Name	Solid tumour/cancer
ICD	ICD-11: 2A00-2F9Z

In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[1]
Response Summary	m6A induced ERR-Gamma confers chemoresistance of cancer cells through upregulation of ATP-dependent translocase ABCB1 (ABCB1) and CPT1B.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Pathway Response	ABC transporters			hsa02010
	Fatty acid metabolism			hsa01212
	Fatty acid degradation			hsa00071
Cell Process	Fatty acid oxidation
In-vitro Model	A-549	Lung adenocarcinoma	Homo sapiens	CVCL_0023
	Hep-G2	Hepatoblastoma	Homo sapiens	CVCL_0027
	MCF-7	Invasive breast carcinoma	Homo sapiens	CVCL_0031
	MDA-MB-231	Breast adenocarcinoma	Homo sapiens	CVCL_0062
In-vivo Model	Both sh-control and sh- ERRγ HepG2/ADR cells (5 × 106 per mouse, n=5 for each group) were diluted in 200uL PBS + 200 uL Matrigel (BD Biosciences) and subcutaneously injected into immunodeficient mice.

In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[1]
Response Summary	m6A induced ERR-Gamma confers chemoresistance of cancer cells through upregulation of ABCB1 and Carnitine O-palmitoyltransferase 1, muscle isoform (CPT1B).
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Pathway Response	ABC transporters			hsa02010
	Fatty acid metabolism			hsa01212
	Fatty acid degradation			hsa00071
Cell Process	Fatty acid oxidation
In-vitro Model	A-549	Lung adenocarcinoma	Homo sapiens	CVCL_0023
	Hep-G2	Hepatoblastoma	Homo sapiens	CVCL_0027
	MCF-7	Invasive breast carcinoma	Homo sapiens	CVCL_0031
	MDA-MB-231	Breast adenocarcinoma	Homo sapiens	CVCL_0062
In-vivo Model	Both sh-control and sh- ERRγ HepG2/ADR cells (5 × 106 per mouse, n=5 for each group) were diluted in 200uL PBS + 200 uL Matrigel (BD Biosciences) and subcutaneously injected into immunodeficient mice.

In total 2 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[2]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Responsed Drug	Arsenite		Phase 2	Drug Info
Target Regulator	YTH domain-containing family protein 1 (YTHDF1)		READER	Regulator Info
Target Regulation	Down regulation
Pathway Response	p53 signaling pathway			hsa04115
In-vitro Model	HaCaT	Normal	Homo sapiens	CVCL_0038
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene				[2]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Responsed Drug	Arsenite		Phase 2	Drug Info
Target Regulator	Methyltransferase-like 3 (METTL3)		WRITER	Regulator Info
Target Regulation	Up regulation
Pathway Response	p53 signaling pathway			hsa04115
In-vitro Model	HaCaT	Normal	Homo sapiens	CVCL_0038

In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[3]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Target Regulator	Fat mass and obesity-associated protein (FTO)		ERASER	Regulator Info
Pathway Response	Autophagy			hsa04140
Cell Process	Cellular Processes, Transport and catabolism
	Cell autophagy
In-vitro Model	HaCaT	Normal	Homo sapiens	CVCL_0038
	HEK293T	Normal	Homo sapiens	CVCL_0063
	HeLa	Endocervical adenocarcinoma	Homo sapiens	CVCL_0030
	MEF (Mouse embryonic fibroblasts)
In-vivo Model	As cells (5 million) in Matrigel or As-T (1 million) cells in PBS with or without gene manipulations were injected subcutaneously into the right flanks of female mice (6-8 weeks of age). For treatment with CS1 or CS2, As-T cells (1 million) in PBS were injected subcutaneously into the right flanks of 6-week-old female nude mice.

