (ADAR) enzymes, resulting in upregulated A-to-I editing on the same m6A-depleted transcripts."
item3472	REG00007	M6ATAR01522	.	.	.	29304330	"Both the presence and extent of A-to-I sites in m6A-negative RNA transcripts suggest a negative correlation between m6A and A-to-I. Suppression of m6A-catalyzing enzymes results in global A-to-I RNA editing changes. Further depletion of m6A modification increases the association of m6A-depleted transcripts with adenosine deaminase acting on RNA (ADAR) enzymes, resulting in upregulated A-to-I editing on the same m6A-depleted transcripts."
item3473	REG00007	M6ATAR01523	.	.	.	29304330	"Both the presence and extent of A-to-I sites in m6A-negative RNA transcripts suggest a negative correlation between m6A and A-to-I. Suppression of m6A-catalyzing enzymes results in global A-to-I RNA editing changes. Further depletion of m6A modification increases the association of m6A-depleted transcripts with adenosine deaminase acting on RNA (ADAR) enzymes, resulting in upregulated A-to-I editing on the same m6A-depleted transcripts."
item3474	REG00007	M6ATAR01524	.	.	.	29304330	"Both the presence and extent of A-to-I sites in m6A-negative RNA transcripts suggest a negative correlation between m6A and A-to-I. Suppression of m6A-catalyzing enzymes results in global A-to-I RNA editing changes. Further depletion of m6A modification increases the association of m6A-depleted transcripts with adenosine deaminase acting on RNA (ADAR) enzymes, resulting in upregulated A-to-I editing on the same m6A-depleted transcripts."
item3475	REG00007	M6ATAR01525	Up	M6ADIS0035	.	37694982	m6A methyltransferase METTL3-mediated METTL1 promotes cell proliferation of head and neck squamous cell carcinoma (HNSC) through m7G modification of the cell-cycle regulator CDK4.
item3476	REG00008	M6ATAR00705	Up	.	.	36070699	A subset of endogenous circular RNAs that harbor m6A and associate with YTHDF2 in an HRSP12-dependent manner is also subjected to m1A-facilitated rapid degradation.
item3477	REG00008	M6ATAR00705	Up	.	.	36070699	A subset of endogenous circular RNAs that harbor m6A and associate with YTHDF2 in an HRSP12-dependent manner is also subjected to m1A-facilitated rapid degradation.
item3478	REG00008	M6ATAR00814	Up	.	.	36070699	A subset of endogenous circular RNAs that harbor m6A and associate with YTHDF2 in an HRSP12-dependent manner is also subjected to m1A-facilitated rapid degradation.
item3479	REG00008	M6ATAR00814	Up	.	.	36070699	A subset of endogenous circular RNAs that harbor m6A and associate with YTHDF2 in an HRSP12-dependent manner is also subjected to m1A-facilitated rapid degradation.
item3480	REG00001	M6ATAR00341	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3481	REG00008	M6ATAR00341	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3482	REG00001	M6ATAR00341	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3483	REG00008	M6ATAR00341	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3484	REG00001	M6ATAR00341	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3485	REG00008	M6ATAR00341	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3486	REG00001	M6ATAR00257	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3487	REG00008	M6ATAR00257	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3488	REG00001	M6ATAR00257	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3489	REG00008	M6ATAR00257	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3490	REG00001	M6ATAR00257	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3491	REG00008	M6ATAR00257	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3492	REG00001	M6ATAR01527	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3493	REG00008	M6ATAR01527	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3494	REG00001	M6ATAR01527	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3495	REG00008	M6ATAR01527	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3496	REG00001	M6ATAR01527	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3497	REG00008	M6ATAR01527	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3498	REG00001	M6ATAR00341	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3499	REG00001	M6ATAR00257	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3500	REG00001	M6ATAR01527	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3501	REG00001	M6ATAR01528	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3502	REG00001	M6ATAR01529	Down	.	.	32213595	"TRMT10A ablation not only leads to decreased m1G in tRNA but also significantly increases m6A levels in mRNA. Cross-linking and immunoprecipitation, followed by high-throughput sequencing results show that TRMT10A shares a significant overlap of associated mRNAs with FTO, and these mRNAs have accelerated decay rates potentially through the regulation by a specific m6A reader, YTHDF2."
item3503	REG00007	M6ATAR01418	Up	M6ADIS0132	.	40019372	"ALKBH3 recognizes the m1A methylation sites and prevents YTHDF2-dependent mRNA decay of METTL3 transcript. Subsequently, METTL3 stabilizes collagen type I alpha 1 chain (COL1A1) and fibronectin1 (FN1) mRNAs, two major components of extracellular matrix, and therefore eliciting the pathological transformation of HTS. This observation bridges the understanding of the link between m1A and m6A methylation, the two fundamental RNA modifications, underscoring the participation of ""RNA methylation crosstalk"" in pathological events."
item3504	REG00007	M6ATAR01530	Up	M6ADIS0132	.	40019372	"ALKBH3 recognizes the m1A methylation sites and prevents YTHDF2-dependent mRNA decay of METTL3 transcript. Subsequently, METTL3 stabilizes collagen type I alpha 1 chain (COL1A1) and fibronectin1 (FN1) mRNAs, two major components of extracellular matrix, and therefore eliciting the pathological transformation of HTS. This observation bridges the understanding of the link between m1A and m6A methylation, the two fundamental RNA modifications, underscoring the participation of ""RNA methylation crosstalk"" in pathological events."
item3505	REG00007	M6ATAR01418	Up	M6ADIS0132	.	40019372	"ALKBH3 recognizes the m1A methylation sites and prevents YTHDF2-dependent mRNA decay of METTL3 transcript. Subsequently, METTL3 stabilizes collagen type I alpha 1 chain (COL1A1) and fibronectin1 (FN1) mRNAs, two major components of extracellular matrix, and therefore eliciting the pathological transformation of HTS. This observation bridges the understanding of the link between m1A and m6A methylation, the two fundamental RNA modifications, underscoring the participation of ""RNA methylation crosstalk"" in pathological events."
item3506	REG00007	M6ATAR01530	Up	M6ADIS0132	.	40019372	"ALKBH3 recognizes the m1A methylation sites and prevents YTHDF2-dependent mRNA decay of METTL3 transcript. Subsequently, METTL3 stabilizes collagen type I alpha 1 chain (COL1A1) and fibronectin1 (FN1) mRNAs, two major components of extracellular matrix, and therefore eliciting the pathological transformation of HTS. This observation bridges the understanding of the link between m1A and m6A methylation, the two fundamental RNA modifications, underscoring the participation of ""RNA methylation crosstalk"" in pathological events."
item3507	REG00024	M6ATAR01418	Up	M6ADIS0132	.	40019372	"ALKBH3 recognizes the m1A methylation sites and prevents YTHDF2-dependent mRNA decay of METTL3 transcript. Subsequently, METTL3 stabilizes collagen type I alpha 1 chain (COL1A1) and fibronectin1 (FN1) mRNAs, two major components of extracellular matrix, and therefore eliciting the pathological transformation of HTS. This observation bridges the understanding of the link between m1A and m6A methylation, the two fundamental RNA modifications, underscoring the participation of ""RNA methylation crosstalk"" in pathological events."
item3508	REG00024	M6ATAR01530	Up	M6ADIS0132	.	40019372	"ALKBH3 recognizes the m1A methylation sites and prevents YTHDF2-dependent mRNA decay of METTL3 transcript. Subsequently, METTL3 stabilizes collagen type I alpha 1 chain (COL1A1) and fibronectin1 (FN1) mRNAs, two major components of extracellular matrix, and therefore eliciting the pathological transformation of HTS. This observation bridges the understanding of the link between m1A and m6A methylation, the two fundamental RNA modifications, underscoring the participation of ""RNA methylation crosstalk"" in pathological events."
item3509	REG00024	M6ATAR01418	Up	M6ADIS0132	.	40019372	"ALKBH3 recognizes the m1A methylation sites and prevents YTHDF2-dependent mRNA decay of METTL3 transcript. Subsequently, METTL3 stabilizes collagen type I alpha 1 chain (COL1A1) and fibronectin1 (FN1) mRNAs, two major components of extracellular matrix, and therefore eliciting the pathological transformation of HTS. This observation bridges the understanding of the link between m1A and m6A methylation, the two fundamental RNA modifications, underscoring the participation of ""RNA methylation crosstalk"" in pathological events."
item3510	REG00024	M6ATAR01530	Up	M6ADIS0132	.	40019372	"ALKBH3 recognizes the m1A methylation sites and prevents YTHDF2-dependent mRNA decay of METTL3 transcript. Subsequently, METTL3 stabilizes collagen type I alpha 1 chain (COL1A1) and fibronectin1 (FN1) mRNAs, two major components of extracellular matrix, and therefore eliciting the pathological transformation of HTS. This observation bridges the understanding of the link between m1A and m6A methylation, the two fundamental RNA modifications, underscoring the participation of ""RNA methylation crosstalk"" in pathological events."
item3511	REG00013	M6ATAR01531	Up	M6ADIS0066	.	40044032	"SNORD9 induces NFYA m6A methylation by binding to m6A methylase METTL3; modifying IGF2BP2 mRNA by 2'-O-methylation and improve NFYA mRNA stability, thus promote the tumorigenesis of ovarian cancer. Targeting ASO to SNORD9 may have efficacy in the treatment of ovarian cancer."
item3512	REG00012	M6ATAR01532	Up	M6ADIS0006	.	37891494	"IGF2BP1 upregulated MIR4435-2HG expression in HCC through N6-methyladenosine (m6A) modification. Moreover, MIR4435-2HG protected NOP58 from degradation, which raised rRNA 2'-O-Me levels and promoted internal ribosome entry site (IRES)-dependent translation of oncogenes."
item3513	REG00024	M6ATAR00536	Up	.	.	34324489	"The A-to-I RNA editing activity of ADAR1 plays important roles in the YTHDF1-dependent IFN responses. Therefore, we uncover that m6A and YTHDF1 affect innate immune responses through modulating the ADAR1-mediated A-to-I RNA editing."
item3514	REG00024	M6ATAR00536	Up	.	.	34324489	"The A-to-I RNA editing activity of ADAR1 plays important roles in the YTHDF1-dependent IFN responses. Therefore, we uncover that m6A and YTHDF1 affect innate immune responses through modulating the ADAR1-mediated A-to-I RNA editing."
item3515	REG00024	M6ATAR00536	Up	.	.	34324489	"The A-to-I RNA editing activity of ADAR1 plays important roles in the YTHDF1-dependent IFN responses. Therefore, we uncover that m6A and YTHDF1 affect innate immune responses through modulating the ADAR1-mediated A-to-I RNA editing."
item3516	REG00007	M6ATAR00795	.	M6ADIS0065	.	36077054	"Overexpression and knockdown of ADAR1 respectively increased and decreased the expression levels of METTL3 and ARHGAP5 protein in breast cancer. We demonstrate that ADAR1 promotes the proliferation, migration and invasion of breast cancer cells through the METTL3/ARHGAP5/YTHDF1 axis and establish that METTL3 is one of the main targets of ADAR1 controlling biological functions."
item3517	REG00024	M6ATAR00795	.	M6ADIS0065	.	36077054	"Overexpression and knockdown of ADAR1 respectively increased and decreased the expression levels of METTL3 and ARHGAP5 protein in breast cancer. We demonstrate that ADAR1 promotes the proliferation, migration and invasion of breast cancer cells through the METTL3/ARHGAP5/YTHDF1 axis and establish that METTL3 is one of the main targets of ADAR1 controlling biological functions."
item3518	REG00007	M6ATAR01386	.	.	.	35614315	"BMSCs overexpressing Mettl3 and Nsun4 can promote the repair of cartilage defects in vivo. Taken together, our study demonstrates that m5C and m6A co-regulate the translation of Sox9 during the chondrogenic differentiation of BMSCs, which provides a therapeutic target for clinical implications."
item3519	REG00008	M6ATAR01386	.	.	.	35614315	"BMSCs overexpressing Mettl3 and Nsun4 can promote the repair of cartilage defects in vivo. Taken together, our study demonstrates that m5C and m6A co-regulate the translation of Sox9 during the chondrogenic differentiation of BMSCs, which provides a therapeutic target for clinical implications."
item3520	REG00014	M6ATAR01533	Up	M6ADIS0057	.	37582794	"RNA cytosine-C(5)-methyltransferase (NSUN2) was upregulated in GC and high NSUN2 expression was associated with poor prognosis. NR_033928 was identified as an NSUN2-methylated and upregulated lncRNA in GC. Functionally, NR_033928 upregulated the expression of glutaminase (GLS) by interacting with IGF2BP3/HUR complex to promote GLS mRNA stability."
item3521	REG00002	M6ATAR00271	Up	M6ADIS0070	.	31358969	"YBX1 maintains the stability of its target mRNA by recruiting ELAVL1. Moreover, NSUN2 and YBX1 are demonstrated to drive UCB pathogenesis by targeting the m5C methylation site in the HDGF 3' untranslated region."
item3522	REG00002	M6ATAR00271	Up	M6ADIS0070	.	31358969	"YBX1 maintains the stability of its target mRNA by recruiting ELAVL1. Moreover, NSUN2 and YBX1 are demonstrated to drive UCB pathogenesis by targeting the m5C methylation site in the HDGF 3' untranslated region."
item3523	REG00024	M6ATAR01418	Up	M6ADIS0017	.	36841889	"In this study, we demonstrate that 5mC-mediated SOCS3 suppression leads to STAT3 activation. STAT3 transactivates HIF-1alpha and HIF-1alpha subsequentially transactivates YTHDF1, thus linking 5mC- mediated initiation stage and m6A-dependent perpetuation stage of HSC activation cascade."
item3524	REG00024	M6ATAR01559	Up	M6ADIS0017	.	36841889	"In this study, we demonstrate that 5mC-mediated SOCS3 suppression leads to STAT3 activation. STAT3 transactivates HIF-1alpha and HIF-1alpha subsequentially transactivates YTHDF1, thus linking 5mC- mediated initiation stage and m6A-dependent perpetuation stage of HSC activation cascade."
item3525	REG00024	M6ATAR00597	Up	M6ADIS0017	.	36841889	"In this study, we demonstrate that 5mC-mediated SOCS3 suppression leads to STAT3 activation. STAT3 transactivates HIF-1alpha and HIF-1alpha subsequentially transactivates YTHDF1, thus linking 5mC- mediated initiation stage and m6A-dependent perpetuation stage of HSC activation cascade."
item3526	REG00024	M6ATAR01560	Up	M6ADIS0017	.	36841889	"In this study, we demonstrate that 5mC-mediated SOCS3 suppression leads to STAT3 activation. STAT3 transactivates HIF-1alpha and HIF-1alpha subsequentially transactivates YTHDF1, thus linking 5mC- mediated initiation stage and m6A-dependent perpetuation stage of HSC activation cascade."
item3527	REG00024	M6ATAR01561	Up	M6ADIS0017	.	36841889	"In this study, we demonstrate that 5mC-mediated SOCS3 suppression leads to STAT3 activation. STAT3 transactivates HIF-1alpha and HIF-1alpha subsequentially transactivates YTHDF1, thus linking 5mC- mediated initiation stage and m6A-dependent perpetuation stage of HSC activation cascade."
item3528	REG00023	M6ATAR01562	.	.	.	37474847	"RNA N6-methyladenosine (m6A) reader, YTHDC2, occupies genomic loci of the primate-specific TE, LTR7/HERV-H, specifically through its interaction with m6A-modified HERV-H RNAs. Unexpectedly, YTHDC2 recruits the DNA 5-methylcytosine (5mC)-demethylase, TET1, to remove 5mC from LTR7/HERV-H and prevent epigenetic silencing. Functionally, the YTHDC2/LTR7 axis inhibits neural differentiation of hESCs."
item3529	REG00007	M6ATAR01562	.	.	.	37474847	"RNA N6-methyladenosine (m6A) reader, YTHDC2, occupies genomic loci of the primate-specific TE, LTR7/HERV-H, specifically through its interaction with m6A-modified HERV-H RNAs. Unexpectedly, YTHDC2 recruits the DNA 5-methylcytosine (5mC)-demethylase, TET1, to remove 5mC from LTR7/HERV-H and prevent epigenetic silencing. Functionally, the YTHDC2/LTR7 axis inhibits neural differentiation of hESCs."
item3530	REG00007	.	.	M6ADIS0056	.	36071173	"Here, we show that METTL3-mediated RNA N6-methyladenosine (m6A) formation leads to DNA demethylation in nearby genomic loci in normal and cancer cells, which is mediated by the interaction between m6A reader FXR1 and DNA 5-methylcytosine dioxygenase TET1. Upon recognizing RNA m6A, FXR1 recruits TET1 to genomic loci to demethylate DNA, leading to reprogrammed chromatin accessibility and gene transcription."
item3531	REG00051	.	.	M6ADIS0056	.	36071173	"Here, we show that METTL3-mediated RNA N6-methyladenosine (m6A) formation leads to DNA demethylation in nearby genomic loci in normal and cancer cells, which is mediated by the interaction between m6A reader FXR1 and DNA 5-methylcytosine dioxygenase TET1. Upon recognizing RNA m6A, FXR1 recruits TET1 to genomic loci to demethylate DNA, leading to reprogrammed chromatin accessibility and gene transcription."
item3532	REG00007	M6ATAR00637	Down	.	.	36375665	"Our study revealed that METTL3 targeted TET1 mRNA via m6A methylation, and TET1, in turn, mediated DNA methylation targeting METTL3 to affect mRNA m6A methylation, thus forming a negative feedback loop that regulated myoblast differentiation."
item3533	REG00008	M6ATAR00637	Down	.	.	36375665	"Our study revealed that METTL3 targeted TET1 mRNA via m6A methylation, and TET1, in turn, mediated DNA methylation targeting METTL3 to affect mRNA m6A methylation, thus forming a negative feedback loop that regulated myoblast differentiation."
item3534	REG00007	M6ATAR00637	Down	.	.	36375665	"Our study revealed that METTL3 targeted TET1 mRNA via m6A methylation, and TET1, in turn, mediated DNA methylation targeting METTL3 to affect mRNA m6A methylation, thus forming a negative feedback loop that regulated myoblast differentiation."
item3535	REG00022	M6ATAR00096	Down	M6ADIS0032	.	36284300	"FENDRR overexpression inhibited hypoxia-induced HPAEC pyroptosis. Additionally, DRP1 is a downstream target gene of FENDRR, and FENDRR formed an RNA-DNA triplex with the promoter of DRP1, which led to an increase in DRP1 promoter methylation that decreased the transcriptional level of DRP1. Notably, we illustrated that the m6A reader YTHDC1 plays an important role in m6A-modified FENDRR degradation."
item3536	REG00007	M6ATAR01564	.	M6ADIS0068	.	38658974	"Moreover, our findings first emphasized the functional importance of IGF2BPs as epigenetic R-loop readers in transcriptional genetic regulation and cancer biology. In addition, our research provides a novel RBM15/IGF2BPs/DNMT1 trans-omics regulation m6A axis, indicating the new crosstalk between RNA m6A methylation and DNA methylation in prostate cancer."
item3537	REG00020	M6ATAR01564	.	M6ADIS0068	.	38658974	"Moreover, our findings first emphasized the functional importance of IGF2BPs as epigenetic R-loop readers in transcriptional genetic regulation and cancer biology. In addition, our research provides a novel RBM15/IGF2BPs/DNMT1 trans-omics regulation m6A axis, indicating the new crosstalk between RNA m6A methylation and DNA methylation in prostate cancer."
item3538	REG00013	M6ATAR01564	.	M6ADIS0068	.	38658974	"Moreover, our findings first emphasized the functional importance of IGF2BPs as epigenetic R-loop readers in transcriptional genetic regulation and cancer biology. In addition, our research provides a novel RBM15/IGF2BPs/DNMT1 trans-omics regulation m6A axis, indicating the new crosstalk between RNA m6A methylation and DNA methylation in prostate cancer."
item3539	REG00014	M6ATAR01564	.	M6ADIS0068	.	38658974	"Moreover, our findings first emphasized the functional importance of IGF2BPs as epigenetic R-loop readers in transcriptional genetic regulation and cancer biology. In addition, our research provides a novel RBM15/IGF2BPs/DNMT1 trans-omics regulation m6A axis, indicating the new crosstalk between RNA m6A methylation and DNA methylation in prostate cancer."
item3540	REG00008	M6ATAR01564	.	M6ADIS0068	.	38658974	"Moreover, our findings first emphasized the functional importance of IGF2BPs as epigenetic R-loop readers in transcriptional genetic regulation and cancer biology. In addition, our research provides a novel RBM15/IGF2BPs/DNMT1 trans-omics regulation m6A axis, indicating the new crosstalk between RNA m6A methylation and DNA methylation in prostate cancer."
item3541	REG00005	M6ATAR00404	Up	M6ADIS0007	.	34016959	"We conclude that loss of LKB1 promotes ALKBH5transcription by a DNA methylation mechanism, reduces m6A modification, and increases the stability of m6A target oncogenes, thus contributing to aggressive phenotypes of KRAS-mutated lung cancer."
item3542	REG00005	M6ATAR00397	Up	M6ADIS0007	.	34016959	"We conclude that loss of LKB1 promotes ALKBH5transcription by a DNA methylation mechanism, reduces m6A modification, and increases the stability of m6A target oncogenes, thus contributing to aggressive phenotypes of KRAS-mutated lung cancer."
item3543	REG00005	M6ATAR00341	Up	M6ADIS0007	.	34016959	"We conclude that loss of LKB1 promotes ALKBH5transcription by a DNA methylation mechanism, reduces m6A modification, and increases the stability of m6A target oncogenes, thus contributing to aggressive phenotypes of KRAS-mutated lung cancer."
item3544	REG00008	M6ATAR00404	Down	M6ADIS0007	.	34016959	"We conclude that loss of LKB1 promotes ALKBH5transcription by a DNA methylation mechanism, reduces m6A modification, and increases the stability of m6A target oncogenes, thus contributing to aggressive phenotypes of KRAS-mutated lung cancer."
item3545	REG00008	M6ATAR00397	Down	M6ADIS0007	.	34016959	"We conclude that loss of LKB1 promotes ALKBH5transcription by a DNA methylation mechanism, reduces m6A modification, and increases the stability of m6A target oncogenes, thus contributing to aggressive phenotypes of KRAS-mutated lung cancer."
item3546	REG00008	M6ATAR00341	Down	M6ADIS0007	.	34016959	"We conclude that loss of LKB1 promotes ALKBH5transcription by a DNA methylation mechanism, reduces m6A modification, and increases the stability of m6A target oncogenes, thus contributing to aggressive phenotypes of KRAS-mutated lung cancer."
item3547	REG00007	M6ATAR01568	.	M6ADIS0317	.	37270777	"IGFBP7-OT suppresses the occupancy of DNMT1 and DNMT3a on the IGFBP7 promoter, thereby inhibiting methylation of the IGFBP7 promoter. The upregulation of IGFBP7-OT in OA is partially controlled by METTL3-mediated N-methyladenosine (mA) modification. Collectively, our findings reveal that mA modification of IGFBP7-OT promotes OA progression by regulating the DNMT1/DNMT3a-IGFBP7 axis and provide a potential therapeutical target for OA treatment."
item3548	REG00007	M6ATAR01568	.	M6ADIS0317	.	37270777	"IGFBP7-OT suppresses the occupancy of DNMT1 and DNMT3a on the IGFBP7 promoter, thereby inhibiting methylation of the IGFBP7 promoter. The upregulation of IGFBP7-OT in OA is partially controlled by METTL3-mediated N-methyladenosine (mA) modification. Collectively, our findings reveal that mA modification of IGFBP7-OT promotes OA progression by regulating the DNMT1/DNMT3a-IGFBP7 axis and provide a potential therapeutical target for OA treatment."
item3549	REG00007	.	.	M6ADIS0100	M6ADRUG0209	38314261	"In addition, this study revealed that the DNMT1/METTL3 pathway affected Ang II-induced apoptosis in NRCMs. Finally, this study found that DNMT1, but not METTL3, might directly regulated the ANP and BNP expression. Collectively, our findings revealed the role of the DNMT1/METTL3 pathway in cardiac hypertrophy and provided a novel molecular mechanism describing the physiological and pathological processes."
item3550	REG00007	M6ATAR01569	.	M6ADIS0007	.	38586389	"METTL3-mediated m6A methylation of DNMT1 up-regulates FOXO3a promoter methylation, thereby promoting the progression of NSCLC."
item3551	REG00007	M6ATAR01569	.	.	.	39826545	"METTL3-METTL14 recruits the DNA methyltransferase DNMT1 to chromatin for gene-body methylation. We identify a set of genes whose expression is fine-tuned by both gene-body 5mC, which promotes transcription, and m6A, which destabilizes transcripts. We demonstrate that METTL3-METTL14-dependent 5mC and m6A are both essential for the differentiation of embryonic stem cells into embryoid bodies and that the upregulation of key differentiation genes during early differentiation depends on the dynamic balance between increased 5mC and decreased m6A."
item3552	REG00006	M6ATAR01569	.	.	.	39826545	"METTL3-METTL14 recruits the DNA methyltransferase DNMT1 to chromatin for gene-body methylation. We identify a set of genes whose expression is fine-tuned by both gene-body 5mC, which promotes transcription, and m6A, which destabilizes transcripts. We demonstrate that METTL3-METTL14-dependent 5mC and m6A are both essential for the differentiation of embryonic stem cells into embryoid bodies and that the upregulation of key differentiation genes during early differentiation depends on the dynamic balance between increased 5mC and decreased m6A."
