m6A-centered Crosstalk Information

Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation

m6A Modification:
Crosstalk ID	M6ACROT00496				[1], [2], [3]
RNA modification MIR222 MIR222 ADAR Methylation : modification sites Indirect Inhibition m⁶A modification CDKN1B CDKN1B IGF2BP3 : m⁶A sites
m6A Regulator	Insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3)			READER	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 IGF2BP3-mediated m6A modification.
In-vitro Model	MKN28	Gastric tubular adenocarcinoma	Homo sapiens		CVCL_1416
	SGC-7901	Gastric carcinoma	Homo sapiens		CVCL_0520
	624-mel	Melanoma	Homo sapiens		CVCL_8054

References

Ref 1	IGF2BP3 functions as a potential oncogene and is a crucial target of miR-34a in gastric carcinogenesis. Mol Cancer. 2017 Apr 11;16(1):77. doi: 10.1186/s12943-017-0647-2.
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.