In total 2 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[4]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Target Regulator	Methyltransferase-like 14 (METTL14)		WRITER	Regulator Info
Target Regulation	Up regulation
Cell Process	RNA stability
	Cell apoptosis
In-vitro Model	BT-549	Invasive breast carcinoma	Homo sapiens	CVCL_1092
	DU145	Prostate carcinoma	Homo sapiens	CVCL_0105
	HeLa	Endocervical adenocarcinoma	Homo sapiens	CVCL_0030
	Hep-G2	Hepatoblastoma	Homo sapiens	CVCL_0027
	MCF-7	Invasive breast carcinoma	Homo sapiens	CVCL_0031
	MDA-MB-231	Breast adenocarcinoma	Homo sapiens	CVCL_0062
	MDA-MB-468	Breast adenocarcinoma	Homo sapiens	CVCL_0419
In-vivo Model	For tumor xenograft studies, MDA-MB-231 cells transfected with scrambled-siRNA or METTL14-siRNA or ALKBH5-siRNA (2 × 106) were mixed with Matrigel and injected subcutaneously in the flank of 6-week-old female athymic nude mice.
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene				[4]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Target Regulator	RNA demethylase ALKBH5 (ALKBH5)		ERASER	Regulator Info
Target Regulation	Up regulation
Cell Process	RNA stability
	Cell apoptosis
In-vitro Model	BT-549	Invasive breast carcinoma	Homo sapiens	CVCL_1092
	DU145	Prostate carcinoma	Homo sapiens	CVCL_0105
	HeLa	Endocervical adenocarcinoma	Homo sapiens	CVCL_0030
	Hep-G2	Hepatoblastoma	Homo sapiens	CVCL_0027
	MCF-7	Invasive breast carcinoma	Homo sapiens	CVCL_0031
	MDA-MB-231	Breast adenocarcinoma	Homo sapiens	CVCL_0062
	MDA-MB-468	Breast adenocarcinoma	Homo sapiens	CVCL_0419
In-vivo Model	For tumor xenograft studies, MDA-MB-231 cells transfected with scrambled-siRNA or METTL14-siRNA or ALKBH5-siRNA (2 × 106) were mixed with Matrigel and injected subcutaneously in the flank of 6-week-old female athymic nude mice.

In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[5]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Target Regulator	Fat mass and obesity-associated protein (FTO)		ERASER	Regulator Info
Target Regulation	Down regulation
Cell Process	Deficiency of lipid accumulation
	Cellular apoptosis
In-vitro Model	Hep-G2	Hepatoblastoma	Homo sapiens	CVCL_0027

In total 2 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[6]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Target Regulator	Zinc finger CCCH domain-containing protein 13 (ZC3H13)		WRITER	Regulator Info
In-vitro Model	SK-LMS-1	Vulvar leiomyosarcoma	Homo sapiens	CVCL_0628
	MDA-MB-157	Breast carcinoma	Homo sapiens	CVCL_0618
	MCF-7	Invasive breast carcinoma	Homo sapiens	CVCL_0031
In-vivo Model	BALB/c nude mice (5 weeks old) were purchased from the Beijing HFK Bioscience Co. Ltd. 2×106 cells (50 uL) were mixed with 50 uL Matrigel (BD Biosciences, San Jose, CA, USA) were injected subcutaneously in the rear flank fat pad of the nude mice (N = 6, per group).
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene				[6]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Target Regulator	E3 ubiquitin-protein ligase Hakai (CBLL1)		WRITER	Regulator Info
In-vitro Model	SK-LMS-1	Vulvar leiomyosarcoma	Homo sapiens	CVCL_0628
	MDA-MB-157	Breast carcinoma	Homo sapiens	CVCL_0618
	MCF-7	Invasive breast carcinoma	Homo sapiens	CVCL_0031
In-vivo Model	BALB/c nude mice (5 weeks old) were purchased from the Beijing HFK Bioscience Co. Ltd. 2×106 cells (50 uL) were mixed with 50 uL Matrigel (BD Biosciences, San Jose, CA, USA) were injected subcutaneously in the rear flank fat pad of the nude mice (N = 6, per group).

In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[7]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]

In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[7]
Response Summary	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).
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]

In total 2 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[7]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene				[8]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Target Regulator	Fat mass and obesity-associated protein (FTO)		ERASER	Regulator Info
Target Regulation	Down regulation
Pathway Response	Wnt signaling pathway			hsa04310
	Central carbon metabolism in cancer			hsa05230
	Glycolysis / Gluconeogenesis			hsa00010
Cell Process	Glycolysis
In-vitro Model	NCI-H322	Minimally invasive lung adenocarcinoma	Homo sapiens	CVCL_1556
	HEK293T	Normal	Homo sapiens	CVCL_0063
In-vivo Model	Mice were randomized into several groups. For the subcutaneous implantation model, 1?×?106 cells were injected subcutaneously into the flank regions of female BALB/c nude mice (4-5 weeks). For lung colonization assays, 1 × 106 cells were injected into the tail vein of female NOD/SCID mice (6-7 weeks), and 6 weeks later the lung was removed and fixed with 10% formalin.

