m6A-centered Crosstalk Information

Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation

m6A Modification:
Crosstalk ID	M6ACROT00680				[1], [2], [3]
m⁶A modification MicroRNA-92a MicroRNA-92a METTL3 Methylation : m⁶A sites Indirect Enhancement RNA modification ITGA6 ITGA6 FTO Demethylation : modification sites
m6A Regulator	Methyltransferase-like 3 (METTL3)			WRITER	Regulator Info
m6A Target	microRNA-92a				Targert Gene
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type	RNA modification (RNAMod) >> N6,2'-O-dimethyladenosine (m6Am)
Epigenetic Regulator	Fat mass and obesity-associated protein (FTO)			ERASER	View Details
Regulated Target	Integrin alpha-6 (ITGA6)				View Details
Crosstalk Relationship	m6A → m6Am			Enhancement
Crosstalk Mechanism	m6A modification indirectly impacts RNA modification through downstream signaling pathways
Crosstalk Summary	METTL3 interacts with microRNA-92a, decreasing its m6A level and promoting its physical interaction with Integrin alpha-6 (ITGA6), which was regulated by FTO-mediated m6Am modification.
In-vitro Model	HT-1376	Bladder carcinoma	Homo sapiens		CVCL_1292
	HT-1197	Recurrent bladder carcinoma	Homo sapiens		CVCL_1291
	MKN45	Gastric adenocarcinoma	Homo sapiens		CVCL_0434

References

Ref 1	The tumor-suppressive effects of alpha-ketoglutarate-dependent dioxygenase FTO via N6-methyladenosine RNA methylation on bladder cancer patients. Bioengineered. 2021 Dec;12(1):5323-5333. doi: 10.1080/21655979.2021.1964893.
Ref 2	N(6)-methyladenosine-dependent pri-miR-17-92 maturation suppresses PTEN/TMEM127 and promotes sensitivity to everolimus in gastric cancer. Cell Death Dis. 2020 Oct 9;11(10):836. doi: 10.1038/s41419-020-03049-w.
Ref 3	Long non-coding RNA OIP5-AS1 suppresses microRNA-92a to augment proliferation and metastasis of ovarian cancer cells through upregulating ITGA6. J Ovarian Res. 2022 Feb 16;15(1):25. doi: 10.1186/s13048-021-00937-3.