item3553	REG00009	M6ATAR01569	.	M6ADIS0257	.	40093271	WTAP expression is elevated in HG-induced HUVECs and epigenetically regulates the m6A modification of DNMT1 to impair diabetic wound healing.
item3554	REG00007	M6ATAR00141	Up	.	M6ADRUG0210	36327957	"METTL3 stabilized MALAT1 expression by promoting m6A modification of MALAT1. MALAT1 promoted SFRP2 methylation and led to reduced SFRP2 expression by recruiting DNMT1, DNMT3A, and DNMT3B to the promoter region of SFRP2. Furthermore, SFRP2 facilitated activation of the Wnt/beta-catenin signaling. By this mechanism, METTL3 suppressed autism-like symptoms and hippocampal neuron apoptosis."
item3555	REG00007	M6ATAR00141	Up	.	M6ADRUG0210	36327957	"METTL3 stabilized MALAT1 expression by promoting m6A modification of MALAT1. MALAT1 promoted SFRP2 methylation and led to reduced SFRP2 expression by recruiting DNMT1, DNMT3A, and DNMT3B to the promoter region of SFRP2. Furthermore, SFRP2 facilitated activation of the Wnt/beta-catenin signaling. By this mechanism, METTL3 suppressed autism-like symptoms and hippocampal neuron apoptosis."
item3556	REG00007	M6ATAR00141	Up	.	M6ADRUG0210	36327957	"METTL3 stabilized MALAT1 expression by promoting m6A modification of MALAT1. MALAT1 promoted SFRP2 methylation and led to reduced SFRP2 expression by recruiting DNMT1, DNMT3A, and DNMT3B to the promoter region of SFRP2. Furthermore, SFRP2 facilitated activation of the Wnt/beta-catenin signaling. By this mechanism, METTL3 suppressed autism-like symptoms and hippocampal neuron apoptosis."
item3557	REG00017	M6ATAR00388	Down	M6ADIS0312	M6ADRUG0210	38334797	These results confirm the crucial role of METTL16 in restraining PTC progression through SCD1-activated lipid metabolism in cooperation with YTHDC2. This suggests that the combination of METTL16 and anti-SCD1 blockade might constitute an effective therapy for PTC.
item3558	REG00023	M6ATAR00388	Down	M6ADIS0312	M6ADRUG0210	38334797	These results confirm the crucial role of METTL16 in restraining PTC progression through SCD1-activated lipid metabolism in cooperation with YTHDC2. This suggests that the combination of METTL16 and anti-SCD1 blockade might constitute an effective therapy for PTC.
item3559	REG00001	M6ATAR00610	Down	M6ADIS0113	.	35712246	"The comprehensive functional annotations indicated these genes might mediate a detailed immune or inflammatory response or signaling pathways in the OLF pathogenesis. SOCS3 was identified as a core gene, which was associated with multiple immune infiltrates and 5mC/m6A modifiers in OLF, and the crosstalk between DNMT1 and FTO on affecting SOCS3 expression might play a significant role in OLF pathogenesis."
item3560	REG00029	M6ATAR01414	Down	M6ADIS0038	.	36264362	"USP7 was able to recruit DNMT1 to the FMR1 promoter region, which increased promoter methylation rates and suppressed FMR1 expression. TBK1 or FMR1 overexpression could reverse the effects of USP7 on cell functions. Inhibition of USP7 alleviated renal ischemia-reperfusion injury in rats."
item3561	REG00030	.	.	M6ADIS0065	.	28393842	"Because IGFBP3 is an established target of DNMT3a, we investigated the effect of MTA1 upon IGFBP3 expression, and found a coactivator role of MTA1/c-Jun/Pol II coactivator complex upon the IGFBP3 transcription. In addition, MTA1 overexpression correlates well with low levels of DNMT3a which, in turn also correlates with a high IGFBP3 status in breast cancer patients and predicts a poor clinical outcome for breast cancer patients."
item3562	REG00030	.	.	M6ADIS0006	.	19070387	"By contrast, the transcription of CDH6 and IGFBP3 was triggered by HBx through the deprivation of DNMT3A from their promoters. Transcriptional levels of target genes in hepatocellular carcinoma (HCC) specimens were strongly correlated with the occurrence of HBx."
item3563	REG00030	.	.	M6ADIS0059	M6ADRUG0005	34790580	"Functionally, HOXD10 acts as a tumor suppressor gene, in which HOXD10-expressing cells showed suppressed cell proliferation, colony formation ability, and migration and invasion capacity. Mechanistically, DNMT1, DNMT3B, and MeCP2 were recruited in the HOXD10 promoter, and demethylation by 5-Aza-2'-deoxycytidine (5-Aza-CdR) treatment or MeCP2 knockdown can sufficiently induce HOXD10 expression. HOXD10regulates the expressions of miR-7 and IGFBP3 in a promoter-dependent manner."
item3564	REG00030	.	.	M6ADIS0059	M6ADRUG0005	34790580	"Functionally, HOXD10 acts as a tumor suppressor gene, in which HOXD10-expressing cells showed suppressed cell proliferation, colony formation ability, and migration and invasion capacity. Mechanistically, DNMT1, DNMT3B, and MeCP2 were recruited in the HOXD10 promoter, and demethylation by 5-Aza-2'-deoxycytidine (5-Aza-CdR) treatment or MeCP2 knockdown can sufficiently induce HOXD10 expression. HOXD10regulates the expressions of miR-7 and IGFBP3 in a promoter-dependent manner."
item3565	REG00002	M6ATAR01491	Up	M6ADIS0268	.	40086625	This study suggests that ELAVL1 regulates DNMT3a expression and nuclear translocation to modulate dendritic cell function and Th17/Treg balance through DACH1/c-Jun pathway in COPD.
item3566	REG00008	M6ATAR01491	Down	M6ADIS0268	.	40086625	This study suggests that ELAVL1 regulates DNMT3a expression and nuclear translocation to modulate dendritic cell function and Th17/Treg balance through DACH1/c-Jun pathway in COPD.
item3567	REG00002	M6ATAR00658	Up	M6ADIS0091	.	36173508	"ELAVL1 plays a critical role in protecting against ferroptosis-induced cerebral I/R and subsequent brain damage via DNMT3B/PINK1 axis, thus providing a new potential target for ischemic stroke treatment."
item3568	REG00024	M6ATAR00658	Up	M6ADIS0057	.	39185313	"Furthermore, methylated RNA immunoprecipitation and RNA Immunoprecipitation assays revealed that YTHDF1 elevated the expression of DNMT3B, which synergistically promoted the initiation and development of GC. We elucidated the molecular mechanism underlying the regulation of DNMT3B by YTHDF1 and explored the crosstalk between m6A and 5mC modification."
item3569	REG00012	M6ATAR00341	Up	M6ADIS0006	.	33051595	"We identified IGF2BP1 as a novel PTPN13-interacting gene and demonstrated that PTPN13 influences c-Myc expression by directly and competitively binding to IGF2BP1 to decrease the intracellular concentration of functional IGF2BP1. Overexpressing PTPN13 promoted c-Myc mRNA degradation independent of the protein tyrosine phosphatase (PTP) activity of PTPN13. Importantly, we discovered that the PTPN13-IGF2BP1-c-Myc axis was important for cancer cell growth through promoting metabolic reprogramming."
item3570	REG00001	M6ATAR01573	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3571	REG00001	M6ATAR00833	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3572	REG00001	M6ATAR01574	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3573	REG00001	M6ATAR00844	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3574	REG00001	M6ATAR01573	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3575	REG00001	M6ATAR00833	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3576	REG00001	M6ATAR01574	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3577	REG00001	M6ATAR00844	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3578	REG00007	M6ATAR01573	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3579	REG00007	M6ATAR00833	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3580	REG00007	M6ATAR01574	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3581	REG00007	M6ATAR00844	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3582	REG00007	M6ATAR01573	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3583	REG00007	M6ATAR00833	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3584	REG00007	M6ATAR01574	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3585	REG00007	M6ATAR00844	.	M6ADIS0370	.	36161325	"The Fto promoter was hypomethylated due to the lower expression of Dnmt1 and Dnmt3a. At the same time, there was a lower occupancy of transcription factor C/EBPalpha on the Fto promoter. Conversely, C/ebp-alpha transcript was downregulated via induced miR-124-3p expression."
item3587	REG00051	M6ATAR01381	.	M6ADIS0006	.	38486042	"METTL3 and METTL14-induced m6A modification upregulated SREBF2-AS1 expression through increasing SREBF2-AS1 transcript stability. Functional assays showed that only m6A-modified, but not non-modified SREBF2-AS1 promoted HCC progression and sorafenib resistance. Mechanistic investigations revealed that m6A-modified SREBF2-AS1 bound and recruited m6A reader FXR1 and DNA 5-methylcytosine dioxygenase TET1 to SREBF2 promoter, leading to DNA demethylation at SREBF2 promoter and the upregulation of SREBF2 transcription. Functional rescue assays showed that SREBF2 was the critical mediator of the oncogenic roles of SREBF2-AS1 in HCC. Together, this study showed that m6A-modified SREBF2-AS1 exerted oncogenic roles in HCC through inducing DNA demethylation and transcriptional activation of SREBF2, and suggested m6A-modified SREBF2-AS1 as a prognostic biomarker and therapeutic target for HCC."
item3588	REG00006	M6ATAR00118	Down	M6ADIS0065	.	35022519	Silencing lncRNA UCA1 curbed the progression of breast cancer through the METTL14-miR-375-SOX12 axis.
item3589	REG00006	M6ATAR00118	Down	M6ADIS0065	.	35022519	Silencing lncRNA UCA1 curbed the progression of breast cancer through the METTL14-miR-375-SOX12 axis.
item3590	REG00006	M6ATAR00118	Down	M6ADIS0065	.	35022519	Silencing lncRNA UCA1 curbed the progression of breast cancer through the METTL14-miR-375-SOX12 axis.
item3591	REG00007	M6ATAR01491	Up	M6ADIS0057	.	37477089	"Linc00942 recruits RNA methyltransferase METTL3 to stimulate N6-methyladenosine (m6A) deposit on DNMT3a transcripts, triggering IGF2BP3/HuR to recognize modified mRNA for reinforced stability. SQSTM1/p62 recruits Linc00942 for autophagic degradation which can be abrogated after autophagy inhibition by p62 knockdown or chloroquine treatment."
item3592	REG00014	M6ATAR01491	Up	M6ADIS0057	.	37477089	"Linc00942 recruits RNA methyltransferase METTL3 to stimulate N6-methyladenosine (m6A) deposit on DNMT3a transcripts, triggering IGF2BP3/HuR to recognize modified mRNA for reinforced stability. SQSTM1/p62 recruits Linc00942 for autophagic degradation which can be abrogated after autophagy inhibition by p62 knockdown or chloroquine treatment."
item3593	REG00024	M6ATAR01577	Up	M6ADIS0375	.	40048660	"YTHDF1 recognizes target MeCP2 mRNA and induces its translation. SLC31A1 inhibition due to increased MeCP2-recognized methylating CpG islands of SLC31A1 in the promoter region restrains its transcription. Conversely, MeCP2 knockdown rescued SLC31A1 expression, resulting in contradictory effects."
item3594	REG00051	M6ATAR01578	.	M6ADIS0326	.	40293529	"MIR670HG interacts with the m6A reader FXR1 and DNA 5-methylcytosine dioxygenase TET1 in an m6A modification-dependent manner. These interactions reduce the binding of TET1 to CD24 promoter, leading to increased DNA methylation at CD24 promoter and transcriptional suppression of CD24."
item3595	REG00005	M6ATAR00186	Down	M6ADIS0107	.	39993647	"Folic acid reduces the expression of m6A demethylase AlkB homolog 5 (ALKHB5) via promoter DNA hypermethylation. Decreased ALKBH5 causes increased m6A modification and increased expression of ATG12 in a demethylase activity-dependent manner, thereby promoting autophagy and preventing hepatic steatosis."
item3596	REG00001	M6ATAR01579	Up	M6ADIS0057	.	39351597	IGFBP7 is regulated by DNA methylation at the genetic level and that the RNA m6A demethylase FTO modulates it at the posttranscriptional level.
item3597	REG00001	M6ATAR01579	Up	M6ADIS0057	.	39351597	IGFBP7 is regulated by DNA methylation at the genetic level and that the RNA m6A demethylase FTO modulates it at the posttranscriptional level.
item3598	REG00007	M6ATAR01580	Up	M6ADIS0335	.	39337381	"The suppression of 5mC demethylation or m6A hypermethylation significantly alleviates the upregulation of PCK2 and proinflammatory cytokines in LPS-challenged KCs. Further reciprocal tests indicate 5mC demethylation is upstream of m6A hypermethylation. Specifically, CpG islands in the promoters of PCK2 and RNA methyltransferase (METTL3 and METTL14) genes are demethylated, while the 3'UTR of PCK2 mRNA is m6A hypermethylated, in LPS-stimulated KCs. These modifications contribute to the transactivation of the PCK2 gene as well as increased PCK2 mRNA stability and protein production via a m6A-mediated mechanism with IGF2BP1 as the reader protein. These results indicate that DNA 5mC and RNA m6A collaborate to upregulate PCK2 expression, respectively, at the transcriptional and post-transcriptional levels during KC activation."
item3599	REG00006	M6ATAR01580	Up	M6ADIS0335	.	39337381	"The suppression of 5mC demethylation or m6A hypermethylation significantly alleviates the upregulation of PCK2 and proinflammatory cytokines in LPS-challenged KCs. Further reciprocal tests indicate 5mC demethylation is upstream of m6A hypermethylation. Specifically, CpG islands in the promoters of PCK2 and RNA methyltransferase (METTL3 and METTL14) genes are demethylated, while the 3'UTR of PCK2 mRNA is m6A hypermethylated, in LPS-stimulated KCs. These modifications contribute to the transactivation of the PCK2 gene as well as increased PCK2 mRNA stability and protein production via a m6A-mediated mechanism with IGF2BP1 as the reader protein. These results indicate that DNA 5mC and RNA m6A collaborate to upregulate PCK2 expression, respectively, at the transcriptional and post-transcriptional levels during KC activation."
item3600	REG00012	M6ATAR01580	Up	M6ADIS0335	.	39337381	"The suppression of 5mC demethylation or m6A hypermethylation significantly alleviates the upregulation of PCK2 and proinflammatory cytokines in LPS-challenged KCs. Further reciprocal tests indicate 5mC demethylation is upstream of m6A hypermethylation. Specifically, CpG islands in the promoters of PCK2 and RNA methyltransferase (METTL3 and METTL14) genes are demethylated, while the 3'UTR of PCK2 mRNA is m6A hypermethylated, in LPS-stimulated KCs. These modifications contribute to the transactivation of the PCK2 gene as well as increased PCK2 mRNA stability and protein production via a m6A-mediated mechanism with IGF2BP1 as the reader protein. These results indicate that DNA 5mC and RNA m6A collaborate to upregulate PCK2 expression, respectively, at the transcriptional and post-transcriptional levels during KC activation."
item3601	REG00007	.	.	.	.	33505026	"METTL3 also interacts physically with the histone 3 lysine 9 (H3K9) tri-methyltransferase SETDB1 and its cofactor TRIM28, and is important for their localization to IAPs. Our findings demonstrate that METTL3-catalysed m6A modification of RNA is important for the integrity of IAP heterochromatin in mouse embryonic stem cells, revealing a mechanism of heterochromatin regulation in mammals."
item3602	REG00022	.	.	.	.	32778823	"We demonstrate that the methyltransferase METTL3/METTL14 regulates H3K9me2 modification. We observe a genome-wide correlation between m6A and occupancy by the H3K9me2 demethylase KDM3B, and we find that the m6A reader YTHDC1 physically interacts with and recruits KDM3B to m6A-associated chromatin regions, promoting H3K9me2 demethylation and gene expression. This study establishes a direct link between m6A and dynamic chromatin modification and provides mechanistic insight into the co-transcriptional interplay between RNA modifications and histone modifications."
item3603	REG00006	.	.	.	.	32778823	"We demonstrate that the methyltransferase METTL3/METTL14 regulates H3K9me2 modification. We observe a genome-wide correlation between m6A and occupancy by the H3K9me2 demethylase KDM3B, and we find that the m6A reader YTHDC1 physically interacts with and recruits KDM3B to m6A-associated chromatin regions, promoting H3K9me2 demethylation and gene expression. This study establishes a direct link between m6A and dynamic chromatin modification and provides mechanistic insight into the co-transcriptional interplay between RNA modifications and histone modifications."
item3604	REG00007	.	.	.	.	32778823	"We demonstrate that the methyltransferase METTL3/METTL14 regulates H3K9me2 modification. We observe a genome-wide correlation between m6A and occupancy by the H3K9me2 demethylase KDM3B, and we find that the m6A reader YTHDC1 physically interacts with and recruits KDM3B to m6A-associated chromatin regions, promoting H3K9me2 demethylation and gene expression. This study establishes a direct link between m6A and dynamic chromatin modification and provides mechanistic insight into the co-transcriptional interplay between RNA modifications and histone modifications."
item3605	REG00008	M6ATAR00658	Down	M6ADIS0168	.	35340126	"Consistently, DNase I sensitivity assay also showed consistent change of chromatin accessibility of the ALKBH5 promoter in KDM4A-overexpressed and TNFalpha-induced senescent NPCs39 (Figure 2Q). Collectively, the above data demonstrated upregulation of ALKBH5 in the senescence process of NPCs was due to epigenetic decrease of H3K9me3 in the promoter."
item3606	REG00006	M6ATAR01597	Down	.	.	29335608	"Thus, our finding that m6A RNA methylation regulates specific histone modifications, including H3K27me3, H3K27ac and H3K4me3, represents a previously unknown mechanism of gene regulation. Among these modifications, H3K27ac and H3K4me3 are associated with gene activation, and H3K27me3e with repression, consistent with our observations that there is no marked bias toward gene activation or repression in Mettl14-KO NSCs compared with controls."
item3607	REG00006	M6ATAR01598	Down	.	.	29335608	"Thus, our finding that m6A RNA methylation regulates specific histone modifications, including H3K27me3, H3K27ac and H3K4me3, represents a previously unknown mechanism of gene regulation. Among these modifications, H3K27ac and H3K4me3 are associated with gene activation, and H3K27me3e with repression, consistent with our observations that there is no marked bias toward gene activation or repression in Mettl14-KO NSCs compared with controls."
item3608	REG00006	M6ATAR01597	Down	.	.	29335608	"Thus, our finding that m6A RNA methylation regulates specific histone modifications, including H3K27me3, H3K27ac and H3K4me3, represents a previously unknown mechanism of gene regulation. Among these modifications, H3K27ac and H3K4me3 are associated with gene activation, and H3K27me3e with repression, consistent with our observations that there is no marked bias toward gene activation or repression in Mettl14-KO NSCs compared with controls."
item3609	REG00006	M6ATAR01598	Down	.	.	29335608	"Thus, our finding that m6A RNA methylation regulates specific histone modifications, including H3K27me3, H3K27ac and H3K4me3, represents a previously unknown mechanism of gene regulation. Among these modifications, H3K27ac and H3K4me3 are associated with gene activation, and H3K27me3e with repression, consistent with our observations that there is no marked bias toward gene activation or repression in Mettl14-KO NSCs compared with controls."
item3610	REG00006	M6ATAR01597	Down	.	.	29335608	"Thus, our finding that m6A RNA methylation regulates specific histone modifications, including H3K27me3, H3K27ac and H3K4me3, represents a previously unknown mechanism of gene regulation. Among these modifications, H3K27ac and H3K4me3 are associated with gene activation, and H3K27me3e with repression, consistent with our observations that there is no marked bias toward gene activation or repression in Mettl14-KO NSCs compared with controls."
item3611	REG00006	M6ATAR01598	Down	.	.	29335608	"Thus, our finding that m6A RNA methylation regulates specific histone modifications, including H3K27me3, H3K27ac and H3K4me3, represents a previously unknown mechanism of gene regulation. Among these modifications, H3K27ac and H3K4me3 are associated with gene activation, and H3K27me3e with repression, consistent with our observations that there is no marked bias toward gene activation or repression in Mettl14-KO NSCs compared with controls."
item3612	REG00007	M6ATAR00249	Up	.	.	31154015	"m6A was present on the transcripts of histone methyltransferase Ezh2, and its reduction upon Mettl3 knockdown decreased both Ezh2 protein expression and consequent H3K27me3 levels. The defects of neurogenesis and neuronal development induced by Mettl3depletion could be rescued by Ezh2 overexpression. Collectively, our results uncover a crosstalk between RNA and histone modifications and indicate that Mettl3-mediated m6A modification plays an important role in regulating neurogenesis and neuronal development through modulating Ezh2."
item3613	REG00008	M6ATAR01264	Down	M6ADIS0125	.	32875102	"The mRNA of lysine demethylase 6B (KDM6B) was m6A-modified and its decay mediated by YTHDF2. YTHDF2 deficiency stabilized KDM6B to promote H3K27me3 demethylation of multiple proinflammatory cytokines and subsequently enhanced their transcription. Furthermore, we identified H3K27me3 as a barrier for m6A modification during transcription. KDM6B recruits the m6A methyltransferase complex to facilitate the methylation of m6A in transcribing mRNA by removing adjacent H3K27me3 barriers. These results revealed cross-talk between m6A and H3K27me3 during bacterial infection, which has broader implications for deciphering epitranscriptomics in immune homeostasis."
item3614	REG00007	M6ATAR01264	Down	M6ADIS0125	.	32875102	"The mRNA of lysine demethylase 6B (KDM6B) was m6A-modified and its decay mediated by YTHDF2. YTHDF2 deficiency stabilized KDM6B to promote H3K27me3 demethylation of multiple proinflammatory cytokines and subsequently enhanced their transcription. Furthermore, we identified H3K27me3 as a barrier for m6A modification during transcription. KDM6B recruits the m6A methyltransferase complex to facilitate the methylation of m6A in transcribing mRNA by removing adjacent H3K27me3 barriers. These results revealed cross-talk between m6A and H3K27me3 during bacterial infection, which has broader implications for deciphering epitranscriptomics in immune homeostasis."
item3615	REG00006	M6ATAR01264	Down	M6ADIS0125	.	32875102	"The mRNA of lysine demethylase 6B (KDM6B) was m6A-modified and its decay mediated by YTHDF2. YTHDF2 deficiency stabilized KDM6B to promote H3K27me3 demethylation of multiple proinflammatory cytokines and subsequently enhanced their transcription. Furthermore, we identified H3K27me3 as a barrier for m6A modification during transcription. KDM6B recruits the m6A methyltransferase complex to facilitate the methylation of m6A in transcribing mRNA by removing adjacent H3K27me3 barriers. These results revealed cross-talk between m6A and H3K27me3 during bacterial infection, which has broader implications for deciphering epitranscriptomics in immune homeostasis."
item3616	REG00009	.	.	M6ADIS0125	.	32875102	"The mRNA of lysine demethylase 6B (KDM6B) was m6A-modified and its decay mediated by YTHDF2. YTHDF2 deficiency stabilized KDM6B to promote H3K27me3 demethylation of multiple proinflammatory cytokines and subsequently enhanced their transcription. Furthermore, we identified H3K27me3 as a barrier for m6A modification during transcription. KDM6B recruits the m6A methyltransferase complex to facilitate the methylation of m6A in transcribing mRNA by removing adjacent H3K27me3 barriers. These results revealed cross-talk between m6A and H3K27me3 during bacterial infection, which has broader implications for deciphering epitranscriptomics in immune homeostasis."
item3617	REG00007	.	.	M6ADIS0125	.	32875102	"The mRNA of lysine demethylase 6B (KDM6B) was m6A-modified and its decay mediated by YTHDF2. YTHDF2 deficiency stabilized KDM6B to promote H3K27me3 demethylation of multiple proinflammatory cytokines and subsequently enhanced their transcription. Furthermore, we identified H3K27me3 as a barrier for m6A modification during transcription. KDM6B recruits the m6A methyltransferase complex to facilitate the methylation of m6A in transcribing mRNA by removing adjacent H3K27me3 barriers. These results revealed cross-talk between m6A and H3K27me3 during bacterial infection, which has broader implications for deciphering epitranscriptomics in immune homeostasis."
item3618	REG00006	.	.	M6ADIS0125	.	32875102	"The mRNA of lysine demethylase 6B (KDM6B) was m6A-modified and its decay mediated by YTHDF2. YTHDF2 deficiency stabilized KDM6B to promote H3K27me3 demethylation of multiple proinflammatory cytokines and subsequently enhanced their transcription. Furthermore, we identified H3K27me3 as a barrier for m6A modification during transcription. KDM6B recruits the m6A methyltransferase complex to facilitate the methylation of m6A in transcribing mRNA by removing adjacent H3K27me3 barriers. These results revealed cross-talk between m6A and H3K27me3 during bacterial infection, which has broader implications for deciphering epitranscriptomics in immune homeostasis."
item3619	REG00006	.	Up	.	.	30867593	"The identification of the histone mark H3K36me3 as a determinant of m6A RNA modification via METTL14 reveals a cross-talk between histone modification and RNA methylation, and adds another layer of complexity to the control of gene expression in normal and pathological biological processes."
item3620	REG00007	.	Up	.	.	30867593	"The identification of the histone mark H3K36me3 as a determinant of m6A RNA modification via METTL14 reveals a cross-talk between histone modification and RNA methylation, and adds another layer of complexity to the control of gene expression in normal and pathological biological processes."