In total 2 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[2]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Responsed Drug	Arsenite		Phase 2	Drug Info
Target Regulator	YTH domain-containing family protein 1 (YTHDF1)		READER	Regulator Info
Target Regulation	Down regulation
Pathway Response	p53 signaling pathway			hsa04115
In-vitro Model	HaCaT	Normal	Homo sapiens	CVCL_0038
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene				[2]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Responsed Drug	Arsenite		Phase 2	Drug Info
Target Regulator	Methyltransferase-like 3 (METTL3)		WRITER	Regulator Info
Target Regulation	Up regulation
Pathway Response	p53 signaling pathway			hsa04115
In-vitro Model	HaCaT	Normal	Homo sapiens	CVCL_0038

In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[9]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Target Regulator	Methyltransferase-like 3 (METTL3)		WRITER	Regulator Info
Target Regulation	Up regulation
Pathway Response	Glycerolipid metabolism			hsa00561
Cell Process	Glycolysis
In-vitro Model	SiHa	Cervical squamous cell carcinoma	Homo sapiens	CVCL_0032
	MDA-MB-231	Breast adenocarcinoma	Homo sapiens	CVCL_0062
	Huh-7	Adult hepatocellular carcinoma	Homo sapiens	CVCL_0336
	Hep-G2	Hepatoblastoma	Homo sapiens	CVCL_0027
	HeLa	Endocervical adenocarcinoma	Homo sapiens	CVCL_0030
In-vivo Model	As to the subcutaneous transplanted model, WT Vec, Mettl3 Mut/-+vec, WTPDK4, Mettl3 Mut/-+vecPDK4 cells (2 × 10 6 per mouse, n = 10 for each group) were diluted in 200 uL normal medium + 200 uL Matrigel (BD Biosciences) and subcutaneously injected into immunodeficient mice to investigate tumor growth.

In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[3]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Target Regulator	Fat mass and obesity-associated protein (FTO)		ERASER	Regulator Info
Target Regulation	Down regulation
Pathway Response	Autophagy			hsa04140
Cell Process	Cellular Processes, Transport and catabolism
	Cell autophagy
In-vitro Model	HaCaT	Normal	Homo sapiens	CVCL_0038
	HEK293T	Normal	Homo sapiens	CVCL_0063
	HeLa	Endocervical adenocarcinoma	Homo sapiens	CVCL_0030
	MEF (Mouse embryonic fibroblasts)
In-vivo Model	As cells (5 million) in Matrigel or As-T (1 million) cells in PBS with or without gene manipulations were injected subcutaneously into the right flanks of female mice (6-8 weeks of age). For treatment with CS1 or CS2, As-T cells (1 million) in PBS were injected subcutaneously into the right flanks of 6-week-old female nude mice.

In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[10]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Target Regulator	Methyltransferase-like 3 (METTL3)		WRITER	Regulator Info
Target Regulation	Down regulation
Pathway Response	Homologous recombination			hsa03440
	p53 signaling pathway			hsa04115
In-vitro Model	BJAB	Burkitt lymphoma	Homo sapiens	CVCL_5711
	Raji	EBV-related Burkitt lymphoma	Homo sapiens	CVCL_0511

In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[11]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Target Regulator	Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1)		READER	Regulator Info
Target Regulation	Up regulation
Cell Process	Cell growth
	Cell invasion
In-vitro Model	A-549	Lung adenocarcinoma	Homo sapiens	CVCL_0023
	Hep-G2	Hepatoblastoma	Homo sapiens	CVCL_0027
	K-562	Chronic myelogenous leukemia	Homo sapiens	CVCL_0004

In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[7]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]

