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 m7A 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 m7A 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 M6ADIS0045 . 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 M6ADIS0045 . 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 Up 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 . M6ADIS0012 . 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 M6ADIS0012 . 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 M6ADIS0012 . 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 M6ADIS0012 . 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 M6ADIS0012 . 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 . M6ADIS0012 . 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 M6ADIS0012 . 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, 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 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 . . 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-Kappa-B 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-Kappa-B 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-Kappa-B 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-Kappa-B 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 M6ATAR00050 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 M6ATAR00050 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 M6ADIS0012 . 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 M6ADIS0012 . 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 . M6ADIS0012 . 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 . . 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 . 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 MA2, a chemical inhibitor of FTO, dramatically suppressed GSC-induced tumorigenesis and prolonged lifespan in GSC-grafted animals. item1013 REG00006 M6ATAR00171 Down M6ADIS0001 . 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 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 beta-hydroxybutyrate (BHB) transiently increases FTO expression in both mouse hypothalamus and cultured cells. item1015 REG00001 . . M6ADIS0095 . 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. item1016 REG00001 M6ATAR00410 Down . . 30046135 The m6A changes caused by FTO influence the stability of ULK1 transcripts, likely through a YTHDF2-dependent manner.Under both basal and 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 . . 30046135 The m6A changes caused by FTO influence the stability of ULK1 transcripts, likely through a YTHDF2-dependent manner.Under both basal and 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 . . 30046135 The m6A changes caused by FTO influence the stability of ULK1 transcripts, likely through a YTHDF2-dependent manner.Under both basal and 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(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(FB23 and FB23-2) holds potential to treat acute myeloid leukemia. item1021 REG00015 M6ATAR00209 Up M6ADIS0065 . 31285549 KIAA1429 acts as an oncogenic factor in breast cancer by regulating CDK1 in an N6-methyladenosine-independent manner.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 . 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 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 (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 (PT2385) restored YTHDF2-programed epigenetic machinery and repressed liver cancer. item1025 REG00001 M6ATAR00348 Up M6ADIS0130 . 31923814 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 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). Cycloleucine (Cyc) was used to block m6 A methylation in UM cells. item1028 . . . 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 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 AFB1 and resveratrol in m6A RNA methylation and their crosstalk in the regulation of hepatic function in mice. item1030 REG00007 M6ATAR00249 Up M6ADIS0007 . 32373962 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 . 32518161 Mammalian target of rapamycin complex 1 (mTORC1) pathway is highly activated in rbm15-deficient hepatocytes. 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 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 . 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 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), 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, 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 . 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 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 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. 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, 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 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 . 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 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 . 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 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 . 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 rapamycin treatment. item1045 REG00007 M6ATAR00175 Up M6ADIS0011 . 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 rapamycin treatment. item1046 REG00007 M6ATAR00339 Up M6ADIS0011 . 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 rapamycin treatment. item1047 REG00007 M6ATAR00313 Up M6ADIS0011 . 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 rapamycin treatment. item1048 REG00007 M6ATAR00159 Down M6ADIS0011 . 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 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. 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 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 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 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 . 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 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 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 . 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 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 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 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 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 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 lipopolysaccharide (LPS) compromises female reproduction, especially oocyte maturation and competence. 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 lipopolysaccharide (LPS) compromises female reproduction, especially oocyte maturation and competence. 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, 4-PBA. item1063 REG00007 . . M6ADIS0046 . 33902106 inhibition of METTL3 by 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 . 33972683 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 . 33972683 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 . . 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. 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. 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. 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, 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, 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, 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, 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, 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, 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, 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, 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 . 34869024 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 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 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 M6ADIS0029 . 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 M6ATAR00005 . 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 M6ATAR00005 . M6ADIS0012 . 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 M6ATAR00005 . 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 . M6ADIS0029 . 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 M6ATAR00005 . 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 M6ATAR00005 . 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 M6ATAR00005 . 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 M6ATAR00005 . 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 M6ATAR00789 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 M6ATAR00790 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 M6ATAR00005 . 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 M6ADIS0012 . 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 M6ATAR00005 . 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 M6ATAR00005 . 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 M6ATAR00005 . . . 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 M6ATAR00005 . . . 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 M6ATAR00005 . 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 M6ADIS0012 . 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 M6ADIS0012 . 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 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 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 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 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 . M6ATAR00543 . 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 M6ADIS0012 . 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 . 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 M6ADIS0012 . 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 M6ADIS0012 . 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 . . M6ADIS0012 . 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 . 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 . 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 M6ADIS0012 . 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 M6ADIS0012 . 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.