item3621	REG00006	M6ATAR01599	Up	.	.	31601799	"Among validating hits are genes coding for the N6-methyladenosine (m6A) mRNA methyltransferase (MTase) complex, including, METTL14, METTL3, and WTAP. We demonstrate that m6A MTase activity promotes erythroid gene expression programs through selective translation of ~300 m6A marked mRNAs, including those coding for SETD histone methyltransferases, ribosomal components, and polyA RNA binding proteins. Remarkably, loss of m6A marks results in dramatic loss of H3K4me3 marks across key erythroid-specific KLF1 transcriptional targets."
item3622	REG00006	M6ATAR01600	Up	.	.	31601799	"Among validating hits are genes coding for the N6-methyladenosine (m6A) mRNA methyltransferase (MTase) complex, including, METTL14, METTL3, and WTAP. We demonstrate that m6A MTase activity promotes erythroid gene expression programs through selective translation of ~300 m6A marked mRNAs, including those coding for SETD histone methyltransferases, ribosomal components, and polyA RNA binding proteins. Remarkably, loss of m6A marks results in dramatic loss of H3K4me3 marks across key erythroid-specific KLF1 transcriptional targets."
item3623	REG00006	M6ATAR01601	Up	.	.	31601799	"Among validating hits are genes coding for the N6-methyladenosine (m6A) mRNA methyltransferase (MTase) complex, including, METTL14, METTL3, and WTAP. We demonstrate that m6A MTase activity promotes erythroid gene expression programs through selective translation of ~300 m6A marked mRNAs, including those coding for SETD histone methyltransferases, ribosomal components, and polyA RNA binding proteins. Remarkably, loss of m6A marks results in dramatic loss of H3K4me3 marks across key erythroid-specific KLF1 transcriptional targets."
item3624	REG00007	M6ATAR01599	Up	.	.	31601799	"Among validating hits are genes coding for the N6-methyladenosine (m6A) mRNA methyltransferase (MTase) complex, including, METTL14, METTL3, and WTAP. We demonstrate that m6A MTase activity promotes erythroid gene expression programs through selective translation of ~300 m6A marked mRNAs, including those coding for SETD histone methyltransferases, ribosomal components, and polyA RNA binding proteins. Remarkably, loss of m6A marks results in dramatic loss of H3K4me3 marks across key erythroid-specific KLF1 transcriptional targets."
item3625	REG00007	M6ATAR01600	Up	.	.	31601799	"Among validating hits are genes coding for the N6-methyladenosine (m6A) mRNA methyltransferase (MTase) complex, including, METTL14, METTL3, and WTAP. We demonstrate that m6A MTase activity promotes erythroid gene expression programs through selective translation of ~300 m6A marked mRNAs, including those coding for SETD histone methyltransferases, ribosomal components, and polyA RNA binding proteins. Remarkably, loss of m6A marks results in dramatic loss of H3K4me3 marks across key erythroid-specific KLF1 transcriptional targets."
item3626	REG00007	M6ATAR01601	Up	.	.	31601799	"Among validating hits are genes coding for the N6-methyladenosine (m6A) mRNA methyltransferase (MTase) complex, including, METTL14, METTL3, and WTAP. We demonstrate that m6A MTase activity promotes erythroid gene expression programs through selective translation of ~300 m6A marked mRNAs, including those coding for SETD histone methyltransferases, ribosomal components, and polyA RNA binding proteins. Remarkably, loss of m6A marks results in dramatic loss of H3K4me3 marks across key erythroid-specific KLF1 transcriptional targets."
item3627	REG00009	M6ATAR01599	Up	.	.	31601799	"Among validating hits are genes coding for the N6-methyladenosine (m6A) mRNA methyltransferase (MTase) complex, including, METTL14, METTL3, and WTAP. We demonstrate that m6A MTase activity promotes erythroid gene expression programs through selective translation of ~300 m6A marked mRNAs, including those coding for SETD histone methyltransferases, ribosomal components, and polyA RNA binding proteins. Remarkably, loss of m6A marks results in dramatic loss of H3K4me3 marks across key erythroid-specific KLF1 transcriptional targets."
item3628	REG00009	M6ATAR01600	Up	.	.	31601799	"Among validating hits are genes coding for the N6-methyladenosine (m6A) mRNA methyltransferase (MTase) complex, including, METTL14, METTL3, and WTAP. We demonstrate that m6A MTase activity promotes erythroid gene expression programs through selective translation of ~300 m6A marked mRNAs, including those coding for SETD histone methyltransferases, ribosomal components, and polyA RNA binding proteins. Remarkably, loss of m6A marks results in dramatic loss of H3K4me3 marks across key erythroid-specific KLF1 transcriptional targets."
item3629	REG00009	M6ATAR01601	Up	.	.	31601799	"Among validating hits are genes coding for the N6-methyladenosine (m6A) mRNA methyltransferase (MTase) complex, including, METTL14, METTL3, and WTAP. We demonstrate that m6A MTase activity promotes erythroid gene expression programs through selective translation of ~300 m6A marked mRNAs, including those coding for SETD histone methyltransferases, ribosomal components, and polyA RNA binding proteins. Remarkably, loss of m6A marks results in dramatic loss of H3K4me3 marks across key erythroid-specific KLF1 transcriptional targets."
item3630	REG00008	M6ATAR00405	Down	M6ADIS0059	.	32552762	"Both the univariate and multivariate Cox regression analysis indicated that METTL14 was an independent prognostic factor in CRC. Moreover, lysine-specific histone demethylase 5C(KDM5C)-mediated demethylation of histone H3 lysine 4 tri-methylation(H3K4me3) in the promoter of METTL14 inhibited METTL15 transcription."
item3631	REG00007	M6ATAR00249	Down	M6ADIS0001	M6ADRUG0010	34586728	"METTL3 is required to maintain the features of GBM stem cells. When combined with TMZ, METTL3 silencing suppressed orthotopic TMZ-resistant xenograft growth in a cooperative manner. Mechanistically, TMZ induced a SOX4-mediated increase in chromatin accessibility at the METTL3 locus by promoting H3K27ac levels and recruiting RNA polymerase II. Moreover, METTL3 depletion affected the deposition of m6A on histone modification-related gene transcripts, such as EZH2, leading to nonsense-mediated mRNA decay."
item3632	REG00007	M6ATAR00249	Down	M6ADIS0001	M6ADRUG0010	34586728	"METTL3 is required to maintain the features of GBM stem cells. When combined with TMZ, METTL3 silencing suppressed orthotopic TMZ-resistant xenograft growth in a cooperative manner. Mechanistically, TMZ induced a SOX4-mediated increase in chromatin accessibility at the METTL3 locus by promoting H3K27ac levels and recruiting RNA polymerase II. Moreover, METTL3 depletion affected the deposition of m6A on histone modification-related gene transcripts, such as EZH2, leading to nonsense-mediated mRNA decay."
item3633	REG00007	M6ATAR01602	Down	M6ADIS0007	.	37742030	"METTL3 knockdown also reduced VGF expression by increasing H3K36me3 modification at the VGF promoter. Further research revealed that METTL3 knockdown upregulated the expression of histone methylase SETD2, the major H3K36me3 methyltransferase, by methylating the m6A site in the 3'UTR of SETD2 mRNA in LUAD cells."
item3634	REG00023	M6ATAR00375	Down	M6ADIS0308	.	38190286	We discovered that YTHDC2 inhibition increased the expression of PTEN while it decreased the expression of the PRC2 component SUZ12 and the levels of the histone modification H3K27me3.
item3635	REG00007	M6ATAR00200	Up	M6ADIS0113	.	40133819	"LDHA knockdown-mediated inhibition of endogenous lactylation suppressed osteogenic differentiation, a phenotype that was rescued by METTL3 overexpression. In conclusion, this study elucidates that histone lactylation-mediated upregulation of METTL3 promotes OLF progression through IGF2BP1-dependent m6A methylation of BMP2, providing novel insights into potential therapeutic strategies for OLF management."
item3636	REG00012	M6ATAR00200	Up	M6ADIS0113	.	40133819	"LDHA knockdown-mediated inhibition of endogenous lactylation suppressed osteogenic differentiation, a phenotype that was rescued by METTL3 overexpression. In conclusion, this study elucidates that histone lactylation-mediated upregulation of METTL3 promotes OLF progression through IGF2BP1-dependent m6A methylation of BMP2, providing novel insights into potential therapeutic strategies for OLF management."
item3637	REG00017	M6ATAR01602	Down	M6ADIS0057	.	40095756	"Furthermore, through the MeRIP-qPCR and dual-luciferase reporter assays, we found that knocking down METTL16 reduced the m6A modification level of the UBXN1 coding sequence in GC. Interestingly, the silencing of METTL16 also downregulated UBXN1 expression by promoting H3K36me3 modification at the UBXN1 promoter."
item3638	REG00024	M6ATAR00619	Up	M6ADIS0072	.	37466203	"First, we found that ocular melanoma cells presented vulnerability towards HDACis. HDACis triggered the elevation of m6A RNA modification in ocular melanoma. Further studies revealed that METTL14 served as a downstream candidate for HDACis. METTL14was silenced by the hypo-histone acetylation status, whereas HDACi restored the normal histone acetylation level of METTL14, thereby inducing its expression. Subsequently, METTL14 served as a tumor suppressor by promoting the expression of FAT4, a tumor suppressor, in a m6A-YTH N6-methyladenosine RNA-binding protein 1-dependent manner. Taken together, we found that HDACi restored the histone acetylation level of METTL14 and subsequently elicited METTL14-mediated m6A modification in tumorigenesis."
item3639	REG00024	M6ATAR00619	Up	M6ADIS0072	.	37466203	"First, we found that ocular melanoma cells presented vulnerability towards HDACis. HDACis triggered the elevation of m6A RNA modification in ocular melanoma. Further studies revealed that METTL14 served as a downstream candidate for HDACis. METTL14was silenced by the hypo-histone acetylation status, whereas HDACi restored the normal histone acetylation level of METTL14, thereby inducing its expression. Subsequently, METTL14 served as a tumor suppressor by promoting the expression of FAT4, a tumor suppressor, in a m6A-YTH N6-methyladenosine RNA-binding protein 1-dependent manner. Taken together, we found that HDACi restored the histone acetylation level of METTL14 and subsequently elicited METTL14-mediated m6A modification in tumorigenesis."
item3640	REG00006	.	.	.	.	37314930	"METTL14 enhances H3K27me3 and reduces H3K4me3 by interacting with and probably recruiting the H3K27 methyltransferase polycomb repressive complex 2 (PRC2) and H3K4 demethylase KDM5B to chromatin. Our findings identify an METTL3-independent role of METTL14 in maintaining the integrity of bivalent domains in mESCs, thus indicating a mechanism of bivalent domain regulation in mammals."
item3641	REG00006	.	.	.	.	37314930	"METTL14 enhances H3K27me3 and reduces H3K4me3 by interacting with and probably recruiting the H3K27 methyltransferase polycomb repressive complex 2 (PRC2) and H3K4 demethylase KDM5B to chromatin. Our findings identify an METTL3-independent role of METTL14 in maintaining the integrity of bivalent domains in mESCs, thus indicating a mechanism of bivalent domain regulation in mammals."
item3642	REG00006	.	.	.	.	37030005	"METTL14, but not METTL3, binds H3K27me3 and recruits KDM6B to induce H3K27me3 demethylation independent of METTL3."
item3643	REG00022	M6ATAR01488	Down	M6ADIS0180	.	38852200	"Lactate regulates N6-methyladenosine (m6A) modification levels by facilitating p300-mediated H3K18la binding to the METTL3 promoter site. The METTL3-mediated m6A modification is enriched in ACSL4, and its mRNA stability is regulated through a YTHDC1-dependent pathway."
item3644	REG00022	M6ATAR01488	Down	M6ADIS0180	.	38852200	"Lactate regulates N6-methyladenosine (m6A) modification levels by facilitating p300-mediated H3K18la binding to the METTL3 promoter site. The METTL3-mediated m6A modification is enriched in ACSL4, and its mRNA stability is regulated through a YTHDC1-dependent pathway."
item3645	REG00022	M6ATAR00150	.	M6ADIS0055	.	36468944	"Low expression of MEG3 is caused by H3K27me3 modification of the MEG3 gene locus, and this is associated with the poor prognosis of OSCC.MEG3 was modified by m6A and bound to YTHDC1."
item3646	REG00006	M6ATAR01603	Up	M6ADIS0398	M6ADRUG0212	39046182	"METTL14-mediated upregulation of HOTAIR resulted in the repression of PP1alpha, which in turn facilitated the recruitment of LSD1, thus catalyzing H3K4me1 demethylation and promoting oxycodone addiction."
item3647	REG00006	M6ATAR01604	Up	M6ADIS0007	.	38888105	"KDM5B downregulated METTL14 expression at the transcriptional level in a H3K4me3-dependent manner, while METTL14 modulated LINC02747 expression via m6A modification. Our results demonstrate a synergy of multiple mechanisms in regulating the malignant phenotype of NSCLC, revealing the complex regulation involved in the occurrence and development of cancer."
item3648	REG00024	M6ATAR01069	Up	M6ADIS0006	.	37817227	METTL16 regulated PRDM15 protein expression via YTHDF1-dependent translation.the histone acetyltransferase p300 cooperated with the transcription factor YY1 to regulate METTL16 gene expression via histone H3 lysine 27 (H3K27) acetylation in CCA cells.
item3649	REG00004	M6ATAR01471	Up	.	.	31320558	"The arginine demethylase JMJD6 promotes the demethylation of hnRNPA2B1 at Arg226 and activates its translocation to cytoplasm, which further magnifies the expression of CGAS, IFI16, and STING."
item3650	REG00004	M6ATAR01606	Up	.	.	31320558	"The arginine demethylase JMJD6 promotes the demethylation of hnRNPA2B1 at Arg226 and activates its translocation to cytoplasm, which further magnifies the expression of CGAS, IFI16, and STING."
item3651	REG00004	M6ATAR00419	Up	.	.	31320558	"The arginine demethylase JMJD6 promotes the demethylation of hnRNPA2B1 at Arg226 and activates its translocation to cytoplasm, which further magnifies the expression of CGAS, IFI16, and STING."
item3652	REG00013	M6ATAR01608	Up	M6ADIS0017	.	38443347	"IGF2BP2 regulates the expression of Aldolase A (ALDOA), a key target in the glycolytic metabolic pathway, which in turn regulates HSCs activation."
item3653	REG00005	M6ATAR00249	Up	M6ADIS0144	.	38344897	"Increased EZH2 expression was due to the increased expression of m6A demethylase ALKBH5 and decreased expression of the m6A reader protein YTHDF2. YTHDF2 directly bind to the m6A modification site of EZH2 to promote EZH2 mRNA degradation in ESCs.Enhancer of zeste homology 2 (EZH2) is a methyltransferase which catalyses H3K27Me3, leading to decreased expression levels of target genes."
item3654	REG00008	M6ATAR00249	Down	M6ADIS0144	.	38344897	"Increased EZH2 expression was due to the increased expression of m6A demethylase ALKBH5 and decreased expression of the m6A reader protein YTHDF2. YTHDF2 directly bind to the m6A modification site of EZH2 to promote EZH2 mRNA degradation in ESCs.Enhancer of zeste homology 2 (EZH2) is a methyltransferase which catalyses H3K27Me3, leading to decreased expression levels of target genes."
item3655	REG00008	M6ATAR01609	Up	M6ADIS0059	.	39269733	The m6A methyltransferase METTL3 modifies Kcnk6 promoting on inflammation associated carcinogenesis is essential for colon homeostasis and defense system through histone lactylation dependent YTHDF2 binding.Histone lactylation activates the transcription of YTHDF2 through H3K18la modification.
item3656	REG00001	M6ATAR00210	Up	M6ADIS0015	.	40281307	"FTO affected EC features via modulating CDK2 mRNA stability in an m6A-YTHDF2-dependent manner. FTO up-regulation under diabetic conditions was driven by lactate-mediated histone lactylation. FB23-2, an inhibitor to FTO's m6A demethylase activity, suppressed angiogenic phenotypes in vitro."
item3657	REG00008	M6ATAR00210	Down	M6ADIS0015	M6ADRUG0152	40281307	"FTO affected EC features via modulating CDK2 mRNA stability in an m6A-YTHDF2-dependent manner. FTO up-regulation under diabetic conditions was driven by lactate-mediated histone lactylation. FB23-2, an inhibitor to FTO's m6A demethylase activity, suppressed angiogenic phenotypes in vitro."
item3658	REG00005	M6ATAR01610	Down	M6ADIS0142	.	38858351	"Demethylase alkB homolog 5 (Alkbh5) was found to reduce m6A methylation levels on Kat2a mRNA, leading to its upregulation. YTH domain family 2 (Ythdf2) played a crucial role as an m6A reader protein mediating the degradation of Kat2a mRNA. Furthermore, Kat2a promoted ferroptosis by increasing Tfrc and Hmox1 expression via enhancing the enrichment of H3K27ac and H3K9ac on their promoter regions. In conclusion, our findings unveil a novel role for the Kat2a-ferroptosis axis in DCM pathogenesis, providing valuable insights for potential clinical interventions."
item3659	REG00008	M6ATAR01610	Up	M6ADIS0142	.	38858351	"Demethylase alkB homolog 5 (Alkbh5) was found to reduce m6A methylation levels on Kat2a mRNA, leading to its upregulation. YTH domain family 2 (Ythdf2) played a crucial role as an m6A reader protein mediating the degradation of Kat2a mRNA. Furthermore, Kat2a promoted ferroptosis by increasing Tfrc and Hmox1 expression via enhancing the enrichment of H3K27ac and H3K9ac on their promoter regions. In conclusion, our findings unveil a novel role for the Kat2a-ferroptosis axis in DCM pathogenesis, providing valuable insights for potential clinical interventions."
item3660	REG00005	M6ATAR01610	Down	M6ADIS0142	.	38858351	"Demethylase alkB homolog 5 (Alkbh5) was found to reduce m6A methylation levels on Kat2a mRNA, leading to its upregulation. YTH domain family 2 (Ythdf2) played a crucial role as an m6A reader protein mediating the degradation of Kat2a mRNA. Furthermore, Kat2a promoted ferroptosis by increasing Tfrc and Hmox1 expression via enhancing the enrichment of H3K27ac and H3K9ac on their promoter regions. In conclusion, our findings unveil a novel role for the Kat2a-ferroptosis axis in DCM pathogenesis, providing valuable insights for potential clinical interventions."
item3661	REG00008	M6ATAR01610	Up	M6ADIS0142	.	38858351	"Demethylase alkB homolog 5 (Alkbh5) was found to reduce m6A methylation levels on Kat2a mRNA, leading to its upregulation. YTH domain family 2 (Ythdf2) played a crucial role as an m6A reader protein mediating the degradation of Kat2a mRNA. Furthermore, Kat2a promoted ferroptosis by increasing Tfrc and Hmox1 expression via enhancing the enrichment of H3K27ac and H3K9ac on their promoter regions. In conclusion, our findings unveil a novel role for the Kat2a-ferroptosis axis in DCM pathogenesis, providing valuable insights for potential clinical interventions."
item3662	REG00005	M6ATAR01611	Down	M6ADIS0006	.	36419136	"UBR7 regulates H2BK120ub to bind to Keap1 promoter through H2BK120ub monoubiquitination, thereby modulating Keap1 expression and downstream Nrf2/Bach1/HK2 signaling. Pharmaceutical and genetic inhibition of glycolytic enzymes attenuate the promoting effect of UBR7 deficiency on tumor growth. In addition, methyltransferase ALKBH5, downregulated in HCC, regulated UBR7 expression in an m6A-dependent manner."
item3663	REG00022	M6ATAR01612	Up	.	.	33658714	"YTHDC1 binds to the transcripts of retrotransposons (such as intracisternal A particles, ERVK and LINE1) in mouse ES cells and its depletion results in the reactivation of these silenced retrotransposons, accompanied by a global decrease in SETDB1-mediated trimethylation at lysine 9 of histone H3 (H3K9me3)."
item3664	REG00022	M6ATAR01613	Up	.	.	33658714	"YTHDC1 binds to the transcripts of retrotransposons (such as intracisternal A particles, ERVK and LINE1) in mouse ES cells and its depletion results in the reactivation of these silenced retrotransposons, accompanied by a global decrease in SETDB1-mediated trimethylation at lysine 9 of histone H3 (H3K9me3)."
item3665	REG00009	M6ATAR00605	Up	M6ADIS0117	M6ADRUG0214	35761192	"Histone acetyltransferase p300 promotes WTAP transcription through H3K27 acetylation.WTAP-mediated N6-methyladenosine modification of NLRP3 mRNA in kidney injury of diabetic nephropathy.WTAP expression in HK-2 cells was examined with the introduction of C646, a histone acetyltransferase p300 inhibitor."
item3666	REG00007	M6ATAR01614	.	.	.	39169036	"SUV39H1/H2 protein, the methyltransferases catalyzing H3K9me3 were dramatically elevated in METTL3/METTL14 deficient cells, which causes an accumulation and infiltration of H3K9me3 across the whole nucleolus and impairs the LLPS. Mechanistically, METTL3/METTL14 complex serves as an essential adapter for CRL4 E3 ubiquitin ligase targeting SUV39H1/H2 for polyubiquitination and proteasomal degradation and therefore prevents H3K9me3 accumulation in nucleoli."
item3667	REG00007	M6ATAR01614	.	.	.	39169036	"SUV39H1/H2 protein, the methyltransferases catalyzing H3K9me3 were dramatically elevated in METTL3/METTL14 deficient cells, which causes an accumulation and infiltration of H3K9me3 across the whole nucleolus and impairs the LLPS. Mechanistically, METTL3/METTL14 complex serves as an essential adapter for CRL4 E3 ubiquitin ligase targeting SUV39H1/H2 for polyubiquitination and proteasomal degradation and therefore prevents H3K9me3 accumulation in nucleoli."
item3668	REG00006	M6ATAR01614	.	.	.	39169036	"SUV39H1/H2 protein, the methyltransferases catalyzing H3K9me3 were dramatically elevated in METTL3/METTL14 deficient cells, which causes an accumulation and infiltration of H3K9me3 across the whole nucleolus and impairs the LLPS. Mechanistically, METTL3/METTL14 complex serves as an essential adapter for CRL4 E3 ubiquitin ligase targeting SUV39H1/H2 for polyubiquitination and proteasomal degradation and therefore prevents H3K9me3 accumulation in nucleoli."
item3669	REG00006	M6ATAR01614	.	.	.	39169036	"SUV39H1/H2 protein, the methyltransferases catalyzing H3K9me3 were dramatically elevated in METTL3/METTL14 deficient cells, which causes an accumulation and infiltration of H3K9me3 across the whole nucleolus and impairs the LLPS. Mechanistically, METTL3/METTL14 complex serves as an essential adapter for CRL4 E3 ubiquitin ligase targeting SUV39H1/H2 for polyubiquitination and proteasomal degradation and therefore prevents H3K9me3 accumulation in nucleoli."
item3670	REG00005	M6ATAR01615	Up	M6ADIS0184	M6ADRUG0215	38520019	"PLK3 methylation decreases PLK3 phosphorylation of HIF1alpha and thereby increases HIF1alpha stability. HIF1alpha, in turn, upregulates ALKBH5 to reduce m6A modification of LINC00115, resulting in attenuated degradation of YTHDF2-dependent m6A-modified RNA and enhanced LINC00115 stability. Thus, this positive feedback loop provokes BCSC phenotypes and enhances chemoresistance and metastasis in triple-negative breast cancer. SETDB1 inhibitor TTD-IN with LINC00115 ASO sensitizes PTX-resistant cell response to chemotherapy in a xenograft animal model. Correlative expression of LINC00115, methylation PLK3, SETDB1, and HIF1alpha are prognostic for clinical triple-negative breast cancers."
item3671	REG00008	M6ATAR01615	Down	M6ADIS0184	M6ADRUG0215	38520019	"PLK3 methylation decreases PLK3 phosphorylation of HIF1alpha and thereby increases HIF1alpha stability. HIF1alpha, in turn, upregulates ALKBH5 to reduce m6A modification of LINC00115, resulting in attenuated degradation of YTHDF2-dependent m6A-modified RNA and enhanced LINC00115 stability. Thus, this positive feedback loop provokes BCSC phenotypes and enhances chemoresistance and metastasis in triple-negative breast cancer. SETDB1 inhibitor TTD-IN with LINC00115 ASO sensitizes PTX-resistant cell response to chemotherapy in a xenograft animal model. Correlative expression of LINC00115, methylation PLK3, SETDB1, and HIF1alpha are prognostic for clinical triple-negative breast cancers."
item3672	REG00007	M6ATAR00341	Up	M6ADIS0056	.	39502790	"AP001885.4 was overexpressed in ESCC cells because of a higher H3K18la level in the promoter and amplification, then enhanced histone lactylation- and NF-kappaB (p65)-dependent transcription activation and METTL3-mediated mRNA stability of c-myc eventually upregulated c-myc and promoted cell proliferation."
item3673	REG00007	M6ATAR00605	Up	M6ADIS0007	.	37156816	"H3K27Ac led to the activation of LINC00969 expression. LINC00969 interacts with EZH2 and METTL3, transcriptionally regulates the level of H3K27me3 in the NLRP3 promoter region, and posttranscriptionally modifies the m6A level of NLRP3 in an m6A-YTHDF2-dependent manner."
item3674	REG00008	M6ATAR00605	Up	M6ADIS0007	.	37156816	"H3K27Ac led to the activation of LINC00969 expression. LINC00969 interacts with EZH2 and METTL3, transcriptionally regulates the level of H3K27me3 in the NLRP3 promoter region, and posttranscriptionally modifies the m6A level of NLRP3 in an m6A-YTHDF2-dependent manner."