In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[12]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Target Regulator	Methyltransferase-like 3 (METTL3)		WRITER	Regulator Info
Target Regulation	Up regulation
Pathway Response	Adherens junction			hsa04520
Cell Process	Epithelial-mesenchymal transition
In-vitro Model	HeLa	Endocervical adenocarcinoma	Homo sapiens	CVCL_0030

In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[13]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Pathway Response	PI3K-Akt signaling pathway			hsa04151
	mTOR signaling pathway			hsa04150
Cell Process	Microsatellite instability
	Mismatch repair
In-vitro Model	U-2 OS cell line (Human osteosarcoma cells)

In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene				[12]
Response Summary	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.
Responsed Disease	Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Target Regulator	Methyltransferase-like 3 (METTL3)		WRITER	Regulator Info
Target Regulation	Up regulation
Pathway Response	Adherens junction			hsa04520
Cell Process	Epithelial-mesenchymal transition
In-vitro Model	HeLa	Endocervical adenocarcinoma	Homo sapiens	CVCL_0030

Ref 1	N6-methyladenosine-induced ERRGamma triggers chemoresistance of cancer cells through upregulation of ABCB1 and metabolic reprogramming. Theranostics. 2020 Feb 10;10(8):3382-3396. doi: 10.7150/thno.40144. eCollection 2020.
Ref 2	N(6)-methyladenosine mediates arsenite-induced human keratinocyte transformation by suppressing p53 activation. Environ Pollut. 2020 Apr;259:113908. doi: 10.1016/j.envpol.2019.113908. Epub 2020 Jan 7.
Ref 3	Autophagy of the m(6)A mRNA demethylase FTO is impaired by low-level arsenic exposure to promote tumorigenesis. Nat Commun. 2021 Apr 12;12(1):2183. doi: 10.1038/s41467-021-22469-6.
Ref 4	Cross-talk among writers, readers, and erasers of m(6)A regulates cancer growth and progression. Sci Adv. 2018 Oct 3;4(10):eaar8263. doi: 10.1126/sciadv.aar8263. eCollection 2018 Oct.
Ref 5	Fat mass and obesity-associated protein regulates lipogenesis via m(6) A modification in fatty acid synthase mRNA. Cell Biol Int. 2021 Feb;45(2):334-344. doi: 10.1002/cbin.11490. Epub 2020 Nov 8.
Ref 6	Ginsenoside Rh2 reduces m6A RNA methylation in cancer via the KIF26B-SRF positive feedback loop. J Ginseng Res. 2021 Nov;45(6):734-743. doi: 10.1016/j.jgr.2021.05.004. Epub 2021 May 25.
Ref 7	Aberrant expression of enzymes regulating m(6)A mRNA methylation: implication in cancer. Cancer Biol Med. 2018 Nov;15(4):323-334. doi: 10.20892/j.issn.2095-3941.2018.0365.
Ref 8	WNT/Beta-catenin-suppressed FTO expression increases m(6)A of c-Myc mRNA to promote tumor cell glycolysis and tumorigenesis. Cell Death Dis. 2021 May 8;12(5):462. doi: 10.1038/s41419-021-03739-z.
Ref 9	N(6)-methyladenosine regulates glycolysis of cancer cells through PDK4. Nat Commun. 2020 May 22;11(1):2578. doi: 10.1038/s41467-020-16306-5.
Ref 10	N6-methyladenosine regulates ATM expression and downstream signaling. J Cancer. 2021 Oct 17;12(23):7041-7051. doi: 10.7150/jca.64061. eCollection 2021.
Ref 11	IGF2BP1 promotes SRF-dependent transcription in cancer in a m6A- and miRNA-dependent manner. Nucleic Acids Res. 2019 Jan 10;47(1):375-390. doi: 10.1093/nar/gky1012.
Ref 12	N6-Methyladenosine Regulates the Expression and Secretion of TGFBeta1 to Affect the Epithelial-Mesenchymal Transition of Cancer Cells. Cells. 2020 Jan 25;9(2):296. doi: 10.3390/cells9020296.
Ref 13	A Comprehensive Multiomics Analysis Identified Ubiquilin 4 as a Promising Prognostic Biomarker of Immune-Related Therapy in Pan-Cancer. J Oncol. 2021 Sep 7;2021:7404927. doi: 10.1155/2021/7404927. eCollection 2021.