m6A-centered Crosstalk Information

Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation

m6A Modification:
Crosstalk ID	M6ACROT00498				[1], [2], [3]
RNA modification MIR222 MIR222 ADAR Methylation : modification sites Indirect Inhibition m⁶A modification CDKN1B CDKN1B METTL14 Methylation : m⁶A sites
m6A Regulator	Methyltransferase-like 14 (METTL14)			WRITER	Regulator Info
m6A Target	Cyclin-dependent kinase inhibitor 1B (CDKN1B/p27)				Targert Gene
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type	RNA modification (RNAMod) >> Adenosine-to-Inosine editing (A-to-I)
Epigenetic Regulator	Interferon-inducible protein 4 (ADAR1)			WRITER	View Details
Regulated Target	MicroRNA 222 (MIR222)				View Details
Crosstalk Relationship	A-to-I → m6A			Inhibition
Crosstalk Mechanism	RNA modification indirectly impacts m6A modification through downstream signaling pathways
Crosstalk Summary	ADAR1 interacts with MicroRNA 222 (MIR222), increasing it's A-to-I level and inhibiting its physical interaction with Cyclin-dependent kinase inhibitor 1B (CDKN1B/p27), which was regulated by METTL14-mediated m6A modification.
In-vitro Model	HEC-1-A	Endometrial adenocarcinoma	Homo sapiens		CVCL_0293
In-vitro Model	624-mel	Melanoma	Homo sapiens		CVCL_8054

References

Ref 1	m(6)A mRNA methylation regulates AKT activity to promote the proliferation and tumorigenicity of endometrial cancer. Nat Cell Biol. 2018 Sep;20(9):1074-1083. doi: 10.1038/s41556-018-0174-4. Epub 2018 Aug 27.
Ref 2	A novel immune resistance mechanism of melanoma cells controlled by the ADAR1 enzyme. Oncotarget. 2015 Oct 6;6(30):28999-9015. doi: 10.18632/oncotarget.4905.
Ref 3	MiR-222 promotes the progression of polycystic ovary syndrome by targeting p27 Kip1. Pathol Res Pract. 2019 May;215(5):918-923. doi: 10.1016/j.prp.2019.01.038. Epub 2019 Jan 28.