item3675	REG00007	M6ATAR00605	Up	M6ADIS0007	.	37156816	"H3K27Ac led to the activation of LINC00969 expression. LINC00969 interacts with EZH2 and METTL3, transcriptionally regulates the level of H3K27me3 in the NLRP3 promoter region, and posttranscriptionally modifies the m6A level of NLRP3 in an m6A-YTHDF2-dependent manner."
item3676	REG00008	M6ATAR00605	Up	M6ADIS0007	.	37156816	"H3K27Ac led to the activation of LINC00969 expression. LINC00969 interacts with EZH2 and METTL3, transcriptionally regulates the level of H3K27me3 in the NLRP3 promoter region, and posttranscriptionally modifies the m6A level of NLRP3 in an m6A-YTHDF2-dependent manner."
item3677	REG00007	M6ATAR01616	Up	M6ADIS0073	.	38900084	"Mechanistically, SETMAR methylates dimethylated H3K36 in the SMARCA2 promoter region to promote SMARCA2 transcription. SMARCA2 can bind to enhancers of the thyroid differentiation transcription factors (TTFs) PAX8, and FOXE1 to promote their expression by enhancing chromatin accessibility. Moreover, METTL3-mediated m6A methylation of SETAMR mRNA is observed and showed that this medication can affect SETMAR expression in an IGF2BP3-dependent manner."
item3678	REG00014	M6ATAR01616	Up	M6ADIS0073	.	38900084	"Mechanistically, SETMAR methylates dimethylated H3K36 in the SMARCA2 promoter region to promote SMARCA2 transcription. SMARCA2 can bind to enhancers of the thyroid differentiation transcription factors (TTFs) PAX8, and FOXE1 to promote their expression by enhancing chromatin accessibility. Moreover, METTL3-mediated m6A methylation of SETAMR mRNA is observed and showed that this medication can affect SETMAR expression in an IGF2BP3-dependent manner."
item3679	REG00007	M6ATAR01616	Up	M6ADIS0073	.	38900084	"Mechanistically, SETMAR methylates dimethylated H3K36 in the SMARCA2 promoter region to promote SMARCA2 transcription. SMARCA2 can bind to enhancers of the thyroid differentiation transcription factors (TTFs) PAX8, and FOXE1 to promote their expression by enhancing chromatin accessibility. Moreover, METTL3-mediated m6A methylation of SETAMR mRNA is observed and showed that this medication can affect SETMAR expression in an IGF2BP3-dependent manner."
item3680	REG00014	M6ATAR01616	Up	M6ADIS0073	.	38900084	"Mechanistically, SETMAR methylates dimethylated H3K36 in the SMARCA2 promoter region to promote SMARCA2 transcription. SMARCA2 can bind to enhancers of the thyroid differentiation transcription factors (TTFs) PAX8, and FOXE1 to promote their expression by enhancing chromatin accessibility. Moreover, METTL3-mediated m6A methylation of SETAMR mRNA is observed and showed that this medication can affect SETMAR expression in an IGF2BP3-dependent manner."
item3681	REG00014	M6ATAR00800	Up	M6ADIS0046	.	38822351	"SENP1 can desumoylate HDAC2, which enhances EGFR transcription and activates the AKT pathway. In addition, we found that IGF2BP3 expression was upregulated in high-risk AML patients and was positively correlated with SENP1 expression. MERIP-qPCR and RIP-qPCR showed that IGF2BP3 binds SENP1 3-UTR in an m6A manner, enhances SENP1 expression, and promotes AKT pathway conduction."
item3682	REG00022	M6ATAR01617	Down	M6ADIS0343	.	35974388	We identified a novel YY1/HDAC2/YTHDC1/ANXA1 axis modulating the progression and chemosensitivity of ccRCC.
item3683	REG00008	M6ATAR01618	Up	M6ADIS0006	.	38247171	"Trimethylated histone H3 lysine 4 and H3 lysine 27 acetylation modification in the promoter region of YTHDF2 enhanced its expression in HCC, and upregulated YTHDF2 in HCC predicted a worse prognosis.YTHDF2 recognized the m6A modification in the 5'-untranslational region of ETS variant transcription factor 5 (ETV5) mRNA and recruited eukaryotic translation initiation factor 3 subunit B to facilitate its translation."
item3684	REG00008	M6ATAR01618	Up	M6ADIS0006	.	38247171	"Trimethylated histone H3 lysine 4 and H3 lysine 27 acetylation modification in the promoter region of YTHDF2 enhanced its expression in HCC, and upregulated YTHDF2 in HCC predicted a worse prognosis.YTHDF2 recognized the m6A modification in the 5'-untranslational region of ETS variant transcription factor 5 (ETV5) mRNA and recruited eukaryotic translation initiation factor 3 subunit B to facilitate its translation."
item3685	REG00001	M6ATAR01486	Down	M6ADIS0059	.	39888307	"HDACi reduces ferroptosis suppressor protein (FSP1) by promoting its mRNA degradation. Specifically, it is confirmed that HDACi specifically targets HDAC1 and promotes the H3K27ac modification of fat mass- and obesity-associated gene (FTO) and AlkB Homolog 5, RNA Demethylase (ALKBH5), which results in significant activation of FTO and ALKBH5. The activation of FTO and ALKBH5 reduces N6-methyladenosine (m6A) modification on FSP1 mRNA, leading to its degradation. Crucially, lactylation of HDAC1K412is essential for ferroptosis regulation. Both Vorinostat (SAHA) and Trichostatin A (TSA) notably diminish HDAC1K412lactylation in comparison to other HDAC1 inhibitors, exhibiting a consistent trend of increasing susceptibility to ferroptosis."
item3686	REG00005	M6ATAR01486	Down	M6ADIS0059	.	39888307	"HDACi reduces ferroptosis suppressor protein (FSP1) by promoting its mRNA degradation. Specifically, it is confirmed that HDACi specifically targets HDAC1 and promotes the H3K27ac modification of fat mass- and obesity-associated gene (FTO) and AlkB Homolog 5, RNA Demethylase (ALKBH5), which results in significant activation of FTO and ALKBH5. The activation of FTO and ALKBH5 reduces N6-methyladenosine (m6A) modification on FSP1 mRNA, leading to its degradation. Crucially, lactylation of HDAC1K412is essential for ferroptosis regulation. Both Vorinostat (SAHA) and Trichostatin A (TSA) notably diminish HDAC1K412lactylation in comparison to other HDAC1 inhibitors, exhibiting a consistent trend of increasing susceptibility to ferroptosis."
item3687	REG00012	M6ATAR01486	Up	M6ADIS0059	.	39888307	"HDACi reduces ferroptosis suppressor protein (FSP1) by promoting its mRNA degradation. Specifically, it is confirmed that HDACi specifically targets HDAC1 and promotes the H3K27ac modification of fat mass- and obesity-associated gene (FTO) and AlkB Homolog 5, RNA Demethylase (ALKBH5), which results in significant activation of FTO and ALKBH5. The activation of FTO and ALKBH5 reduces N6-methyladenosine (m6A) modification on FSP1 mRNA, leading to its degradation. Crucially, lactylation of HDAC1K412is essential for ferroptosis regulation. Both Vorinostat (SAHA) and Trichostatin A (TSA) notably diminish HDAC1K412lactylation in comparison to other HDAC1 inhibitors, exhibiting a consistent trend of increasing susceptibility to ferroptosis."
item3688	REG00005	.	.	.	.	37369679	ALKBH5 is acetylated at lysine 235 (K235) by lysine acetyltransferase 8 and deacetylated by histone deacetylase 7.the m6A demethylation activity of ALKBH5 is orchestrated by its K235 acetylation and regulatory subunit PSPC1 and that K235 acetylation is necessary for the m6A demethylase activity and oncogenic roles of ALKBH5.
item3689	REG00013	M6ATAR01619	Up	M6ADIS0007	.	38281999	This feeds back upon the IGF2BP2 promoter region by further increasing the trimethyl modification at lysine 4 of histone H3 (H3K4me3) level to upregulate IGF2BP2 expression. We demonstrated that this positive feedback loop between IGF2BP2 and SLC7A5 promotes lung cancer radioresistance through the AKT/mTOR pathway.
item3690	REG00005	M6ATAR01620	Up	M6ADIS0161	.	38285939	"Histone deacetylase 11 downregulation induced by nerve injury increases histone H3 lysine 27 acetylation (H3K27ac), facilitating the binding of the transcription factor forkhead box protein D3 (FOXD3) to the Alkbh5 promoter and promoting Alkbh5 transcription. The increased ALKBH5 erases m6A sites in Htr3a messenger RNA (mRNA), resulting in an inability of YT521-B homology domain 2 (YTHDF2) to bind to Htr3a mRNA, thus causing an increase in 5-HT3A protein expression and 5-HT3 channel currents."
item3691	REG00008	M6ATAR01620	Down	M6ADIS0161	.	38285939	"Histone deacetylase 11 downregulation induced by nerve injury increases histone H3 lysine 27 acetylation (H3K27ac), facilitating the binding of the transcription factor forkhead box protein D3 (FOXD3) to the Alkbh5 promoter and promoting Alkbh5 transcription. The increased ALKBH5 erases m6A sites in Htr3a messenger RNA (mRNA), resulting in an inability of YT521-B homology domain 2 (YTHDF2) to bind to Htr3a mRNA, thus causing an increase in 5-HT3A protein expression and 5-HT3 channel currents."
item3692	REG00005	M6ATAR01621	Down	M6ADIS0057	.	38589927	Histone acetylation causes HSPA4 upregulation in GC tumor tissues. HSPA4 upregulation increases the protein stability of m6A demethylase ALKBH5. ALKBH5 decreases CD58 in GC cells through m6A methylation regulation.H3K27ac modification plays an important role in HSPA4 overexpression in GC tissues.
item3693	REG00013	M6ATAR01536	Up	M6ADIS0061	.	39616247	"CTCF interacts with HNRNPU through a FLG-AS1-dependent mechanism, facilitating the recruitment of EP300 and activation of the m6A reader IGF2BP2. This activation promotes histone lactylation at the promoter region of IGF2BP2 stimulating the proliferation of PDAC cells. IGF2BP2 enhanced the mRNA stability of CSF1 and MYC."
item3694	REG00013	M6ATAR00341	Up	M6ADIS0061	.	39616247	"CTCF interacts with HNRNPU through a FLG-AS1-dependent mechanism, facilitating the recruitment of EP300 and activation of the m6A reader IGF2BP2. This activation promotes histone lactylation at the promoter region of IGF2BP2 stimulating the proliferation of PDAC cells. IGF2BP2 enhanced the mRNA stability of CSF1 and MYC."
item3695	REG00007	M6ATAR00388	Up	M6ADIS0107	.	39903889	"LDHA-induced H3K18lac promoted NAFLD progression, where LDHA-induced H3K18lac in METTL3 promoter elevated METTL3 expression, thereby promoting m6A methylation and stabilizing SCD1 via a YTHDF1-dependent manner. Keywords: Nonalcoholic fatty liver disease, LDHA, METTL3, YTHDF1, Histone lactylation."
item3696	REG00024	M6ATAR00388	Up	M6ADIS0107	.	39903889	"LDHA-induced H3K18lac promoted NAFLD progression, where LDHA-induced H3K18lac in METTL3 promoter elevated METTL3 expression, thereby promoting m6A methylation and stabilizing SCD1 via a YTHDF1-dependent manner. Keywords: Nonalcoholic fatty liver disease, LDHA, METTL3, YTHDF1, Histone lactylation."
item3697	REG00022	M6ATAR00140	Up	M6ADIS0006	.	39725144	"Histone lactylation in HCC induces increased expression of YTHDC1, increasing the stability of m6A-modified NEAT1. The histone acetyltransferase p300 is then recruited by NEAT1 and activates SCD by increasing the level of histone acetylation at the SCD promoter, thus facilitating HCC progression via hepatocellular lipid metabolism remodeling. Taken together, these discoveries suggest a close link between the epigenetic machinery and lipid metabolic abnormalities, which promotes cancer progression."
item3698	REG00022	M6ATAR00140	Up	M6ADIS0006	.	39725144	"Histone lactylation in HCC induces increased expression of YTHDC1, increasing the stability of m6A-modified NEAT1. The histone acetyltransferase p300 is then recruited by NEAT1 and activates SCD by increasing the level of histone acetylation at the SCD promoter, thus facilitating HCC progression via hepatocellular lipid metabolism remodeling. Taken together, these discoveries suggest a close link between the epigenetic machinery and lipid metabolic abnormalities, which promotes cancer progression.YTHDC1 enhances NEAT1 stability, tethering p300, and increasing H3K27ac level at SCD promoter."
item3699	REG00025	M6ATAR01622	Up	M6ADIS0342	.	40022822	H3K18la -regulated YTHDF3 is involved in SEV-induced microglial pyroptosis.YTHDF3 stabilizes PRDX3 mRNA through m6A modification.H3K18la regulates YTHDF3/PRDX3 mediated pyroptosis to mitigating SEV-induced cognitive dysfunction in neonatal mice.
item3700	REG00006	M6ATAR00451	Down	M6ADIS0184	.	39563370	"The loss of METTL14 expression results from lysine-specific demethylase 1 (LSD1)-mediated removal of histone H3 lysine 4 methylation at the promoter region, which is critical for LSD1-driven stemness in TNBC."
item3701	REG00008	M6ATAR00451	Down	M6ADIS0184	.	39563370	"The loss of METTL14 expression results from lysine-specific demethylase 1 (LSD1)-mediated removal of histone H3 lysine 4 methylation at the promoter region, which is critical for LSD1-driven stemness in TNBC."
item3702	REG00007	M6ATAR00140	Up	.	.	39362776	The genome-protective role of NEAT1 is mediated by the RNA methyltransferase 3 (METTL3) and involves the release of the chromodomain helicase DNA binding protein 4 (CHD4) from NEAT1 to fine-tune histone acetylation at DSBs. Our data suggest a direct role for NEAT1 in DDR.
item3703	REG00007	.	.	M6ADIS0374	.	39109795	"H3K36 methylation plays an important role in HSCR, confirming that the methyltransferase SMYD2 can affect m6A methylation levels and intestinal nervous system development by regulating METTL3 expression."
item3704	REG00007	M6ATAR00197	Down	.	.	38773376	"CAT upregulated NRF1, NRF1 activated METTL3 via KAT2A transcription, and METTL3 inhibited Beclin-1 via m6A modification."
item3705	REG00007	M6ATAR01624	Up	.	.	37963393	Mettl3 determines endocrine lineage by modulating Hdac1 activity during the transition of bipotent progenitors might help in the development of targeted endocrine cell protocols for diabetes treatment.
item3706	REG00052	M6ATAR01625	Down	.	.	40068772	"METTL7B suppressed the expression of USP38 via m6A dependent mRNA degradation, resulting in increasing ubiquitylation of HDAC3, which is a proven histone lysine delactylases."
item3707	REG00052	M6ATAR01625	Down	.	.	40068772	"METTL7B suppressed the expression of USP38 via m6A dependent mRNA degradation, resulting in increasing ubiquitylation of HDAC3, which is a proven histone lysine delactylases."
item3708	REG00007	M6ATAR01610	Down	M6ADIS0007	.	38943137	"METTL3 regulates the expression of KAT2A, a histone acetyltransferase, by methylating the m6A site in the 3'UTR of KAT2A mRNA in NSCLC cells. Intriguingly, NFIC was also found to negatively regulate the expression of KAT2A by directly binding to its promoter region."
item3709	REG00007	M6ATAR01626	Up	.	.	39535388	"Depletion of METTL3-mediated m6A modification leads to abnormally elongated cilia via suppressing HDAC6-dependent deacetylation of axonemal alpha-tubulin, ultimately attenuating cell growth and cervical cancer development."
item3710	REG00007	M6ATAR00360	.	M6ADIS0125	.	37858336	"G9a promotes m6A methyltransferase activity of METTL3 at translational/post-translational level by regulating its expression, its methylation, and its cytosolic localization during ET."
item3711	REG00007	M6ATAR01369	.	M6ADIS0125	.	37858336	"G9a promotes m6A methyltransferase activity of METTL3 at translational/post-translational level by regulating its expression, its methylation, and its cytosolic localization during ET."
item3712	REG00007	M6ATAR01282	.	M6ADIS0125	.	37858336	"G9a promotes m6A methyltransferase activity of METTL3 at translational/post-translational level by regulating its expression, its methylation, and its cytosolic localization during ET."
item3713	REG00006	M6ATAR01628	Up	M6ADIS0054	.	39021049	"METTL14 catalysed m6A modification on ANKRD22 messenger ribonucleic acid (mRNA), recognized by the reader IGF2BP2, leading to increased mRNA stability and higher translational efficiency.our findings highlighted elevated ANKRD22-mediated histone H3 lysine 27 acetylation (H3K27AC) signals near the METTL14 promoter, which contributes to a positive feedback loop perpetuating malignant progression in NPC."
item3714	REG00013	M6ATAR01628	Up	M6ADIS0054	.	39021049	"METTL14 catalysed m6A modification on ANKRD22 messenger ribonucleic acid (mRNA), recognized by the reader IGF2BP2, leading to increased mRNA stability and higher translational efficiency.our findings highlighted elevated ANKRD22-mediated histone H3 lysine 27 acetylation (H3K27AC) signals near the METTL14 promoter, which contributes to a positive feedback loop perpetuating malignant progression in NPC."
item3715	REG00005	M6ATAR00605	Down	.	.	39900266	"G6PT deficiency induces intracellular lactate accumulation, which enhances histone H3K18 lactylation and upregulates ALKBH5 expression; ALKBH5 demethylates m6A modification on NLRP3 mRNA, leading to NLRP3 mRNA degradation and diminished inflammasome activation."
item3716	REG00006	M6ATAR01629	Down	M6ADIS0007	.	40011892	"JMJD6 affects METTL14 expression in an arginine demethylase dependent manner, and mediates m6A modification of SLC3A2 to regulate its expression level, thereby affecting the sensitivity of lung cancer cells to ferroptosis."
item3717	REG00006	M6ATAR01630	Down	M6ADIS0057	.	39497511	"Histone H3 lactylation at Lys18 was found to upregulate METTL14 expression. In conclusion, METTL14 knockdown promotes stemness in GC by mediating m6A modification of ATF5 mRNA, which activates the WDR74/beta-catenin axis, making METTL14 a potential therapeutic target for gastric cancer treatment."
item3718	REG00020	.	.	M6ADIS0007	.	40135634	"Lactate uptake mediated by Monocarboxylate transporter 1 (MCT1) is essential for RBM15 induction. Subsequent investigations revealed that L-lactate promotes lactylation of RBM15 majorly at Lys850 (K850), while histone deacetylase 3 (HDAC3) acts as the delactylase for RBM15. Importantly, lactylation of RBM15 stabilizes itself by inhibiting proteasome-mediated ubiquitin degradation. Mutation of the lactylation site K850R disrupts the association between RBM15 and METTL3, leading to a reduction in global m6A levels. Moreover, K850R significantly abrogated RBM15-mediated cell proliferation and migration in LUAD cells. Collectively, these findings unveil lactylation as a novel regulatory mechanism affecting both stability and m6A methylation activity of RBM15 in LUAD cells."
item3719	REG00005	M6ATAR00399	Down	M6ADIS0017	.	38938016	"KDM4C decreases H3K9me3 methylation to upregulate ALKBH5 and subsequently inhibits snail1, ultimately impeding liver fibrosis."
item3720	REG00007	M6ATAR01632	Down	M6ADIS0168	.	39572532	KMT2A regulates the autophagy-GATA4 axis through METTL3-mediated m6A modification of ATG4a to promote NPCs senescence and IVDD progression.
item3721	REG00008	M6ATAR01632	Down	M6ADIS0168	.	39572532	KMT2A regulates the autophagy-GATA4 axis through METTL3-mediated m6A modification of ATG4a to promote NPCs senescence and IVDD progression.
item3722	REG00022	M6ATAR01633	Up	M6ADIS0348	.	39501105	YTHDC1 is a therapeutic target for B-cell acute lymphoblastic leukemia by attenuating DNA damage response through the KMT2C-H3K4me1/me3 epigenetic axis.
item3723	REG00022	M6ATAR01633	Up	M6ADIS0348	.	39501105	YTHDC1 is a therapeutic target for B-cell acute lymphoblastic leukemia by attenuating DNA damage response through the KMT2C-H3K4me1/me3 epigenetic axis.
item3724	REG00008	M6ATAR01634	Down	M6ADIS0107	.	39107881	YTHDF2-mediated degradation of m6A-modified circ-SLC9A6 was found to be essential for the regulation of SLC9A6-126aa expression.
item3725	REG00007	M6ATAR01635	Down	.	.	39934221	"Mettl3 deletion in the endometrium alters mRNA m6A methylation via Eed interaction. This reduces m6A recognized by Ythdc1, which recruits Eed to suppress H3K27me3 modification co-transcriptionally. The reduction of H3K27me3 disrupts chromatin accessibility and impairs transcription of genes critical for endometrial receptivity. Collectively, these results shed light on a Mettl3-Eed-m6A-Ythdc1 axis that links m6A and histone modification in regulating local chromatin state and gene expression, advancing our understanding of the epigenetic crosstalk between RNA and DNA modification in infertility disease."
item3726	REG00007	.	.	M6ADIS0042	M6ADRUG0216	37456679	"METTL3 interacts with RNA polymerase II and active histone modifications such as H3K9ac, H3K27ac, and H3K36me3 to maintain the expression of proteasome-related genes."
item3727	REG00007	.	.	M6ADIS0042	M6ADRUG0216	37456679	"METTL3 interacts with RNA polymerase II and active histone modifications such as H3K9ac, H3K27ac, and H3K36me3 to maintain the expression of proteasome-related genes."
item3728	REG00007	.	.	M6ADIS0042	M6ADRUG0216	37456679	"METTL3 interacts with RNA polymerase II and active histone modifications such as H3K9ac, H3K27ac, and H3K36me3 to maintain the expression of proteasome-related genes."
item3729	REG00007	M6ATAR00578	.	M6ADIS0008	.	35987795	"The transcription factor ETS1 recruited P300 and WDR5 which separately mediated H3K27ac and H3K4me3 histone modification in the promoter of METTL3 and induced METTL3 transcription activation. Furthermore, we identified TXNDC5 as a target of METTL3-mediated m6A modification through MeRIP-seq, and revealed that METTL3-mediated TXNDC5 expression relied on the m6A reader-dependent manner."
item3730	REG00007	M6ATAR00578	.	M6ADIS0008	.	35987795	"The transcription factor ETS1 recruited P300 and WDR5 which separately mediated H3K27ac and H3K4me3 histone modification in the promoter of METTL3 and induced METTL3 transcription activation. Furthermore, we identified TXNDC5 as a target of METTL3-mediated m6A modification through MeRIP-seq, and revealed that METTL3-mediated TXNDC5 expression relied on the m6A reader-dependent manner."
item3731	REG00008	M6ATAR00578	.	M6ADIS0008	.	35987795	"The transcription factor ETS1 recruited P300 and WDR5 which separately mediated H3K27ac and H3K4me3 histone modification in the promoter of METTL3 and induced METTL3 transcription activation. Furthermore, we identified TXNDC5 as a target of METTL3-mediated m6A modification through MeRIP-seq, and revealed that METTL3-mediated TXNDC5 expression relied on the m6A reader-dependent manner."
item3732	REG00008	M6ATAR00578	.	M6ADIS0008	.	35987795	"The transcription factor ETS1 recruited P300 and WDR5 which separately mediated H3K27ac and H3K4me3 histone modification in the promoter of METTL3 and induced METTL3 transcription activation. Furthermore, we identified TXNDC5 as a target of METTL3-mediated m6A modification through MeRIP-seq, and revealed that METTL3-mediated TXNDC5 expression relied on the m6A reader-dependent manner."
item3733	REG00022	M6ATAR01635	Down	.	.	39934221	"Mettl3 deletion in the endometrium alters mRNA m6A methylation via Eed interaction. This reduces m6A recognized by Ythdc1, which recruits Eed to suppress H3K27me3 modification co-transcriptionally. The reduction of H3K27me3 disrupts chromatin accessibility and impairs transcription of genes critical for endometrial receptivity. Collectively, these results shed light on a Mettl3-Eed-m6A-Ythdc1 axis that links m6A and histone modification in regulating local chromatin state and gene expression, advancing our understanding of the epigenetic crosstalk between RNA and DNA modification in infertility disease."
item3734	REG00001	M6ATAR01460	Down	M6ADIS0094	.	39410722	"FTO deletion and METTL16 overexpression significantly increased m6A levels. This led to the downregulation of the methyltransferase SUV39H1, resulting in reduced H3K9me3 expression."
item3735	REG00017	M6ATAR01460	Up	M6ADIS0094	.	39410722	"FTO deletion and METTL16 overexpression significantly increased m6A levels. This led to the downregulation of the methyltransferase SUV39H1, resulting in reduced H3K9me3 expression."
item3736	REG00007	M6ATAR00637	Down	.	.	36375665	"TET1 knockdown contributed to the binding of H3K4me3 and H3K27me3 to METTL3 DNA. Our results revealed a negative feedback regulatory loop between TET1 and METTL3 in myoblast differentiation, which unveiled the interplay among DNA methylation, RNA methylation and histone methylation in skeletal myogenesis."
item3737	REG00007	M6ATAR00637	Down	.	.	36375665	"TET1 knockdown contributed to the binding of H3K4me3 and H3K27me3 to METTL3 DNA. Our results revealed a negative feedback regulatory loop between TET1 and METTL3 in myoblast differentiation, which unveiled the interplay among DNA methylation, RNA methylation and histone methylation in skeletal myogenesis."
