m6A-centered Crosstalk Information

Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation

m6A Modification:
Crosstalk ID	M6ACROT00508				[1], [2], [3]
RNA modification MIR222 MIR222 ADAR Methylation : modification sites Indirect Inhibition m⁶A modification ATF3 ATF3 YTHDF2 : m⁶A sites
m6A Regulator	YTH domain-containing family protein 2 (YTHDF2)			READER	Regulator Info
m6A Target	Cyclic-AMP-dependent transcription factor ATF-3 (ATF3)				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 Cyclic-AMP-dependent transcription factor ATF-3 (ATF3), which was regulated by YTHDF2-mediated m6A modification.
In-vitro Model	MCF-7	Invasive breast carcinoma	Homo sapiens		CVCL_0031
In-vitro Model	624-mel	Melanoma	Homo sapiens		CVCL_8054

References

Ref 1	ATF3 Modulates the Resistance of Breast Cancer Cells to Tamoxifen through an N(6)-Methyladenosine-Based Epitranscriptomic Mechanism. Chem Res Toxicol. 2021 Jul 19;34(7):1814-1821. doi: 10.1021/acs.chemrestox.1c00206. Epub 2021 Jul 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	Extracellular vesicles-derived microRNA-222 promotes immune escape via interacting with ATF3 to regulate AKT1 transcription in colorectal cancer. BMC Cancer. 2021 Apr 1;21(1):349. doi: 10.1186/s12885-021-08063-5.