item3738	REG00008	M6ATAR00637	Down	.	.	36375665	"TET1 knockdown contributed to the binding of H3K4me3 and H3K27me3 to METTL3 DNA. Our results revealed a negative feedback regulatory loop between TET1 and METTL3 in myoblast differentiation, which unveiled the interplay among DNA methylation, RNA methylation and histone methylation in skeletal myogenesis."
item3739	REG00008	M6ATAR00637	Down	.	.	36375665	"TET1 knockdown contributed to the binding of H3K4me3 and H3K27me3 to METTL3 DNA. Our results revealed a negative feedback regulatory loop between TET1 and METTL3 in myoblast differentiation, which unveiled the interplay among DNA methylation, RNA methylation and histone methylation in skeletal myogenesis."
item3740	REG00025	M6ATAR01636	Down	M6ADIS0054	.	36310139	"The m6A-modified CBX1 mRNA transcript is recognized and destabilized by the m6A reader YTHDF3. Furthermore, it is revealed that CBX1 promotes NPC cell migration, invasion, and proliferation through transcriptional repression of MAP7 via H3K9me3-mediated heterochromatin formation."
item3741	REG00018	.	.	.	.	36111643	"Inhibition of METTL5 reduced the activity of phosphorylated ribosomal protein S6, decreased the levels of the repressive histone modification H3K27me3 and increased the expression of activating histone modifications H3K27ac and H3K4me3 and mRNA levels of some 2-cell-specific genes."
item3742	REG00018	.	.	.	.	36111643	"Inhibition of METTL5 reduced the activity of phosphorylated ribosomal protein S6, decreased the levels of the repressive histone modification H3K27me3 and increased the expression of activating histone modifications H3K27ac and H3K4me3 and mRNA levels of some 2-cell-specific genes."
item3743	REG00018	.	.	.	.	36111643	"Inhibition of METTL5 reduced the activity of phosphorylated ribosomal protein S6, decreased the levels of the repressive histone modification H3K27me3 and increased the expression of activating histone modifications H3K27ac and H3K4me3 and mRNA levels of some 2-cell-specific genes."
item3744	REG00009	M6ATAR01637	Up	M6ADIS0010	.	39433619	"WTAP act as an N6-methyladenosine transferase to regulate the m6A modification of long noncoding RNA TEX41. Then, the upregulated m6A modification destabilized TEX41 in a YTHDF2-dependent manner. Furthermore, TEX41 interacted with the SUZ12 protein and increased the histone methyltransferase activity of SUZ12, resulting in HDAC1 silencing."
item3745	REG00008	M6ATAR01637	Up	M6ADIS0010	.	39433619	"WTAP act as an N6-methyladenosine transferase to regulate the m6A modification of long noncoding RNA TEX41. Then, the upregulated m6A modification destabilized TEX41 in a YTHDF2-dependent manner. Furthermore, TEX41 interacted with the SUZ12 protein and increased the histone methyltransferase activity of SUZ12, resulting in HDAC1 silencing."
item3746	REG00001	M6ATAR00976	Up	M6ADIS0061	.	38789418	FTO-mediated KDM5B stabilization in the context of loss of Smad4 activate DLG1/YAP1 pathway to promote tumorigenesis by reprogramming lipid accumulation in PDAC.
item3747	REG00001	M6ATAR00976	Up	M6ADIS0061	.	38789418	FTO-mediated KDM5B stabilization in the context of loss of Smad4 activate DLG1/YAP1 pathway to promote tumorigenesis by reprogramming lipid accumulation in PDAC.
item3748	REG00005	M6ATAR01638	Up	M6ADIS0006	.	34112124	"Mechanically, the highly expressed ALKBH5 is induced by HBx-mediated H3K4me3 modification of ALKBH5 gene promoter in a WDR5-dependent manner after HBV infection. The increased ALKBH5 protein catalyzes the m6A demethylation of HBx mRNA, thus stabilizing and favoring a higher HBx expression level."
item3749	REG00005	M6ATAR01011	Up	M6ADIS0046	.	39465506	"ALKBH5 removed m6A modification to stabilize TUG1 expression in a YTHDF2-dependent manner, enhancing H3K9me2 levels on the SH3BGRL promoter and suppressing SH3BGRL expression, thus promoting ADR resistance in AML cells."
item3750	REG00008	M6ATAR01011	Down	M6ADIS0046	.	39465506	"ALKBH5 removed m6A modification to stabilize TUG1 expression in a YTHDF2-dependent manner, enhancing H3K9me2 levels on the SH3BGRL promoter and suppressing SH3BGRL expression, thus promoting ADR resistance in AML cells."
item3751	REG00023	M6ATAR00990	Up	M6ADIS0182	.	36753389	"METTL3 promoted the expression of absent, small, or homeotic-like 1 (ASH1L) via enhancing its stability in a YT521-B homology domain containing 2 (YTHDC2)-dependent manner, which further decreased the expression of IL-17 and IL-23 receptor (IL-23R), resulting in reduced pathogenic Th17 responses."
item3752	REG00006	M6ATAR01639	Up	M6ADIS0091	.	39448421	"METTL14 induced HDAC3 m6A modification in an IGF2BP3-dependent manner, and could activate cGAS-STING pathway through HDAC3."
item3753	REG00014	M6ATAR01639	Up	M6ADIS0091	.	39448421	"METTL14 induced HDAC3 m6A modification in an IGF2BP3-dependent manner, and could activate cGAS-STING pathway through HDAC3."
item3754	REG00007	M6ATAR01640	Up	M6ADIS0117	.	35354439	METTL3 promoted m6A modification of NDS2 mRNA and enhanced its stability by YTHDF1. METTL3 overexpression alleviated renal impairment and fibrosis in vivo and in vitro. But the protective role was blocked upon NSD2 silencing.
item3755	REG00024	M6ATAR01640	Up	M6ADIS0117	.	35354439	METTL3 promoted m6A modification of NDS2 mRNA and enhanced its stability by YTHDF1. METTL3 overexpression alleviated renal impairment and fibrosis in vivo and in vitro. But the protective role was blocked upon NSD2 silencing.
item3756	REG00007	M6ATAR01640	Up	M6ADIS0117	.	35354439	METTL3 promoted m6A modification of NDS2 mRNA and enhanced its stability by YTHDF1. METTL3 overexpression alleviated renal impairment and fibrosis in vivo and in vitro. But the protective role was blocked upon NSD2 silencing.
item3757	REG00024	M6ATAR01640	Up	M6ADIS0117	.	35354439	METTL3 promoted m6A modification of NDS2 mRNA and enhanced its stability by YTHDF1. METTL3 overexpression alleviated renal impairment and fibrosis in vivo and in vitro. But the protective role was blocked upon NSD2 silencing.
item3758	REG00020	M6ATAR01641	Down	M6ADIS0311	.	39709463	"MLL1 elevated RBM15 expression by increasing H3K4me3 on RBM15 promoter. RBM15 promoted the binding of TRIM72 to YTHDF2 by enhancing m6A modification on TRIM72 mRNA, thereby repressing TRIM72 expression. TRIM72 bound to ADAM9 and ubiquitinated it for degradation."
item3759	REG00008	M6ATAR01641	Down	M6ADIS0311	.	39709463	"MLL1 elevated RBM15 expression by increasing H3K4me3 on RBM15 promoter. RBM15 promoted the binding of TRIM72 to YTHDF2 by enhancing m6A modification on TRIM72 mRNA, thereby repressing TRIM72 expression. TRIM72 bound to ADAM9 and ubiquitinated it for degradation."
item3760	REG00024	M6ATAR01146	Up	.	M6ADRUG0217	39581460	"The metabolite beta-hydroxybutyrate (BHBA) secreted after acute exercise upregulates m6A modification in WAT. This enhances m6A-dependent translation of the histone acetyltransferase CREBBP, promoting the transcription of key beiging genes by increasing chromatin accessibility."
item3761	REG00008	M6ATAR01146	Up	.	M6ADRUG0217	39581460	"The metabolite beta-hydroxybutyrate (BHBA) secreted after acute exercise upregulates m6A modification in WAT. This enhances m6A-dependent translation of the histone acetyltransferase CREBBP, promoting the transcription of key beiging genes by increasing chromatin accessibility."
item3762	REG00024	M6ATAR01642	Down	.	.	37991435	"YTHDF1, the N6-methyladenine (m6A) RNA reader that was previously known to be mainly cytoplasmic, associates with RNF2, a PRC1 protein that mediates H2AK119ub in human embryonic stem cells (hESCs)."
item3763	REG00008	M6ATAR00375	Down	M6ADIS0001	.	33363140	Histone methyltransferase EZH2 inhibited miR-454-3p through methylation modification and promoted m6A modification of PTEN to induce glioma M2 macrophage polarization.miR-454-3p promoted PTEN expression by inhibiting m6A modification through binding to the enzyme YTHDF2.
item3764	REG00009	M6ATAR01643	Up	M6ADIS0307	.	40038518	"Knockdown of PHF19 precipitates loss of H3K27 trimethylation and enhanced chromatin accessibility, ultimately resulting in upregulated expression of genes involved in the cell cycle and DNA damage checkpoints. Therefore, WTAP/m6A-dependent PHF19 upregulation accelerates leukemia progression by coordinating m6A modification and histone methylation, establishing its status as a novel therapeutic target for t(8;21) AML."
item3765	REG00007	M6ATAR01644	Up	M6ADIS0310	.	40221424	"Histone H3K9 lactylation in the promoter region of the N6-methyladenosine (m6A) writer METTL3 was enriched to enhance METTL3 transcription, leading to the lnc668 m6A modification. Meanwhile, the m6A reader YTHDC1 recognized m6A-modified lnc668 and elevated the METTL3-mediated lnc668 modification."
item3766	REG00022	M6ATAR01644	Up	M6ADIS0310	.	40221424	"Histone H3K9 lactylation in the promoter region of the N6-methyladenosine (m6A) writer METTL3 was enriched to enhance METTL3 transcription, leading to the lnc668 m6A modification. Meanwhile, the m6A reader YTHDC1 recognized m6A-modified lnc668 and elevated the METTL3-mediated lnc668 modification."
item3767	REG00009	M6ATAR00939	Up	M6ADIS0307	.	38660840	"In t(8;21) AML cell lines, WTAP could regulate the expression of KDM4B by regulating the m6A modification of the 3'UTR of KDM4B mRNA, and silencing the expression of KDM4B could inhibit the cellular proliferation in vitro."
item3768	REG00006	M6ATAR01277	Up	.	.	39757292	"PHF20 elevated METTL14 expression by enhancing the enrichment of H3K4me3 on its promoter, and METTL14 strengthened HOXA13 m6A methylation to maintain HOXA13 mRNA stability through IGF2BP3. In conclusion, PHF20 elevates METTL14 expression by enhancing H3K4me3 enrichment on its promoter and enhances HOXA13 mRNA stability via IGF2BP3-mediated m6A modification, thus facilitating HOXA13 expression and eventually inducing osteogenic differentiation of BMSCs."
item3769	REG00014	M6ATAR01277	Up	.	.	39757292	"PHF20 elevated METTL14 expression by enhancing the enrichment of H3K4me3 on its promoter, and METTL14 strengthened HOXA13 m6A methylation to maintain HOXA13 mRNA stability through IGF2BP3. In conclusion, PHF20 elevates METTL14 expression by enhancing H3K4me3 enrichment on its promoter and enhances HOXA13 mRNA stability via IGF2BP3-mediated m6A modification, thus facilitating HOXA13 expression and eventually inducing osteogenic differentiation of BMSCs."
item3770	REG00008	M6ATAR00669	Down	M6ADIS0161	.	32670741	"Peripheral nerve injury increases the expression of the m6A demethylase fat-mass and obesity-associated proteins (FTO) in the injured DRG via the activation of Runx1, a transcription factor that binds to the Fto gene promoter. Mimicking this increase erases m6A in euchromatic histone lysine methyltransferase 2 (Ehmt2) mRNA (encoding the histone methyltransferase G9a) and elevates the level of G9a in DRG and leads to neuropathic pain symptoms. Conversely, blocking this increase reverses a loss of m6A sites in Ehmt2 mRNA and destabilizes the nerve injury-induced G9a upregulation in the injured DRG and alleviates nerve injury-associated pain hypersensitivities. FTO contributes to neuropathic pain likely through stabilizing nerve injury-induced upregulation of G9a, a neuropathic pain initiator, in primary sensory neurons."
item3771	REG00007	M6ATAR01646	Up	M6ADIS0072	.	40252822	"PIR expression is driven by aberrant N6-methyladenosine (m6A) modifications mediated by METTL3 and IGF2BP3. Meanwhile, the high expressed PIR acts as a transcriptional co-regulator by interacting with WDR5, resulting in the regulation of H3K4me3 modifications at the ANAPC10 promoter region and subsequent promotion of ANAPC10 expression."
item3772	REG00014	M6ATAR01646	Up	M6ADIS0072	.	40252822	"PIR expression is driven by aberrant N6-methyladenosine (m6A) modifications mediated by METTL3 and IGF2BP3. Meanwhile, the high expressed PIR acts as a transcriptional co-regulator by interacting with WDR5, resulting in the regulation of H3K4me3 modifications at the ANAPC10 promoter region and subsequent promotion of ANAPC10 expression."
item3773	REG00005	M6ATAR00592	Down	M6ADIS0311	.	34995009	"Inhibition of ALKBH5 promotes KDM3B-mediated ALCAM demethylation by facilitating PPARG mRNA m6A modification, and further activates the Wnt/beta-catenin pathway, and in turn alleviates PE progression.PPARG repressed the H3K9me2 levels at activated leukocyte cell adhesion molecule (ALCAM) promoter region by increasing the expression and activity of lysine demethylase 3B (KDM3B)."
item3774	REG00008	M6ATAR00260	Down	M6ADIS0168	.	39625652	"ROS exposure activated YTHDF2 and promoted the degradation of m6A-modified FOXO3 mRNA, impairing FOXO3's ability to activate TIMP1.FOXO3 recruited histone acetyltransferase CBP (CREB binding protein) and mediator complex subunit 1 (Med1) to activate TIMP1 expression, which inhibited MMP activity and prevented disc degeneration."
item3775	REG00007	M6ATAR01264	Down	.	.	39800682	METTL3 induced H3K27 trimethylation of the SLC7A11 promoter by suppressing the mRNA stability of H3K27 demethylases KDM6B.
item3776	REG00008	M6ATAR01264	Down	.	.	39800682	METTL3 induced H3K27 trimethylation of the SLC7A11 promoter by suppressing the mRNA stability of H3K27 demethylases KDM6B.
item3777	REG00006	.	Down	.	.	40183255	H3K27-me3 Inhibition Induces YTHDF2-Mediated Decay of m6A-Marked Severe Acute Respiratory Syndrome Coronavirus 2 Transcripts.
item3778	REG00006	.	Down	.	.	40183255	H3K27-me3 Inhibition Induces YTHDF2-Mediated Decay of m6A-Marked Severe Acute Respiratory Syndrome Coronavirus 2 Transcripts.
item3779	REG00006	.	Down	.	.	40183255	H3K27-me3 Inhibition Induces YTHDF2-Mediated Decay of m6A-Marked Severe Acute Respiratory Syndrome Coronavirus 2 Transcripts.
item3780	REG00006	.	Down	.	.	40183255	H3K27-me3 Inhibition Induces YTHDF2-Mediated Decay of m6A-Marked Severe Acute Respiratory Syndrome Coronavirus 2 Transcripts.
item3781	REG00008	.	Down	.	.	40183255	H3K27-me3 Inhibition Induces YTHDF2-Mediated Decay of m6A-Marked Severe Acute Respiratory Syndrome Coronavirus 2 Transcripts.
item3782	REG00008	.	Down	.	.	40183255	H3K27-me3 Inhibition Induces YTHDF2-Mediated Decay of m6A-Marked Severe Acute Respiratory Syndrome Coronavirus 2 Transcripts.
item3783	REG00008	.	Down	.	.	40183255	H3K27-me3 Inhibition Induces YTHDF2-Mediated Decay of m6A-Marked Severe Acute Respiratory Syndrome Coronavirus 2 Transcripts.
item3784	REG00008	.	Down	.	.	40183255	H3K27-me3 Inhibition Induces YTHDF2-Mediated Decay of m6A-Marked Severe Acute Respiratory Syndrome Coronavirus 2 Transcripts.
item3785	REG00023	M6ATAR01647	Up	M6ADIS0006	.	39649245	"NUTM2B-AS1 specifically binds to BMPR1A promoter. m6A-methylated NUTM2B-AS1 is recognized by the m6A reader YTHDC2, which further binds to the H3K4 METTL3 and METTL16 induce m6A hypermethylation of NUTM2B-AS1. methyltransferase MLL1. m6A-methylated NUTM2B-AS1 recruits YTHDC2 and MLL1 to BMPR1A promoter, leading to increased H3K4me3 and chromatin accessibility at BMPR1A promoter. Functional rescue assays suggest that BMPR1A is a critical mediator of the oncogenic role of m6A-methylated NUTM2B-AS1 in HCC."
item3786	REG00007	M6ATAR01647	Up	M6ADIS0006	.	39649245	"NUTM2B-AS1 specifically binds to BMPR1A promoter. m6A-methylated NUTM2B-AS1 is recognized by the m6A reader YTHDC2, which further binds to the H3K4 METTL3 and METTL16 induce m6A hypermethylation of NUTM2B-AS1. methyltransferase MLL1. m6A-methylated NUTM2B-AS1 recruits YTHDC2 and MLL1 to BMPR1A promoter, leading to increased H3K4me3 and chromatin accessibility at BMPR1A promoter. Functional rescue assays suggest that BMPR1A is a critical mediator of the oncogenic role of m6A-methylated NUTM2B-AS1 in HCC."
item3787	REG00017	M6ATAR01647	Up	M6ADIS0006	.	39649245	"NUTM2B-AS1 specifically binds to BMPR1A promoter. m6A-methylated NUTM2B-AS1 is recognized by the m6A reader YTHDC2, which further binds to the H3K4 METTL3 and METTL16 induce m6A hypermethylation of NUTM2B-AS1. methyltransferase MLL1. m6A-methylated NUTM2B-AS1 recruits YTHDC2 and MLL1 to BMPR1A promoter, leading to increased H3K4me3 and chromatin accessibility at BMPR1A promoter. Functional rescue assays suggest that BMPR1A is a critical mediator of the oncogenic role of m6A-methylated NUTM2B-AS1 in HCC."
item3788	REG00008	M6ATAR00341	Up	M6ADIS0001	.	33363140	Histone methyltransferase EZH2 inhibited miR-454-3p through methylation modification and promoted m6A modification of PTEN to induce glioma M2 macrophage polarization.miR-454-3p promoted PTEN expression by inhibiting m6A modification through binding to the enzyme YTHDF2.
item3789	REG00008	M6ATAR00731	Down	M6ADIS0001	.	33363140	Histone methyltransferase EZH2 inhibited miR-454-3p through methylation modification and promoted m6A modification of PTEN to induce glioma M2 macrophage polarization.miR-454-3p promoted PTEN expression by inhibiting m6A modification through binding to the enzyme YTHDF2.
item3790	REG00008	M6ATAR00054	Up	M6ADIS0001	.	33363140	Histone methyltransferase EZH2 inhibited miR-454-3p through methylation modification and promoted m6A modification of PTEN to induce glioma M2 macrophage polarization.miR-454-3p promoted PTEN expression by inhibiting m6A modification through binding to the enzyme YTHDF2.
item3791	REG00002	M6ATAR01280	Up	M6ADIS0057	.	34195070	SNHG12 reduced the overall survival of GC patients and promoted GC tumorigenesis by activating the AKT/GSK-3beta pathway and binding with the RNA binding protein ELAVL1 (also known as HuR) and stabilizing YWHAZ expression.
item3792	REG00002	M6ATAR00211	Up	M6ADIS0006	.	34558987	"VPS9D1-AS1 silencing suppressed HCC tumor growth in vivo. Mechanistically, VPS9D1-AS1 was able to bind to the HuR protein and thereby influence the stability and expression of the CDK4 mRNA, thus impacting HCC cell proliferation. The VPS9D1-AS1/HuR/CDK4 signaling axis regulates HCC tumor cell oncogenic activity, highlighting this pathway as a promising therapeutic target."
item3793	REG00012	M6ATAR00341	Up	M6ADIS0061	.	33122827	Epigenetic silencing of LncRNA LINC00261 promotes c-myc-mediated aerobic glycolysis by regulating miR-222-3p/HIPK2/ERK axis and sequestering IGF2BP1.
item3794	REG00014	M6ATAR00671	Up	M6ADIS0006	.	31656043	LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in hepatocellular carcinoma.
item3795	REG00014	M6ATAR01679	Up	M6ADIS0001	M6ADRUG0010	34657141	IGF2BP3 interacted with RMRP and ZNRF3 mRNA. IGF2BP3 knockdown weakened the interaction of Argonaute 2 (Ago2) and ZNRF3. RMRP reduced ZNRF3 expression and mRNA stability by IGF2BP3. A positive feedback loop of lncRNA-RMRP/ZNRF3 axis and Wnt/beta-catenin signaling regulates the progression and temozolomide resistance in glioma.
item3796	REG00012	M6ATAR00341	Up	M6ADIS0006	.	33387362	Long noncoding RNA NBAT1 suppresses hepatocellular carcinoma progression via competitively associating with IGF2BP1 and decreasing c-Myc expression.
item3797	REG00003	M6ATAR00303	Up	M6ADIS0055	.	32549791	Knockdown of LINC00662 represses AK4 and attenuates radioresistance of oral squamous cell carcinoma.LINC00662 modulated the radiosensitivity of OSCC cells via hnRNPC-modulated AK4.
item3798	REG00013	M6ATAR01620	Up	M6ADIS0056	.	34022433	Linc01305 promotes metastasis and proliferation of esophageal squamous cell carcinoma through interacting with IGF2BP2 and IGF2BP3 to stabilize HTR3A mRNA.
item3799	REG00014	M6ATAR01620	Up	M6ADIS0056	.	34022433	Linc01305 promotes metastasis and proliferation of esophageal squamous cell carcinoma through interacting with IGF2BP2 and IGF2BP3 to stabilize HTR3A mRNA.
item3800	REG00003	.	.	.	.	23973260	MALAT-1 interacts with hnRNP C in cell cycle regulation.
item3801	REG00022	M6ATAR01681	Down	M6ADIS0091	.	39407279	METTL3 mediates m6A modification of lncRNA CRNDE to promote ATG10 expression and improve brain ischemia/reperfusion injury through YTHDC1.
item3802	REG00007	M6ATAR00675	.	M6ADIS0059	.	38838765	ABHD11-AS1 interacts with IGF2BP2 and affects CRC development through enhancing FOXM1 stability.
item3803	REG00013	M6ATAR00258	Up	M6ADIS0059	.	38838765	ABHD11-AS1 interacts with IGF2BP2 and affects CRC development through enhancing FOXM1 stability.
item3804	REG00007	M6ATAR01682	Down	.	.	25683224	"Overexpressing miRNAs significantly increased the amount of mRNAs associated with METTL3, whereas downregulating miRNA abundance by antagomirs significantly reduced METTL3 binding on mRNAs (i.e., DGCR2 and TUBB4B, targeted by miR-423-3p and miR-1226-3p, respectively) in HeLa cells ."
item3805	REG00007	M6ATAR01683	Down	.	.	25683224	"Overexpressing miRNAs significantly increased the amount of mRNAs associated with METTL3, whereas downregulating miRNA abundance by antagomirs significantly reduced METTL3 binding on mRNAs (i.e., DGCR2 and TUBB4B, targeted by miR-423-3p and miR-1226-3p, respectively) in HeLa cells ."
item3806	REG00007	M6ATAR01684	Down	.	.	25683224	"Consistently, the amounts of METTL3-crosslinked total RNAs (Figure 5I) and mRNAs (i.e., TCF4 and RPS13) targeted by designed miRNAs."
item3807	REG00007	M6ATAR01685	Down	.	.	25683224	"Consistently, the amounts of METTL3-crosslinked total RNAs (Figure 5I) and mRNAs (i.e., TCF4 and RPS13) targeted by designed miRNAs."
item3808	REG00007	M6ATAR00237	Up	M6ADIS0007	.	27856248	"MiR-33a suppresses proliferation of NSCLC cells via targeting METTL3 mRNA.miR-33a was able to depress the expression of EGFR, TAZ, MAPKAPK2 and DNMT3A at the level of protein."
item3809	REG00007	M6ATAR01160	Up	M6ADIS0007	.	27856248	"MiR-33a suppresses proliferation of NSCLC cells via targeting METTL3 mRNA.miR-33a was able to depress the expression of EGFR, TAZ, MAPKAPK2 and DNMT3A at the level of protein."
item3810	REG00007	M6ATAR01159	Up	M6ADIS0007	.	27856248	"MiR-33a suppresses proliferation of NSCLC cells via targeting METTL3 mRNA.miR-33a was able to depress the expression of EGFR, TAZ, MAPKAPK2 and DNMT3A at the level of protein."
item3811	REG00007	M6ATAR01491	Up	M6ADIS0007	.	27856248	"MiR-33a suppresses proliferation of NSCLC cells via targeting METTL3 mRNA.miR-33a was able to depress the expression of EGFR, TAZ, MAPKAPK2 and DNMT3A at the level of protein."
item3812	REG00009	.	.	M6ADIS0001	.	28212562	"Overexpression of miR-29a in GSCs inhibited expression of WTAP and suppressed both phosphoinositide 3-kinase/AKT and extracellular signal-related kinase pathways by downregulating QKI-6, thereby inhibiting cell proliferation, migration, and invasion but promoting apoptosis."
item3813	REG00012	M6ATAR00341	Up	.	.	32245947	"LINC00266-1 binds to IGF2BP1 and strengthens m6A recognition by IGF2BP1 on RNAs, such as c-Myc mRNA, to increase the mRNA stability and expression of c-Myc, thereby promoting tumorigenesis."
item3814	REG00005	M6ATAR01689	Up	M6ADIS0370	.	32387133	"Overexpressed circSTAG1 captured ALKBH5 and decreased the translocation of ALKBH5 into the nucleus, leading to increased m6A methylation of fatty acid amide hydrolase (FAAH) messenger RNA and degradation of FAAH in astrocytes with subsequent attenuation of depressive-like behaviors and astrocyte loss induced by corticosterone in vitro."
item3815	.	M6ATAR00451	.	M6ADIS0006	.	30361504	m6A modification in the YAP 3'UTR induced the interaction of miR-382-5p and led to the inhibition of YAP.circRNA_104075 stimulates YAP-dependent tumorigenesis through the regulation of HNF4a and may serve as a diagnostic marker in hepatocellular carcinoma.
item3816	REG00008	M6ATAR01691	Down	M6ADIS0223	.	38353178	MiR615-3p inhibited FBLN1 and osteogenic differentiation of umbilical cord mesenchymal stem cells by associated with YTHDF2 in a m6A-miRNA interaction manner.
item3817	REG00005	M6ATAR01692	Up	.	.	39311450	"Knockdown of ALKBH5 resulted in a significant increase in the m6A modification level of lnc-AK311120, accompanied by a downregulation in the expression level of lnc-AK311120.AK311120 interacted with the RNA-binding proteins DExH-Box helicase 9 (DHX9) and YTH domain containing 2 (YTHDC2) to form a ternary complex, while mitogen-activated protein kinase kinase 7 (MAP2K7) served as the shared downstream target gene of DHX9 and YTHDC2."
item3818	REG00023	M6ATAR01693	Up	.	.	39311450	"AK311120 interacted with the RNA-binding proteins DExH-Box helicase 9 (DHX9) and YTH domain containing 2 (YTHDC2) to form a ternary complex, while mitogen-activated protein kinase kinase 7 (MAP2K7) served as the shared downstream target gene of DHX9 and YTHDC2."
item3819	REG00013	M6ATAR00356	Up	M6ADIS0375	.	36384975	"Airn exerts anti-fibrotic effects by directly binding to insulin-like growth factor 2 mRNA-binding protein 2 (IMP2) and further prevents its ubiquitination-dependent degradation. Moreover, we revealed that Airn/IMP2 protected p53 mRNA from degradation in m6A manner, leading to CF cell cycle arrest and reduced cardiac fibrosis."
item3820	REG00007	M6ATAR01287	.	M6ADIS0057	.	39209141	"m6A-modified linc-OIP5 reduced DDX5 ubiquitination and enhanced DDX5 stability by binding to TRIM5, thereby promoting BC cell proliferation, migration and PTX resistance, and inhibiting apoptosis."
item3821	REG00013	M6ATAR01695	Up	M6ADIS0006	.	35266112	"RtcisE2F functions as a scaffold of N-methyladenosine (m6A) reader IGF2BP2 and E2F6/E2F3 mRNA. rtcisE2F promotes the association of E2F6/E2F3 mRNAs with IGF2BP2, and inhibits their association with another m6A reader, YTHDF2. IGF2BP2 inhibits E2F6/E2F3 mRNA decay, whereas YTHDF2 promotes E2F6/E2F3 mRNA decay."
item3822	REG00013	M6ATAR00235	Up	M6ADIS0006	.	35266112	"RtcisE2F functions as a scaffold of N-methyladenosine (m6A) reader IGF2BP2 and E2F6/E2F3 mRNA. rtcisE2F promotes the association of E2F6/E2F3 mRNAs with IGF2BP2, and inhibits their association with another m6A reader, YTHDF2. IGF2BP2 inhibits E2F6/E2F3 mRNA decay, whereas YTHDF2 promotes E2F6/E2F3 mRNA decay."
item3823	REG00008	M6ATAR01695	Down	M6ADIS0006	.	35266112	"RtcisE2F functions as a scaffold of N-methyladenosine (m6A) reader IGF2BP2 and E2F6/E2F3 mRNA. rtcisE2F promotes the association of E2F6/E2F3 mRNAs with IGF2BP2, and inhibits their association with another m6A reader, YTHDF2. IGF2BP2 inhibits E2F6/E2F3 mRNA decay, whereas YTHDF2 promotes E2F6/E2F3 mRNA decay."
item3824	REG00008	M6ATAR00235	Down	M6ADIS0006	.	35266112	"RtcisE2F functions as a scaffold of N-methyladenosine (m6A) reader IGF2BP2 and E2F6/E2F3 mRNA. rtcisE2F promotes the association of E2F6/E2F3 mRNAs with IGF2BP2, and inhibits their association with another m6A reader, YTHDF2. IGF2BP2 inhibits E2F6/E2F3 mRNA decay, whereas YTHDF2 promotes E2F6/E2F3 mRNA decay."
item3825	REG00013	M6ATAR01696	Up	M6ADIS0059	.	35173309	LINC01021 maintains tumorigenicity by enhancing N6-methyladenosine reader IMP2 dependent stabilization of MSX1 and JARID2: implication in colorectal cancer.
item3826	REG00013	M6ATAR01697	Up	M6ADIS0059	.	35173309	LINC01021 maintains tumorigenicity by enhancing N6-methyladenosine reader IMP2 dependent stabilization of MSX1 and JARID2: implication in colorectal cancer.
item3827	REG00001	M6ATAR00348	Up	M6ADIS0274	.	39538055	"LncRNA UCA1 inhibits oxidative stress and ferroptosis, thereby preventing cardiomyocyte aging. This protective effect is likely mediated by increasing the expression of demethylase FTO and reducing m6A modification, which promotes the expression of NRF2."
item3828	REG00007	M6ATAR00379	Up	M6ADIS0008	.	38286198	Transcriptome sequencing analysis reveals miR-30c-5p promotes ferroptosis in cervical cancer and inhibits growth and metastasis of cervical cancer xenografts by targeting the METTL3/KRAS axis.
item3829	REG00002	M6ATAR01699	Up	M6ADIS0068	.	37647111	"m6A-Mediated Biogenesis of circDDIT4 Inhibits Prostate Cancer Progression by Sequestrating ELAVL1/HuR.By competitively binding to ELAV-like RNA binding protein 1 (ELAVL1/HuR) through its 3'-UTR, circDDIT4 acts as a protein sponge to decrease the expression of prostate cancer-overexpressed anoctamin 7 (ANO7)."
item3830	REG00026	.	.	M6ADIS0006	.	35278064	Downregulation of ZC3H13 by miR-362-3p/miR-425-5p is associated with a poor prognosis and adverse outcomes in hepatocellular carcinoma.
item3831	REG00026	.	.	M6ADIS0006	.	35278064	Downregulation of ZC3H13 by miR-362-3p/miR-425-5p is associated with a poor prognosis and adverse outcomes in hepatocellular carcinoma.
item3832	.	M6ATAR01700	.	M6ADIS0061	.	37726400	LncRNA BCAN-AS1 stabilizes c-Myc via N6-methyladenosine-mediated binding with SNIP1 to promote pancreatic cancer.
item3833	REG00048	M6ATAR01701	Up	M6ADIS0185	.	38358439	m6A-Induced lncRNA MEG3 Promotes Cerebral Ischemia-Reperfusion Injury Via Modulating Oxidative Stress and Mitochondrial Dysfunction by hnRNPA1/Sirt2 Axis.
item3834	REG00004	M6ATAR00497	Down	.	.	38811846	DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression.
item3835	REG00029	M6ATAR01702	Up	M6ADIS0110	.	39221886	FAS-AS1 maintained the stability of ADAM8 mRNA by recruiting FMR1. METTL14 knockdown repressed FAS-AS1 expression in an m6A-dependent manner.METTL14-mediated lncRNA-FAS-AS1 promotes osteoarthritis progression by up-regulating ADAM8.
item3836	REG00048	M6ATAR01306	Up	M6ADIS0006	.	39247822	Exosomal SLC16A1-AS1-induced M2 macrophages polarization facilitates hepatocellular carcinoma progression.the HCC exosomal SLC16A1-AS1 enhanced mRNA stabilization of SLC16A1 in macrophage by promoting the interaction between 3' untranslated regions (3'UTR) of SLC16A1 mRNA and heterogeneous nuclear ribonucleoprotein A1 (HNRNPA1).
item3837	REG00007	M6ATAR01703	Down	M6ADIS0100	.	33020597	The piRNA CHAPIR regulates cardiac hypertrophy by controlling METTL3-dependent N6-methyladenosine methylation of Parp10 mRNA.
item3838	REG00024	M6ATAR01704	Up	.	.	36417851	"m6A-modified lincRNA Dubr is required for neuronal development by stabilizing YTHDF1/3 and facilitating mRNA translation.Dubr interacts with m6A-binding proteins, the YTHDF1/3 complex, through its m6A motifs to protect YTHDF1/3 from degradation via the proteasome pathway. Furthermore, Tau and Calmodulin are regulated by YTHDF1/3 and m6A-modified Dubr."
item3839	REG00025	M6ATAR01704	Up	.	.	36417851	"m6A-modified lincRNA Dubr is required for neuronal development by stabilizing YTHDF1/3 and facilitating mRNA translation.Dubr interacts with m6A-binding proteins, the YTHDF1/3 complex, through its m6A motifs to protect YTHDF1/3 from degradation via the proteasome pathway. Furthermore, Tau and Calmodulin are regulated by YTHDF1/3 and m6A-modified Dubr."
item3840	REG00024	M6ATAR01705	Up	.	.	36417851	"m6A-modified lincRNA Dubr is required for neuronal development by stabilizing YTHDF1/3 and facilitating mRNA translation.Dubr interacts with m6A-binding proteins, the YTHDF1/3 complex, through its m6A motifs to protect YTHDF1/3 from degradation via the proteasome pathway. Furthermore, Tau and Calmodulin are regulated by YTHDF1/3 and m6A-modified Dubr."
item3841	REG00025	M6ATAR01705	Up	.	.	36417851	"m6A-modified lincRNA Dubr is required for neuronal development by stabilizing YTHDF1/3 and facilitating mRNA translation.Dubr interacts with m6A-binding proteins, the YTHDF1/3 complex, through its m6A motifs to protect YTHDF1/3 from degradation via the proteasome pathway. Furthermore, Tau and Calmodulin are regulated by YTHDF1/3 and m6A-modified Dubr."
item3842	REG00013	M6ATAR00451	Up	M6ADIS0184	.	39820521	"Triple-negative breast cancer cell derived piR31115 promotes the proliferation and migration of endothelial cells via METTL3-mediated m6A modification of YAP1.Concurrently, the IGF2BP plays a crucial role in stabilizing YAP1 protein expression."
item3843	REG00007	M6ATAR00451	Up	M6ADIS0184	.	39820521	Triple-negative breast cancer cell-derived piR31115 promotes the proliferation and migration of endothelial cells via METTL3-mediated m6A modification of YAP1.
item3844	REG00015	M6ATAR01706	Up	M6ADIS0065	.	31717552	"LINC00667 positively regulated the KIAA1429 via sponging miR-556-5p, forming a KIAA1429/m6A/LINC00667/miR-556-5p feedback loop. Collectively, the central findings of our study suggest that KIAA1429-induced LINC00667 exerted its functions as an oncogene in BC progression through m6A-dependent feedback loop.N6-methyladenine- induced LINC00667 promoted breast cancer progression through m6A/KIAA1429 positive feedback loop."
item3845	REG00015	M6ATAR01706	Up	M6ADIS0065	.	31717552	"LINC00667 positively regulated the KIAA1429 via sponging miR-556-5p, forming a KIAA1429/m6A/LINC00667/miR-556-5p feedback loop. Collectively, the central findings of our study suggest that KIAA1429-induced LINC00667 exerted its functions as an oncogene in BC progression through m6A-dependent feedback loop.N6-methyladenine- induced LINC00667 promoted breast cancer progression through m6A/KIAA1429 positive feedback loop."
item3846	REG00007	M6ATAR01707	Down	M6ADIS0164	.	38134679	"Mechanistically, exosomal lncRNA PAET promoted methyltransferase-like 3 (METTL3) accumulation by increasing its stability, which stimulated N6-methyladenosine (m6A) modification of cytochrome c oxidase subunit 4I1 (COX4I1), and COX4I1 levels were decreased in a mechanism dependent on the m6A ""reader"" YTH domain family 3 (YTHDF3)."
item3847	REG00025	M6ATAR01707	Down	M6ADIS0164	.	38134679	"Mechanistically, exosomal lncRNA PAET promoted methyltransferase-like 3 (METTL3) accumulation by increasing its stability, which stimulated N6-methyladenosine (m6A) modification of cytochrome c oxidase subunit 4I1 (COX4I1), and COX4I1 levels were decreased in a mechanism dependent on the m6A ""reader"" YTH domain family 3 (YTHDF3)."
item3848	REG00005	M6ATAR00404	Up	M6ADIS0340	.	39509294	"Inhibition of miR-155 promoted the expression of HIF-1alpha and attenuated the m6A modification of SOX2 mRNA, thereby promoting the expression of SOX2 and activating the downstream EGFR/MEK/ERK signaling pathway to promote wound healing in an in vitro DFU model."
item3849	REG00013	M6ATAR00206	Up	M6ADIS0059	.	36230970	m6A Modification of Long Non-Coding RNA HNF1A-AS1 Facilitates Cell Cycle Progression in Colorectal Cancer via IGF2BP2-Mediated CCND1 mRNA Stabilization.
item3850	REG00001	M6ATAR01060	Down	M6ADIS0091	.	37002530	"BMSC-derived exosomal KLF4 promoted lncRNA-ZFAS1 expression to repress Drp1 m6A modification by targeting FTO, thus reducing mitochondrial dysfunction and alleviating neuronal injury in ischemic stroke."
item3851	REG00015	M6ATAR01708	Up	M6ADIS0059	.	38843497	"KIAA1429-mediated m6A modification up-regulated lncRNA EBLN3P expression, and lncRNA EBLN3P increased KIAA1429 expression by competitively binding to miR-153-3p, thus reducing ferroptosis and increasing the radioresistance of CRC."
item3852	REG00015	M6ATAR01708	Up	M6ADIS0059	.	38843497	"KIAA1429-mediated m6A modification up-regulated lncRNA EBLN3P expression, and lncRNA EBLN3P increased KIAA1429 expression by competitively binding to miR-153-3p, thus reducing ferroptosis and increasing the radioresistance of CRC."
item3853	REG00003	M6ATAR01709	Up	M6ADIS0068	.	36195720	"LncNAP1L6 activates MMP pathway by stabilizing the m6A-modified NAP1L2 to promote malignant progression in prostate cancer. lncNAP1L6 recruited HNRNPC to m6A-modified NAP1L2, leading to stabilization of NAP1L2 mRNA."
item3854	REG00007	M6ATAR00341	Up	M6ADIS0046	.	35761379	Tumor-suppressive MEG3 induces microRNA-493-5p expression to reduce arabinocytosine chemoresistance of acute myeloid leukemia cells by downregulating the METTL3/MYC axis.
item3855	REG00007	M6ATAR00341	Up	M6ADIS0046	.	35761379	Tumor-suppressive MEG3 induces microRNA-493-5p expression to reduce arabinocytosine chemoresistance of acute myeloid leukemia cells by downregulating the METTL3/MYC axis.
item3856	REG00005	M6ATAR00156	Up	M6ADIS0091	.	36609501	ALKBH5 regulated STAT3 expression by mediating its m6A modification and long noncoding RNA H19/miR-124-3p. ALKBH5 also alleviated the H/Post injury induced by the low expression of STAT3 in senescent cardiomyocytes.
item3857	REG00022	M6ATAR01710	Down	M6ADIS0066	.	39827178	"PiR-26441 inhibits mitochondrial oxidative phosphorylation and tumorigenesis in ovarian cancer through m6A modification by interacting with YTHDC1.piR-26441 could inhibit OC cell growth via the YTHDC1/TSFM signaling axis, underscoring its significant importance in the context of OC, as well as offering potential as a therapeutic target."
item3858	REG00053	M6ATAR00341	Up	M6ADIS0057	M6ADRUG0047	35073459	"LNC942 up-regulated the MSI2 expression by preventing its interaction with SCFbeta-TRCPE3 ubiquitin ligase, eventually inhibiting ubiquitination. Then, LNC942 stabilized c-Myc mRNA in an N6-methyladenosine (m6A)-dependent manner. As a potential m6A recognition protein, MSI2 stabilized c-Myc mRNA with m6A modifications. Moreover, inhibition of the LNC942-MSI2-c-Myc axis was found to restore chemosensitivity both in vitro and in vivo.LNC942 was found to be up-regulated in chemoresistant GC cells."
item3859	REG00047	M6ATAR00348	Up	M6ADIS0001	.	37202791	"Mechanistically, SNAI3-AS1 competitively binds to SND1 and perturbs the m6A-dependent recognition of Nrf2 mRNA 3'UTR by SND1, thereby reducing the mRNA stability of Nrf2. Epigenetically silenced lncRNA SNAI3-AS1 promotes ferroptosis in glioma via perturbing the m6A-dependent recognition of Nrf2 mRNA mediated by SND1."
item3860	REG00013	M6ATAR01711	Up	M6ADIS0007	.	36257938	"The LCAT1-IGF2BP2-CDC6 axis appears to play a vital role in promoting the growth and migration of lung cancer cells, and is a potential therapeutic target for lung cancer."
item3861	REG00005	M6ATAR01712	Down	M6ADIS0056	.	33231844	A positive feedback loop between AlkB homolog 5 and miR-193a-3p promotes growth and metastasis in esophageal squamous cell carcinoma.
item3862	REG00007	M6ATAR00297	Up	M6ADIS0006	.	38680094	MiR-502-3p targeted YTHDF3 to regulate the translation of integrin alpha-6 (ITGA6) and targeted HBXIP to inhibit the m6A modification of ITGA6 through methyltransferase-like 3 (METTL3).Long noncoding RNA SNHG3 interacts with microRNA-502-3p to mediate ITGA6 expression in liver hepatocellular carcinoma.SNHG3 controls the YTHDF3/ITGA6 and HBXIP/METTL3/ITGA6 pathways by repressing miR-502-3p expression to sustain the self-renewal properties of CSC in LIHC.
item3863	REG00007	M6ATAR00297	Up	M6ADIS0006	.	38680094	MiR-502-3p targeted YTHDF3 to regulate the translation of integrin alpha-6 (ITGA6) and targeted HBXIP to inhibit the m6A modification of ITGA6 through methyltransferase-like 3 (METTL3).Long noncoding RNA SNHG3 interacts with microRNA-502-3p to mediate ITGA6 expression in liver hepatocellular carcinoma.SNHG3 controls the YTHDF3/ITGA6 and HBXIP/METTL3/ITGA6 pathways by repressing miR-502-3p expression to sustain the self-renewal properties of CSC in LIHC.
item3864	REG00025	M6ATAR00297	Up	M6ADIS0006	.	38680094	MiR-502-3p targeted YTHDF3 to regulate the translation of integrin alpha-6 (ITGA6) and targeted HBXIP to inhibit the m6A modification of ITGA6 through methyltransferase-like 3 (METTL3).Long noncoding RNA SNHG3 interacts with microRNA-502-3p to mediate ITGA6 expression in liver hepatocellular carcinoma.SNHG3 controls the YTHDF3/ITGA6 and HBXIP/METTL3/ITGA6 pathways by repressing miR-502-3p expression to sustain the self-renewal properties of CSC in LIHC.
item3865	REG00025	M6ATAR00297	Up	M6ADIS0006	.	38680094	MiR-502-3p targeted YTHDF3 to regulate the translation of integrin alpha-6 (ITGA6) and targeted HBXIP to inhibit the m6A modification of ITGA6 through methyltransferase-like 3 (METTL3).Long noncoding RNA SNHG3 interacts with microRNA-502-3p to mediate ITGA6 expression in liver hepatocellular carcinoma.SNHG3 controls the YTHDF3/ITGA6 and HBXIP/METTL3/ITGA6 pathways by repressing miR-502-3p expression to sustain the self-renewal properties of CSC in LIHC.
item3866	REG00024	M6ATAR00341	Up	M6ADIS0007	.	35972892	"Mechanistically, m6A methyltransferase METTL3 enhanced the stability of DLGAP1-AS2 via m6A site binding. Moreover, DLGAP1-AS2 interacted with YTHDF1 to enhance the stability of c-Myc mRNA through DLGAP1-AS2/YTHDF1/m6A/c-Myc mRNA."
item3867	REG00024	M6ATAR00283	Up	M6ADIS0056	.	35389828	"HCP5 was able to directly interact with YTHDF1, a N6-methyladenosine (m6A) reader, enhancing the binding of YTHDF1 to m6A-modified HK2 mRNA, leading to increasing HK2 stability, thereby promoting the Warburg effect (aerobic glycolysis) of ESCC cells."
item3868	REG00024	M6ATAR01713	Up	M6ADIS0057	.	37279381	H19 recruited N 6 -methyladenosine (m 6 A) reader YTHDF1 to promote SCARB1 translation and facilitate angiogenesis in gastric cancer.
item3869	REG00045	M6ATAR01714	Down	M6ADIS0015	.	36174881	m6A transferase METTL3 regulates endothelial-mesenchymal transition in diabetic retinopathy via lncRNA SNHG7/KHSRP/MKL1 axis.
item3870	REG00001	M6ATAR01715	Up	M6ADIS0006	.	35858900	"CircGPR137B, co-localized with miR-4739 in the cytoplasm, acted as a sponge for miR-4739 to upregulate its target FTO, which mediated m6A demethylation of circGPR137B and promoted its expression. Thus, a feedback loop comprising circGPR137B/miR-4739/FTO axis was formed. FTO suppressed cell growth and indicated favorable survival in patients with HCC."
item3871	REG00001	M6ATAR01715	Up	M6ADIS0006	.	35858900	"CircGPR137B, co-localized with miR-4739 in the cytoplasm, acted as a sponge for miR-4739 to upregulate its target FTO, which mediated m6A demethylation of circGPR137B and promoted its expression. Thus, a feedback loop comprising circGPR137B/miR-4739/FTO axis was formed. FTO suppressed cell growth and indicated favorable survival in patients with HCC."
item3872	REG00006	M6ATAR00922	Up	M6ADIS0006	.	36474147	"Exosomes derived from M1 macrophages transferred miR-628-5p to HCC cells to inhibit human methyltransferase-like 14 (METTL14) expression. METTL14 promoted circFUT8 m6A modification and facilitated its nuclear export to the cytoplasm, where M1 macrophages regulated the circFUT8/miR-552-3p/CHMP4B pathway, thereby suppressing HCC progression."
item3873	REG00004	M6ATAR01716	Up	M6ADIS0057	.	36171622	"NEAT1 was upregulated significantly by c-Jun/c-Fos in RPRD1B-overexpressing cells. NEAT1, in turn, increased the stability of the RPRD1B mRNA by recruiting the m6A ""reader"" protein hnRNPA2B1 and reduced the degradation of the RPRD1B protein by inhibiting TRIM25-mediated ubiquitination."
item3874	REG00006	M6ATAR00274	Down	M6ADIS0172	.	37076497	LncRNA UCA1 promotes keratinocyte-driven inflammation via suppressing METTL14 and activating the HIF-1alpha/NF-kappaB axis in psoriasis.
item3875	REG00022	M6ATAR01717	Up	.	.	38842666	Mir22hg facilitates ferritinophagy-mediated ferroptosis in sepsis by recruiting the m6A reader YTHDC1 and enhancing Angptl4 mRNA stability.
item3876	REG00001	M6ATAR01718	Up	M6ADIS0142	.	35132536	"Ang II induced downregulation of circCELF1 expression, while circCELF1 enhanced the expression of DKK2 by adsorbing miR-636. circCELF1 also reduced DKK2 m6A level by upregulating FTO expression, thereby inhibiting the binding of miR-636 to DKK2 and promoting DKK2 expression."
item3877	REG00014	M6ATAR01719	Up	M6ADIS0006	.	37756562	"LINC01089 interacted with heterogeneous nuclear ribonucleoprotein M (hnRNPM) and led to hnRNPM-mediated skipping of DIAPH3 exon 3. Knockdown of LINC01089 increased the inclusion of DIAPH3 exon 3, which contains an important m6A-modification site that is recognized by IGF2BP3 to increase DIAPH3 mRNA stability. Thus, LINC01089 loss increased DIAPH3 protein levels, which suppressed the ERK/Elk1/Snail axis and inhibited EMT of HCC cells."
item3878	REG00001	M6ATAR00341	Down	M6ADIS0046	.	33283713	Hsa-let-7b-5p Inhibits Proliferation of Human Leukemia THP-1 Cells via FTO/m6A/MYC Signaling Pathway.
item3879	REG00054	M6ATAR00216	.	M6ADIS0117	.	38334961	"Mechanically, miR-204 reduced METTL7A expression to CIDEC m6A methylation, thus suppressing OS and mitochondrial dysfunction."
item3880	REG00001	M6ATAR00401	Up	M6ADIS0006	.	37326474	"The encoded micropeptide AC115619-22aa inhibited the progression of HCC by binding to WTAP and impeding the assembly of the N6-methyladenosine (m6A) methyltransferase complex, which regulates the expression of tumor-associated genes, such as SOCS2 and ATG14.Hypoxia-Responsive lncRNA AC115619 Encodes a Micropeptide That Suppresses m6A Modifications and Hepatocellular Carcinoma Progression."
item3881	REG00001	M6ATAR00194	Up	M6ADIS0006	.	37326474	"The encoded micropeptide AC115619-22aa inhibited the progression of HCC by binding to WTAP and impeding the assembly of the N6-methyladenosine (m6A) methyltransferase complex, which regulates the expression of tumor-associated genes, such as SOCS2 and ATG14.Hypoxia-Responsive lncRNA AC115619 Encodes a Micropeptide That Suppresses m6A Modifications and Hepatocellular Carcinoma Progression."
item3882	REG00009	M6ATAR01241	Up	M6ADIS0007	.	39106633	"PiR-27222 could deubiquitinate and stabilize eIF4B by directly binding to eIF4B and reducing its interaction with PARK2. The enhanced expression of eIF4B, in turn, promoted the expression of WTAP, leading to increased m6A modification in the Casp8 transcript."
item3883	REG00013	M6ATAR00283	Up	M6ADIS0006	.	36933158	"LncRNA miR4458HG modulates hepatocellular carcinoma progression by activating m6A-dependent glycolysis and promoting the polarization of tumor-associated macrophages.Mechanistically, miR4458HG bound IGF2BP2 (a key RNA m6A reader) and facilitated IGF2BP2-mediated target mRNA stability, including HK2 and SLC2A1 (GLUT1), and consequently altered HCC glycolysis and tumor cell physiology."
item3884	REG00013	M6ATAR00269	Up	M6ADIS0006	.	36933158	"LncRNA miR4458HG modulates hepatocellular carcinoma progression by activating m6A-dependent glycolysis and promoting the polarization of tumor-associated macrophages.Mechanistically, miR4458HG bound IGF2BP2 (a key RNA m6A reader) and facilitated IGF2BP2-mediated target mRNA stability, including HK2 and SLC2A1 (GLUT1), and consequently altered HCC glycolysis and tumor cell physiology."
item3885	REG00006	M6ATAR01728	Up	M6ADIS0342	.	36336035	"Lnc-Gm10532 increased Fission 1 (FIS1) expression and mitochondrial fission by recruiting the m6A writer methyltransferase-like 14 (METTL14) and enhancing m6A modification of Fis1 mRNA. Moreover, lnc-Gm10532 was also required for chronic Cd-induced mitochondrial dysfunction and memory deficits in a rodent model. Therefore, data of this study reveal a new epigenetic mechanism of chronic Cd neurotoxicity."
item3886	REG00007	M6ATAR00605	Up	M6ADIS0110	.	35842714	"HucMSCs-EVs inhibited the secretion of pro-inflammatory factors and the degradation of cartilage ECM after lowering the m6A level of NLRP3 mRNA with miR-1208 targeting combined with METTL3, thereby alleviating OA progression in mice and providing a novel therapy for clinical OA treatment."
item3887	REG00007	M6ATAR00433	Up	M6ADIS0311	.	39115693	LINC01410 accelerates the invasion of trophoblast cells by modulating METTL3/Fas.
item3888	REG00001	M6ATAR00341	Up	M6ADIS0056	.	36868327	"LINC00858 modulated MYC m6A modification via FTO by recruiting ZNF184, thus facilitating ESCC progression."
item3889	REG00007	M6ATAR01729	Up	M6ADIS0001	.	37580442	"MiR-1208 downregulated the m6A methylation level of NUP214 mRNA by negatively regulating the expression of METTL3, thereby NUP214 expression and TGF-beta pathway activity were suppressed."
item3890	REG00026	M6ATAR01730	Up	M6ADIS0001	M6ADRUG0193	37855702	"Hypoxic GSC-induced neuron activation promotes GBM progression by polarizing microglia via the exosomal miR-200c-3p/ZC3H13/DUSP9/p-ERK pathway. Levetiracetam, an antiepileptic drug, blocks the abnormal activation of neurons in GBM and impairs activity-dependent GBM progression."
item3891	REG00006	.	.	.	.	38320638	"These findings underscore the regulatory role of Linc-smad7 in controlling METTL14 gene expression, thereby mediating m6A modifications to regulate lipid synthesis in mammary epithelial cells."
item3892	REG00007	M6ATAR00944	Up	M6ADIS0184	M6ADRUG0194	36202872	METTL3/LINC00662/miR-186-5p feedback loop regulates docetaxel resistance in triple negative breast cancer .
item3893	REG00007	M6ATAR00944	Up	M6ADIS0184	M6ADRUG0194	36202872	METTL3/LINC00662/miR-186-5p feedback loop regulates docetaxel resistance in triple negative breast cancer .
item3894	REG00007	M6ATAR01731	Up	M6ADIS0073	M6ADRUG0195	38993572	"The METTL3/PAX8/YTHDC1 axis has been revealed to play a pivotal role in repressing tumour occurrence, and is antagonized by miR-493-5p."
item3895	REG00022	M6ATAR01731	Up	M6ADIS0073	M6ADRUG0195	38993572	"The METTL3/PAX8/YTHDC1 axis has been revealed to play a pivotal role in repressing tumour occurrence, and is antagonized by miR-493-5p."
item3896	REG00001	M6ATAR01308	Down	M6ADIS0059	.	39111169	"Mechanistically, the risk allele of rs67734009 increased ESR1 expression via miR-3492 binding and m6A modification. Collectively, this study sheds light on potential genetic and epigenetic mechanisms linking PCB153 exposure and colorectal cancer risk, thereby providing insight into the accurate protection against POPs exposure."
item3897	REG00012	M6ATAR00341	Up	M6ADIS0046	M6ADRUG0165	38048862	"LncRNA GLCC1 served as scaffold to facilitate the formation of the IGF2 mRNA binding protein 1 (IGF2BP1)-c-Myc complex, which led to the activation of the downstream tumor-promoting c-Myc-associated signal pathways."
item3898	REG00006	M6ATAR00223	Up	M6ADIS0125	.	37972448	The facilitation of circMETTL14(11)S/METTL14/CXCR4 on TNF-alpha-induced endothelial inflammation of HUVECs was verified.
item3899	REG00006	M6ATAR01625	Up	M6ADIS0070	.	36288387	"METTL14 overexpression prohibits BCa cell migration, invasion in vitro and tumor metastasis in vivo. METTL14 stabilizes USP38 mRNA by inducing N6-methyladenosine (m6A) modification and enhances USP38 mRNA stability in YTHDF2-dependent manner. METTL14 represses BCa cell migration, invasion and EMT via USP38. Additionally, miR-3165 inhibits METTL14 expression to promote BCa progression."
item3900	REG00008	M6ATAR01625	Up	M6ADIS0070	.	36288387	"METTL14 overexpression prohibits BCa cell migration, invasion in vitro and tumor metastasis in vivo. METTL14 stabilizes USP38 mRNA by inducing N6-methyladenosine (m6A) modification and enhances USP38 mRNA stability in YTHDF2-dependent manner. METTL14 represses BCa cell migration, invasion and EMT via USP38. Additionally, miR-3165 inhibits METTL14 expression to promote BCa progression."
item3901	REG00013	M6ATAR01732	Up	M6ADIS0027	.	37543219	"By competitively binding to IGF2BP2, circCDK1 blocked the m6A modification of CPPED1 in IGF2BP2-dependent manner. Moreover, the circCDK1-mediated decrease of CPPED1 activated the PI3K/AKT signal pathway to facilitate progression of LSCC."
item3902	REG00007	M6ATAR01733	Up	M6ADIS0055	.	35403343	Lnc-H2AFV-1 might be a biomarker that alters m6A modification by regulating the m6A methylases METTL3/14 and FTO and then mediating the downstream target IFT80 to promote HNSCC progression.
item3903	REG00006	M6ATAR01733	Up	M6ADIS0055	.	35403343	Lnc-H2AFV-1 might be a biomarker that alters m6A modification by regulating the m6A methylases METTL3/14 and FTO and then mediating the downstream target IFT80 to promote HNSCC progression.
item3904	REG00001	M6ATAR01733	Down	M6ADIS0055	.	35403343	Lnc-H2AFV-1 might be a biomarker that alters m6A modification by regulating the m6A methylases METTL3/14 and FTO and then mediating the downstream target IFT80 to promote HNSCC progression.
item3905	REG00007	M6ATAR00294	Up	M6ADIS0361	M6ADRUG0196	38991640	"Lnc-HZ06 promotes STAT4-mediated IL1B mRNA transcription, enhances IL1B mRNA stability by promoting the formation of METTL3/HuR/IL1B mRNA ternary complex, and finally up-regulates IL1B expression levels."
item3906	REG00001	M6ATAR00341	Up	M6ADIS0059	.	37957486	Exos-mediated hsa_circ_0001739/lncRNA AC159540.1 competitively inhibited miR-218-5p to elevate FTO and MYC. Tumor cell-derived exosomes mediating hsa_circ_0001739/lncRNA AC159540.1 facilitate liver metastasis in colorectal cancer.
item3907	REG00001	M6ATAR00341	Up	M6ADIS0059	.	37957486	Exos-mediated hsa_circ_0001739/lncRNA AC159540.1 competitively inhibited miR-218-5p to elevate FTO and MYC. Tumor cell-derived exosomes mediating hsa_circ_0001739/lncRNA AC159540.1 facilitate liver metastasis in colorectal cancer.
item3908	REG00001	M6ATAR00341	Up	M6ADIS0059	.	37957486	Exos-mediated hsa_circ_0001739/lncRNA AC159540.1 competitively inhibited miR-218-5p to elevate FTO and MYC. Tumor cell-derived exosomes mediating hsa_circ_0001739/lncRNA AC159540.1 facilitate liver metastasis in colorectal cancer.
item3909	REG00007	M6ATAR00823	Up	M6ADIS0117	.	37389924	"AI662270 promotes CTGF expression at the posttranscriptional stage by recruiting METTL3 to the CTGF promoter and depositing m6A modifications on the nascent mRNA, thereby, uncovering a novel regulatory mechanism of CTGF in the pathogenesis of kidney fibrosis."
item3910	REG00006	M6ATAR00823	Up	M6ADIS0117	.	37389924	"AI662270 promotes CTGF expression at the posttranscriptional stage by recruiting METTL3 to the CTGF promoter and depositing m6A modifications on the nascent mRNA, thereby, uncovering a novel regulatory mechanism of CTGF in the pathogenesis of kidney fibrosis."
item3911	REG00009	M6ATAR00823	Up	M6ADIS0117	.	37389924	"AI662270 promotes CTGF expression at the posttranscriptional stage by recruiting METTL3 to the CTGF promoter and depositing m6A modifications on the nascent mRNA, thereby, uncovering a novel regulatory mechanism of CTGF in the pathogenesis of kidney fibrosis."
item3912	REG00015	M6ATAR00823	Up	M6ADIS0117	.	37389924	"AI662270 promotes CTGF expression at the posttranscriptional stage by recruiting METTL3 to the CTGF promoter and depositing m6A modifications on the nascent mRNA, thereby, uncovering a novel regulatory mechanism of CTGF in the pathogenesis of kidney fibrosis."
item3913	REG00007	M6ATAR01559	.	M6ADIS0375	.	36753405	MetBil as a novel molecular regulator in ischemia-induced cardiac fibrosis via METTL3-mediated m6A modification.
item3914	REG00007	M6ATAR00745	.	M6ADIS0375	.	36753405	MetBil as a novel molecular regulator in ischemia-induced cardiac fibrosis via METTL3-mediated m6A modification.
item3915	REG00013	M6ATAR00451	Up	M6ADIS0007	M6ADRUG0198	38394728	"Mechanically, exosomal circPACRGL bound to IGF2BP2 to improve the stability of YAP1 mRNA and regulate Hippo signaling in polarized THP-1 cells. TMS inhibited NSCLC growth via suppressing Hippo signaling and M2 polarization in vivo."
item3916	REG00024	M6ATAR01734	Up	.	.	39357613	"Mechanistically, miR-381 inhibited IL-18 translation in LMECs by inhibiting YTHDF1 expression via binding to its 3'-UTR. As expected, YTHDF1 overexpression in LMECs abolished the effects of miR-381-overexpressed exosomes on LMECs injury and Treg cell differentiation."
item3917	REG00012	M6ATAR01735	Up	M6ADIS0059	.	38965575	"Mechanistically, LOC101928222 synergized with IGF2BP1 to stabilize HMGCS2 mRNA through an m6A-dependent pathway, leading to increased cholesterol synthesis and, ultimately, the promotion of CRC development."
item3918	REG00006	M6ATAR00217	Down	M6ADIS0008	.	35093098	"METTL14 was a directed target gene of piRNA-14633. Knockdown of METTL14 with siRNA attenuated proliferation, migration and invasion of CC cells. piRNA-14633 increased CYP1B1 expression, while silencing of METTL14 impaired its expression."
item3919	REG00006	M6ATAR00547	Up	.	M6ADRUG0199	36924560	"We demonstrated a novel toxicological mechanism in that BPF disrupted the Keap1-Nrf2 redox system to upregulate miR-141/200b/c which controlled pancreatic insulin production and apoptosis via Mettl14 and Xiap, respectively. As the major surrogates of BPA in various applications, BPF was also diabetogenic, which warrants attention in future research."
item3920	REG00006	M6ATAR00547	Up	.	M6ADRUG0199	36924560	"We demonstrated a novel toxicological mechanism in that BPF disrupted the Keap1-Nrf2 redox system to upregulate miR-141/200b/c which controlled pancreatic insulin production and apoptosis via Mettl14 and Xiap, respectively. As the major surrogates of BPA in various applications, BPF was also diabetogenic, which warrants attention in future research."
item3921	REG00006	M6ATAR00547	Up	.	M6ADRUG0199	36924560	"We demonstrated a novel toxicological mechanism in that BPF disrupted the Keap1-Nrf2 redox system to upregulate miR-141/200b/c which controlled pancreatic insulin production and apoptosis via Mettl14 and Xiap, respectively. As the major surrogates of BPA in various applications, BPF was also diabetogenic, which warrants attention in future research."
item3922	REG00013	M6ATAR01736	Up	M6ADIS0065	M6ADRUG0202	36438499	"LncSNHG5 enhanced ZNF281 mRNA stability by binding with the m6A reader IGF2BP2. Enhanced ZNF281 transcriptionally regulated CCL2 and CCL5 expression to activate P38 MAPK signaling in endothelial cells. High CCL2 and CCL5 expression was associated with tumor metastasis and poor prognosis in BC patients. The inhibitors RS102895, marasviroc and cenicriviroc inhibited angiogenesis and vascular permeability in the PMN by blocking the binding of CCL2/CCR2 and CCL5/CCR5. The lncSNHG5-ZNF281-CCL2/CCL5 signaling axis plays an essential role in inducing premetastatic niche formation to promote BC metastasis."
item3923	REG00013	M6ATAR00833	Up	M6ADIS0059	.	35773744	"CircEZH2 interacts with m6A reader IGF2BP2 and blocks its ubiquitination-dependent degradation. Meanwhile, circEZH2 could serve as a sponge of miR-133b, resulting in the upregulation of IGF2BP2. Particularly, circEZH2/IGF2BP2 enhances the stability of CREB1 mRNA, thus aggravating CRC progression."
item3924	REG00013	M6ATAR00833	Up	M6ADIS0059	.	35773744	"CircEZH2 interacts with m6A reader IGF2BP2 and blocks its ubiquitination-dependent degradation. Meanwhile, circEZH2 could serve as a sponge of miR-133b, resulting in the upregulation of IGF2BP2. Particularly, circEZH2/IGF2BP2 enhances the stability of CREB1 mRNA, thus aggravating CRC progression."
item3925	REG00013	M6ATAR00833	Up	M6ADIS0059	.	35773744	"CircEZH2 interacts with m6A reader IGF2BP2 and blocks its ubiquitination-dependent degradation. Meanwhile, circEZH2 could serve as a sponge of miR-133b, resulting in the upregulation of IGF2BP2. Particularly, circEZH2/IGF2BP2 enhances the stability of CREB1 mRNA, thus aggravating CRC progression."
item3926	REG00001	M6ATAR00399	Up	M6ADIS0061	.	38057853	"Hypoxia-driven E26 transformation-specific sequence-1 (ETS1), as an upstream modulatory mechanism, was essential for the downregulation of GATA6-AS1 in PDAC cells. GATA6-AS1 inhibited the expression of fat mass and obesity-associated protein (FTO), an N6-methyladenosine (m6A) eraser, and repressed SNAI1 mRNA stability in an m6A-dependent manner."
item3927	REG00006	M6ATAR01486	.	M6ADIS0056	M6ADRUG0047	39689599	Exosomal miR-130a-3p confers cisplatin resistance in esophageal cancer by regulating ferroptosis via the suppression of METTL14-mediated m6A RNA methylation of FSP1.
item3928	REG00020	M6ATAR00433	Up	.	.	37478845	"m6A RIP-seq analysis revealed that FTO-IT1 knockout increased mRNA m6A methylation of a subset of p53 transcriptional target genes (e.g., FAS, TP53INP1, and SESN2) and induced PCa cell cycle arrest and apoptosis. FTO-IT1 directly binds RBM15 and inhibits RBM15 binding, m6A methylation, and stability of p53 target mRNAs."
item3929	REG00020	M6ATAR01737	Up	.	.	37478845	"m6A RIP-seq analysis revealed that FTO-IT1 knockout increased mRNA m6A methylation of a subset of p53 transcriptional target genes (e.g., FAS, TP53INP1, and SESN2) and induced PCa cell cycle arrest and apoptosis. FTO-IT1 directly binds RBM15 and inhibits RBM15 binding, m6A methylation, and stability of p53 target mRNAs."
item3930	REG00020	M6ATAR01738	Up	.	.	37478845	"m6A RIP-seq analysis revealed that FTO-IT1 knockout increased mRNA m6A methylation of a subset of p53 transcriptional target genes (e.g., FAS, TP53INP1, and SESN2) and induced PCa cell cycle arrest and apoptosis. FTO-IT1 directly binds RBM15 and inhibits RBM15 binding, m6A methylation, and stability of p53 target mRNAs."
item3931	REG00013	M6ATAR01739	Up	M6ADIS0347	.	38945954	"m6A-modified circRNA was found to increase mRNA stability by functioning as a scaffold for the binding of IGF2BP2 and mRNA. This phenomenon was also observed in the present study, and we identified Krm1 as a target gene of the circHIPK3/IGF2BP2 complex."
item3932	REG00005	M6ATAR01740	Up	M6ADIS0312	.	38485895	"CircNRCAM could competitively bind to ALKBH5, which restrained miR-506-3p expression and promoted NRCAM expression."
item3933	REG00005	M6ATAR01741	Up	M6ADIS0057	.	36864711	LINC00659 cooperated with ALKBH5 to accelerate gastric cancer progression by stabilising JAK1 mRNA in an m6 A-YTHDF2-dependent manner.
item3934	REG00008	M6ATAR01741	Down	M6ADIS0057	.	36864711	LINC00659 cooperated with ALKBH5 to accelerate gastric cancer progression by stabilising JAK1 mRNA in an m6 A-YTHDF2-dependent manner.
item3935	REG00012	M6ATAR01742	Up	M6ADIS0008	.	38180377	"LRRC75A-AS1 competitively binds to IGF2BP1 protein to destabilize SYVN1 mRNA, subsequently suppresses SYVN1-mediated NLRP3 ubiquitination degradation and activates IL1beta/Smad2/3 signaling, thus promoting EMT in cervical cancer. Implication: LRRC75A-AS1 promotes cervical cancer progression, and this study suggests LRRC75A-AS1 as a new therapeutic target for cervical cancer."
item3936	REG00008	M6ATAR01743	Down	M6ADIS0059	.	35986274	"Hypoxia-induced HIF-1alpha transcriptionally upregulates the expression of lncRNA STEAP3-AS1, which interacts competitively with YTHDF2, thus upregulating mRNA stability of STEAP3 and consequent STEAP3 protein expression."
item3937	REG00048	.	.	M6ADIS0057	.	37897508	"OIP5-AS1 prevented Trim21-mediated ubiquitination and degradation of hnRNPA1, stabilizing hnRNPA1 protein and promoting the malignant progression of GC by regulating PKM2 signaling pathway."
item3938	REG00012	.	.	.	.	32179813	MiR-670-3p functions as the regulator of Igf2bp1 expression and plays a crucial role in PA development through m6A modification.
item3939	REG00007	M6ATAR01744	Up	M6ADIS0061	.	37604948	MiR-33a-3p regulates METTL3-mediated AREG stability and alters EMT to inhibit pancreatic cancer invasion and metastasis.
item3940	REG00007	M6ATAR00327	Up	M6ADIS0001	.	38802444	"Our study identifies a novel micropeptide AF127577.4-ORF hidden in a lncRNA, with a potent anti-proliferating function in GBM by diminishing METTL3 protein stability by reducing the ERK2/METTL3 interaction. This micropeptide may be beneficial for development of therapeutic strategies against GBM."
item3941	REG00014	M6ATAR00341	Up	M6ADIS0057	.	36284068	"The interaction between c-MYC mRNA and LIN28B is speculated to be supported by LOC101929709, which binds to both LIN28B and IGF2BP3. Mechanistically, LOC101929709 enriched in the cytoplasm helps LIN28B stabilize c-MYC mRNA."
item3942	REG00055	M6ATAR00341	Up	M6ADIS0057	.	36284068	"The interaction between c-MYC mRNA and LIN28B is speculated to be supported by LOC101929709, which binds to both LIN28B and IGF2BP3. Mechanistically, LOC101929709 enriched in the cytoplasm helps LIN28B stabilize c-MYC mRNA."
item3943	REG00007	M6ATAR00795	.	M6ADIS0065	.	36077054	"ADAR1 edits METTL3 mRNA and changes its binding site to miR532-5p, leading to increased METTL3 protein, which further targets ARHGAP5, recognized by YTHDF1."
item3944	REG00024	M6ATAR00795	.	M6ADIS0065	.	36077054	"ADAR1 edits METTL3 mRNA and changes its binding site to miR532-5p, leading to increased METTL3 protein, which further targets ARHGAP5, recognized by YTHDF1."
item3945	REG00048	M6ATAR00764	Down	M6ADIS0059	M6ADRUG0048	36576581	LINC01615 promoted G6PD expression by competitively binding with hnRNPA1 and facilitating G6PD pre-mRNA splicing.LINC01615 maintains cell survival in adaptation to nutrient starvation through the pentose phosphate pathway and modulates chemosensitivity in colorectal cancer.
item3946	REG00009	M6ATAR00248	Down	M6ADIS0112	.	36541909	WTAP may be involved in the methylation process of ETS1 in RA. ETS1 m6A methylation levels were altered upon WTAP intervention. The overexpression or interference of circ_0066715 decreased or increased WTAP expression.
item3947	REG00013	M6ATAR00419	Up	M6ADIS0059	.	37624989	"CircASPH interacted with insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) to stabilize IGF2BP2 protein, therefore enhancing the stability of m6A-modified STING mRNA."
item3948	REG00007	M6ATAR00605	.	M6ADIS0007	M6ADRUG0030	37156816	"Mechanistically, gain of H3K4me1 and H3K27Ac led to the activation of LINC00969 expression. LINC00969 interacts with EZH2 and METTL3, transcriptionally regulates the level of H3K27me3 in the NLRP3 promoter region, and posttranscriptionally modifies the m6A level of NLRP3 in an m6A-YTHDF2-dependent manner, thus epigenetically repressing NLRP3 expression to suppress the activation of the NLRP3/caspase-1/GSDMD-related classical pyroptosis signalling pathways, thereby endowing an antipyroptotic phenotype and promoting TKI resistance in lung cancer."
item3949	REG00008	M6ATAR00605	.	M6ADIS0007	M6ADRUG0030	37156816	"Mechanistically, gain of H3K4me1 and H3K27Ac led to the activation of LINC00969 expression. LINC00969 interacts with EZH2 and METTL3, transcriptionally regulates the level of H3K27me3 in the NLRP3 promoter region, and posttranscriptionally modifies the m6A level of NLRP3 in an m6A-YTHDF2-dependent manner, thus epigenetically repressing NLRP3 expression to suppress the activation of the NLRP3/caspase-1/GSDMD-related classical pyroptosis signalling pathways, thereby endowing an antipyroptotic phenotype and promoting TKI resistance in lung cancer."
item3950	REG00001	M6ATAR00453	Up	M6ADIS0065	.	36302751	"Mechanistically, senescent neutrophils-derived exosomal piRNA-17560 enhances the expression of fat mass and obesity-associated protein (FTO) in breast cancer cells. The upregulation of FTO further strengthens ZEB1 transcripts stability and expression by decreasing N6-methyladenosine (m6A) RNA methylation, leading to chemoresistance and epithelial-mesenchymal transition (EMT) of tumor cells."
item3951	REG00001	M6ATAR00457	.	M6ADIS0097	.	38761356	"CCRR is a protective lncRNA that acts by maintaining the function of FTO, thereby reducing the m6A RNA methylation level of SERCA2a, ultimately preserving calcium homeostasis for myocardial contractile function in MI."
item3952	REG00007	M6ATAR01747	Down	M6ADIS0006	M6ADRUG0032	39629121	"HNF4A-AS1 interacted with METTL3, leading to m6A modification of DECR1 mRNA, which subsequently decreased DECR1 expression via YTHDF3-dependent mRNA degradation.Our results indicated the pivotal role of lipid metabolism-related and liver-specific HNF4A-AS1 in inhibiting sorafenib resistance by promoting ferroptosis and suggesting that HNF4A-AS1 might be a potential target for HCC."
item3953	REG00025	M6ATAR01747	Down	M6ADIS0006	M6ADRUG0032	39629121	"HNF4A-AS1 interacted with METTL3, leading to m6A modification of DECR1 mRNA, which subsequently decreased DECR1 expression via YTHDF3-dependent mRNA degradation.Our results indicated the pivotal role of lipid metabolism-related and liver-specific HNF4A-AS1 in inhibiting sorafenib resistance by promoting ferroptosis and suggesting that HNF4A-AS1 might be a potential target for HCC."
item3954	REG00014	M6ATAR01748	Up	M6ADIS0010	.	37106446	"HNRNPC mediated circZBTB44 interaction with IGF2BP3 to up-regulate HK3, promoting the proliferation and migration of RCC cells in vitro and tumorigenesis in vivo. The results of the study shed new light on the targeted therapy of RCC."
item3955	REG00024	M6ATAR00399	Up	M6ADIS0057	.	36999803	"PLAGL2 enhances Snail expression and GC progression via the UCA1/miR-145-5p/YTHDF1 axis, suggesting that PLAGL2 may become a therapeutic target for GC treatment."
item3956	REG00005	M6ATAR00334	Up	M6ADIS0008	.	37639643	"Silencing MALAT1 led to down-regulation of the N6-methyladenosine (m6A) demethylase ALKBH5 via regulating miR-141-3p expression, which caused a decrease in the expression levels of matrix metalloproteinase 2 (MMP2) and MMP9 expression, thereby suppressing cell migration and invasion."
item3957	REG00005	M6ATAR00334	Up	M6ADIS0008	.	37639643	"Silencing MALAT1 led to down-regulation of the N6-methyladenosine (m6A) demethylase ALKBH5 via regulating miR-141-3p expression, which caused a decrease in the expression levels of matrix metalloproteinase 2 (MMP2) and MMP9 expression, thereby suppressing cell migration and invasion."
item3958	REG00005	M6ATAR00335	Up	M6ADIS0008	.	37639643	"Silencing MALAT1 led to down-regulation of the N6-methyladenosine (m6A) demethylase ALKBH5 via regulating miR-141-3p expression, which caused a decrease in the expression levels of matrix metalloproteinase 2 (MMP2) and MMP9 expression, thereby suppressing cell migration and invasion."
item3959	REG00005	M6ATAR00335	Up	M6ADIS0008	.	37639643	"Silencing MALAT1 led to down-regulation of the N6-methyladenosine (m6A) demethylase ALKBH5 via regulating miR-141-3p expression, which caused a decrease in the expression levels of matrix metalloproteinase 2 (MMP2) and MMP9 expression, thereby suppressing cell migration and invasion."
item3960	REG00024	M6ATAR00425	Up	M6ADIS0091	.	32890792	MicroRNA-421-3p prevents inflammatory response in cerebral ischemia/reperfusion injury through targeting YTHDF1 to inhibit p65 mRNA translation. These findings provide novel insights into understanding the molecular pathogenesis of cerebral I/R injury.
item3961	REG00056	M6ATAR00755	Down	M6ADIS0006	.	37877357	"CircSTX6 acted as a sponge for HNRNPD protein, facilitating its binding to ATF3 mRNA, consequently promoting ATF3 mRNA decay. Meanwhile, circSTX6-144aa promoted HCC proliferation, migration and invasion independent of circSTX6 itself."
item3962	REG00009	M6ATAR00240	Up	M6ADIS0068	.	35650605	"CircPDE5A blocks the WTAP-dependent N6-methyladenisine (m6A) methylation of eukaryotic translation initiation factor 3c (EIF3C) mRNA by forming the circPDE5A-WTAP complex, and finally disrupts the translation of EIF3C. Moreover, the circPDE5A-dependent decrease in EIF3C expression inactivates the MAPK pathway and then restrains PCa progression."
item3963	REG00014	M6ATAR00277	Up	M6ADIS0070	.	38504159	"IGF2BP3 is negatively regulated by promoter methylation and miR-320a-3p,IGF2BP3 prevent HMGB1 mRNA decay in bladder cancer and development."
item3964	REG00007	M6ATAR00404	Up	M6ADIS0007	.	35467477	"CircVMP1 acted as microRNA-524-5p (miR-524-5p) sponge to up-regulate the expression of methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit (METTL3) and SOX2."
item3965	REG00007	M6ATAR00404	Up	M6ADIS0007	.	35467477	"CircVMP1 acted as microRNA-524-5p (miR-524-5p) sponge to up-regulate the expression of methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit (METTL3) and SOX2."
item3966	REG00014	M6ATAR00484	Up	M6ADIS0006	.	38353724	"LINC00942 suppresses ferroptosis and induces Treg immunosuppression in HCC by recruiting IGF2BP3 to enhance SLC7A11 mRNA stability, which may provide novel therapeutic targets for HCC."
item3967	REG00013	M6ATAR00476	Up	M6ADIS0059	.	34784937	LINC00460 enhanced the protein expression of high-mobility group AT-hook 1 (HMGA1) by directly interacting with IGF2BP2 and DHX9 to bind the 3' untranslated region (UTR) of HMGA1 mRNA and increased the stability of HMGA1 mRNA.
item3968	REG00025	M6ATAR01752	Down	M6ADIS0061	.	35183226	A reciprocal feedback between N6-methyladenosine reader YTHDF3 and lncRNA DICER1-AS1 promotes glycolysis of pancreatic cancer through inhibiting maturation of miR-5586-5p.
item3969	REG00007	M6ATAR00375	Down	M6ADIS0057	.	31711642	"LINC00470-METTL3-mediated PTEN mRNA degradation relied on the m6A reader protein YTHDF2-dependent pathway. Taken together, LINC00470 might serve as a therapeutic target for GC patients."
item3970	REG00008	M6ATAR00375	Down	M6ADIS0057	.	31711642	"LINC00470-METTL3-mediated PTEN mRNA degradation relied on the m6A reader protein YTHDF2-dependent pathway. Taken together, LINC00470 might serve as a therapeutic target for GC patients."
item3971	REG00014	M6ATAR01753	Up	M6ADIS0010	.	33293428	"Mechanistically, DMDRMR bound insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) to stabilize target genes, including the cell-cycle kinase CDK4 and three extracellular matrix components (COL6A1, LAMA5, and FN1), by specifically enhancing IGF2BP3 activity on them in an m6A-dependent manner."
item3972	REG00014	M6ATAR01754	Up	M6ADIS0010	.	33293428	"Mechanistically, DMDRMR bound insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) to stabilize target genes, including the cell-cycle kinase CDK4 and three extracellular matrix components (COL6A1, LAMA5, and FN1), by specifically enhancing IGF2BP3 activity on them in an m6A-dependent manner."
item3973	REG00014	M6ATAR01530	Up	M6ADIS0010	.	33293428	"Mechanistically, DMDRMR bound insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) to stabilize target genes, including the cell-cycle kinase CDK4 and three extracellular matrix components (COL6A1, LAMA5, and FN1), by specifically enhancing IGF2BP3 activity on them in an m6A-dependent manner."
item3974	REG00007	M6ATAR01486	.	M6ADIS0007	.	33781830	METTL3 was confirmed as a direct target gene of miR-4443. Further mechanistic analysis showed that miR-4443 regulated the expression of FSP1 in an m6A manner via METLL3.
item3975	REG00034	M6ATAR00605	Up	M6ADIS0168	.	34412584	"METTL14 was highly present in NP cells from IVDD patients, which stabilize NLRP3 mRNA in an IGFBP2-dependent manner. The elevated NLRP3 levels result in the increase of interleukin 1beta (IL-1beta) and IL-18 levels and trigger pyroptotic NP cell death. Such pathogenic axis could be blocked by hucMSC exosomes, which directly degrade METTL14 through exosomal miR-26a-5p."
item3976	REG00012	M6ATAR00692	Up	M6ADIS0068	.	34537760	"METTL3-mediated m6A modification of KIF3C-mRNA promotes prostate cancer progression and is negatively regulated by miR-320d.METTL3 induced m6A modification on KIF3C, promoting the stabilization of KIF3C-mRNA by IGF2 binding protein 1 (IGF2BP1)."
item3977	REG00013	M6ATAR01757	Up	M6ADIS0065	.	39496940	Hypoxia induced cellular and exosomal RPPH1 promotes breast cancer angiogenesis and metastasis through stabilizing the IGF2BP2/FGFR2 axis.
item3978	REG00008	M6ATAR01415	Down	M6ADIS0243	.	35383152	"Ythdf2 function was a downstream of MIAT in cardiac hypertrophy. Finally, we found that MIAT was a necessary regulator of cardiac hypertrophy due to its regulation of the Ythdf2/PPARalpha/CPT-1a axis. This study indicated a new hypertrophic signaling pathway: MIAT/Ythdf2/PPARalpha/CPT-1a. The results provided a new understanding of the MIAT and m6A RNA methylation reading protein, Ythdf2, function and mechanism in cardiac hypertrophy and highlighted the potential therapeutic benefits in the heart."
item3979	REG00007	M6ATAR00157	Up	M6ADIS0004	.	33749070	"The molecular mechanism underlying the effect of Long intergenic non-protein coding RNA 470 (LINC00470) on chronic myelocytic leukaemia by reducing the PTEN stability via RNA methyltransferase METTL3, thus leading to the inhibition of cell autophagy while promoting chemoresistance in CML."
item3980	REG00013	M6ATAR00276	Up	M6ADIS0059	.	33526059	LINC00460/DHX9/IGF2BP2 complex promotes colorectal cancer proliferation and metastasis by mediating HMGA1 mRNA stability depending on m6A modification.
item3981	REG00008	M6ATAR01535	Down	M6ADIS0077	.	30065315	"ADAR interacts with hsa-mir-18a, increasing it's A-to-I level and promoting its physical interaction with RUNX1, which was regulated by YTHDF2-mediated m6A modification."
item3982	REG00008	M6ATAR01537	Down	M6ADIS0077	.	30065315	"ADAR interacts with hsa-mir-210, increasing it's A-to-I level and promoting its physical interaction with SMAD4, which was regulated by YTHDF2-mediated m6A modification."
item3983	REG00006	M6ATAR01544	Up	.	.	34302813	"ADAR interacts with NEAT1, increasing it's A-to-I level and promoting its physical interaction with hsa-mir-146a, which was regulated by METTL14-mediated m6A modification."
item3984	REG00013	M6ATAR01538	Up	M6ADIS0006	.	34347395	"ADARB1 interacts with hsa-mir-122, increasing it's A-to-I level and inhibiting its physical interaction with SOX6, which was regulated by IGF2BP2-mediated m6A modification."
item3985	REG00006	M6ATAR01538	Up	M6ADIS0006	.	34347395	"ADARB1 interacts with hsa-mir-122, increasing it's A-to-I level and inhibiting its physical interaction with SOX6, which was regulated by METTL14-mediated m6A modification."
item3986	REG00007	M6ATAR01538	Up	M6ADIS0006	.	34347395	"ADARB1 interacts with hsa-mir-122, increasing it's A-to-I level and inhibiting its physical interaction with SOX6, which was regulated by METTL3-mediated m6A modification."
item3987	REG00007	M6ATAR01842	.	M6ADIS0056	.	36071173	"Here, we show that METTL3-mediated RNA N6-methyladenosine (m6A) formation leads to DNA demethylation in nearby genomic loci in normal and cancer cells, which is mediated by the interaction between m6A reader FXR1 and DNA 5-methylcytosine dioxygenase TET1. Upon recognizing RNA m6A, FXR1 recruits TET1 to genomic loci to demethylate DNA, leading to reprogrammed chromatin accessibility and gene transcription. These gene include SATB2, RPIA, WNT7B, BCL6, FAT4 and SAMD9L."
item3988	REG00051	M6ATAR01842	.	M6ADIS0056	.	36071173	"Here, we show that METTL3-mediated RNA N6-methyladenosine (m6A) formation leads to DNA demethylation in nearby genomic loci in normal and cancer cells, which is mediated by the interaction between m6A reader FXR1 and DNA 5-methylcytosine dioxygenase TET1. Upon recognizing RNA m6A, FXR1 recruits TET1 to genomic loci to demethylate DNA, leading to reprogrammed chromatin accessibility and gene transcription. These gene include SATB2, RPIA, WNT7B, BCL6, FAT4 and SAMD9L."
item3989	REG00007	M6ATAR01840	.	M6ADIS0056	.	36071173	"Here, we show that METTL3-mediated RNA N6-methyladenosine (m6A) formation leads to DNA demethylation in nearby genomic loci in normal and cancer cells, which is mediated by the interaction between m6A reader FXR1 and DNA 5-methylcytosine dioxygenase TET1. Upon recognizing RNA m6A, FXR1 recruits TET1 to genomic loci to demethylate DNA, leading to reprogrammed chromatin accessibility and gene transcription. These gene include SATB2, RPIA, WNT7B, BCL6, FAT4 and SAMD9L."
item3990	REG00051	M6ATAR01840	.	M6ADIS0056	.	36071173	"Here, we show that METTL3-mediated RNA N6-methyladenosine (m6A) formation leads to DNA demethylation in nearby genomic loci in normal and cancer cells, which is mediated by the interaction between m6A reader FXR1 and DNA 5-methylcytosine dioxygenase TET1. Upon recognizing RNA m6A, FXR1 recruits TET1 to genomic loci to demethylate DNA, leading to reprogrammed chromatin accessibility and gene transcription. These gene include SATB2, RPIA, WNT7B, BCL6, FAT4 and SAMD9L."
item3991	REG00007	M6ATAR01843	.	M6ADIS0056	.	36071173	"Here, we show that METTL3-mediated RNA N6-methyladenosine (m6A) formation leads to DNA demethylation in nearby genomic loci in normal and cancer cells, which is mediated by the interaction between m6A reader FXR1 and DNA 5-methylcytosine dioxygenase TET1. Upon recognizing RNA m6A, FXR1 recruits TET1 to genomic loci to demethylate DNA, leading to reprogrammed chromatin accessibility and gene transcription. These gene include SATB2, RPIA, WNT7B, BCL6, FAT4 and SAMD9L."
item3992	REG00051	M6ATAR01843	.	M6ADIS0056	.	36071173	"Here, we show that METTL3-mediated RNA N6-methyladenosine (m6A) formation leads to DNA demethylation in nearby genomic loci in normal and cancer cells, which is mediated by the interaction between m6A reader FXR1 and DNA 5-methylcytosine dioxygenase TET1. Upon recognizing RNA m6A, FXR1 recruits TET1 to genomic loci to demethylate DNA, leading to reprogrammed chromatin accessibility and gene transcription. These gene include SATB2, RPIA, WNT7B, BCL6, FAT4 and SAMD9L."
item3993	REG00007	M6ATAR01835	.	M6ADIS0056	.	36071173	"Here, we show that METTL3-mediated RNA N6-methyladenosine (m6A) formation leads to DNA demethylation in nearby genomic loci in normal and cancer cells, which is mediated by the interaction between m6A reader FXR1 and DNA 5-methylcytosine dioxygenase TET1. Upon recognizing RNA m6A, FXR1 recruits TET1 to genomic loci to demethylate DNA, leading to reprogrammed chromatin accessibility and gene transcription. These gene include SATB2, RPIA, WNT7B, BCL6, FAT4 and SAMD9L."
item3994	REG00051	M6ATAR01835	.	M6ADIS0056	.	36071173	"Here, we show that METTL3-mediated RNA N6-methyladenosine (m6A) formation leads to DNA demethylation in nearby genomic loci in normal and cancer cells, which is mediated by the interaction between m6A reader FXR1 and DNA 5-methylcytosine dioxygenase TET1. Upon recognizing RNA m6A, FXR1 recruits TET1 to genomic loci to demethylate DNA, leading to reprogrammed chromatin accessibility and gene transcription. These gene include SATB2, RPIA, WNT7B, BCL6, FAT4 and SAMD9L."
item3995	REG00007	M6ATAR01841	.	M6ADIS0056	.	36071173	"Here, we show that METTL3-mediated RNA N6-methyladenosine (m6A) formation leads to DNA demethylation in nearby genomic loci in normal and cancer cells, which is mediated by the interaction between m6A reader FXR1 and DNA 5-methylcytosine dioxygenase TET1. Upon recognizing RNA m6A, FXR1 recruits TET1 to genomic loci to demethylate DNA, leading to reprogrammed chromatin accessibility and gene transcription. These gene include SATB2, RPIA, WNT7B, BCL6, FAT4 and SAMD9L."
item3996	REG00051	M6ATAR01841	.	M6ADIS0056	.	36071173	"Here, we show that METTL3-mediated RNA N6-methyladenosine (m6A) formation leads to DNA demethylation in nearby genomic loci in normal and cancer cells, which is mediated by the interaction between m6A reader FXR1 and DNA 5-methylcytosine dioxygenase TET1. Upon recognizing RNA m6A, FXR1 recruits TET1 to genomic loci to demethylate DNA, leading to reprogrammed chromatin accessibility and gene transcription. These gene include SATB2, RPIA, WNT7B, BCL6, FAT4 and SAMD9L."
item3997	REG00009	M6ATAR01838	.	M6ADIS0125	.	32875102	"Knockout (KO) of YTHDF2, an m6A reader, markedly enhanced demethylation of H3K27me3 on the promoters of proinflammatory cytokines (e.g., IL-6 and IL-12B). Furthermore, we identified H3K27me3 as a barrier for m6A modification during transcription. KDM6B recruits the m6A methyltransferase complex (METTL3/METTL14/WTAP) to facilitate the methylation of m6A in transcribing mRNA by removing adjacent H3K27me3 barriers. These results revealed cross-talk between m6A and H3K27me3 during bacterial infection, which has broader implications for deciphering epitranscriptomics in immune homeostasis."
item3998	REG00007	M6ATAR01838	.	M6ADIS0125	.	32875102	"Knockout (KO) of YTHDF2, an m6A reader, markedly enhanced demethylation of H3K27me3 on the promoters of proinflammatory cytokines (e.g., IL-6 and IL-12B). Furthermore, we identified H3K27me3 as a barrier for m6A modification during transcription. KDM6B recruits the m6A methyltransferase complex (METTL3/METTL14/WTAP) to facilitate the methylation of m6A in transcribing mRNA by removing adjacent H3K27me3 barriers. These results revealed cross-talk between m6A and H3K27me3 during bacterial infection, which has broader implications for deciphering epitranscriptomics in immune homeostasis."
item3999	REG00006	M6ATAR01838	.	M6ADIS0125	.	32875102	"Knockout (KO) of YTHDF2, an m6A reader, markedly enhanced demethylation of H3K27me3 on the promoters of proinflammatory cytokines (e.g., IL-6 and IL-12B). Furthermore, we identified H3K27me3 as a barrier for m6A modification during transcription. KDM6B recruits the m6A methyltransferase complex (METTL3/METTL14/WTAP) to facilitate the methylation of m6A in transcribing mRNA by removing adjacent H3K27me3 barriers. These results revealed cross-talk between m6A and H3K27me3 during bacterial infection, which has broader implications for deciphering epitranscriptomics in immune homeostasis."
item4000	REG00007	M6ATAR01672	Up	M6ADIS0059	.	34544413	"LINC01605 was regulated by SMYD2-EP300-mediated modifications of histone H3K4me3 as well as H3K27ac. LINC01605 was found to bind to METTL3 and promote the m6A modification of SPTBN2 mRNA, thereby facilitating the translation of SPTBN2. hsa_circ_0000677 and its downstream target ABCC1 were upregulated in CRC cells, induced by the  METTL3-mediated m6A modification of circ_0000677 and SUMO1-mediated SUMOylation of METTL3. This work provided a new strategy for the therapeutic treatment of CRC."
item4001	REG00007	M6ATAR00797	Up	M6ADIS0004	.	32703936	"MALAT1 hijacks both the chimeric mRNAs and fusion proteins in nuclear speckles during chromosomal translocations and mediates the colocalization of oncogenic fusion proteins with METTL14. MALAT1 and fusion protein complexes serve as a functional loading bridge for the interaction of PML-RARalpha mRNA, METTL14, METTL3 and WTAP. MALAT1 regulates chimeric mRNA export in a manner dependent on the YTHDC1 and SRSF3"
item4002	REG00006	M6ATAR00797	Up	M6ADIS0004	.	32703936	"MALAT1 hijacks both the chimeric mRNAs and fusion proteins in nuclear speckles during chromosomal translocations and mediates the colocalization of oncogenic fusion proteins with METTL14. MALAT1 and fusion protein complexes serve as a functional loading bridge for the interaction of PML-RARalpha mRNA, METTL14, METTL3 and WTAP. MALAT1 regulates chimeric mRNA export in a manner dependent on the YTHDC1 and SRSF3"
item4003	REG00009	M6ATAR00797	Up	M6ADIS0004	.	32703936	"MALAT1 hijacks both the chimeric mRNAs and fusion proteins in nuclear speckles during chromosomal translocations and mediates the colocalization of oncogenic fusion proteins with METTL14. MALAT1 and fusion protein complexes serve as a functional loading bridge for the interaction of PML-RARalpha mRNA, METTL14, METTL3 and WTAP. MALAT1 regulates chimeric mRNA export in a manner dependent on the YTHDC1 and SRSF3"
item4004	REG00022	M6ATAR00797	Up	M6ADIS0001	.	32703936	"MALAT1 hijacks both the chimeric mRNAs and fusion proteins in nuclear speckles during chromosomal translocations and mediates the colocalization of oncogenic fusion proteins with METTL14. MALAT1 and fusion protein complexes serve as a functional loading bridge for the interaction of PML-RARalpha mRNA, METTL14, METTL3 and WTAP. MALAT1 regulates chimeric mRNA export in a manner dependent on the YTHDC1 and SRSF3"
item4005	REG00007	M6ATAR01556	Up	M6ADIS0057	M6ADRUG0105	33037176	"METTL3 interacts with hsa-mir-19b-1, decreasing its m6A level and promoting its physical interaction with SIRT1, which was regulated by FTO-mediated m6Am modification. "
item4006	REG00007	M6ATAR01839	Up	.	.	34666602	"METTL3 promoted m6A modification and the binding of DGCR8 to miR-20a-5p to further elevate the miR-20a-5p expression and inhibit NFIC transcription, thus promoting EMT, invasion and migration."
item4007	REG00001	M6ATAR01837	Up	M6ADIS0001	.	33684100	miR-145 induces binding of FTO to CLIP3 mRNA and increases cellular m6A demethylase activity. miRNA-mediated loss of m6A increases nascent translation in glioblastoma
item4008	REG00006	M6ATAR01555	Up	M6ADIS0099	.	32633395	"NSUN2 interacts with H19, increasing its m5C level and promoting its physical interaction with hsa-mir-19a, which was regulated by METTL14-mediated m6A modification."
item4009	REG00007	M6ATAR01555	Up	M6ADIS0057	M6ADRUG0105	33037176	"NSUN2 interacts with H19, increasing its m5C level and promoting its physical interaction with hsa-mir-19a, which was regulated by METTL3-mediated m6A modification."
item4010	REG00050	M6ATAR01836	Down	M6ADIS0004	.	37640841	"RBFOX2 can recruit RBM15, an MTC component, to facilitate methylation of promoter-associated RNAs. RBM15 also physically interacts with YTHDC1 and recruits polycomb repressive complex 2 (PRC2) to the RBFOX2-bound loci for chromatin silencing and transcription suppression. PRC2, a key player in epigenetic regulation, is known to mediate the trimethylation of histone H3 on lysine 27 (H3K27me3). This modification is crucial for the establishment of a repressive chromatin state, effectively preventing the binding of transcriptional activators and thus suppressing gene expression at the loci targeted by RBFOX2 and its associated factors. RBFOX2/m6A/RBM15/YTHDC1/PRC2 axis plays a critical role in myeloid leukaemia. "
item4011	REG00020	M6ATAR01836	Down	M6ADIS0004	.	37640841	"RBFOX2 can recruit RBM15, an MTC component, to facilitate methylation of promoter-associated RNAs. RBM15 also physically interacts with YTHDC1 and recruits polycomb repressive complex 2 (PRC2) to the RBFOX2-bound loci for chromatin silencing and transcription suppression. PRC2, a key player in epigenetic regulation, is known to mediate the trimethylation of histone H3 on lysine 27 (H3K27me3). This modification is crucial for the establishment of a repressive chromatin state, effectively preventing the binding of transcriptional activators and thus suppressing gene expression at the loci targeted by RBFOX2 and its associated factors. RBFOX2/m6A/RBM15/YTHDC1/PRC2 axis plays a critical role in myeloid leukaemia. "
item4012	REG00022	M6ATAR01836	Down	M6ADIS0004	.	37640841	"RBFOX2 can recruit RBM15, an MTC component, to facilitate methylation of promoter-associated RNAs. RBM15 also physically interacts with YTHDC1 and recruits polycomb repressive complex 2 (PRC2) to the RBFOX2-bound loci for chromatin silencing and transcription suppression. PRC2, a key player in epigenetic regulation, is known to mediate the trimethylation of histone H3 on lysine 27 (H3K27me3). This modification is crucial for the establishment of a repressive chromatin state, effectively preventing the binding of transcriptional activators and thus suppressing gene expression at the loci targeted by RBFOX2 and its associated factors. RBFOX2/m6A/RBM15/YTHDC1/PRC2 axis plays a critical role in myeloid leukaemia. "