m6A-centered Crosstalk Information

Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation

m6A Modification:
Crosstalk ID	M6ACROT00477				[1], [2], [3]
m⁶A modification GAS5 GAS5 YTHDF3 : m⁶A sites Indirect Inhibition RNA modification MIR155 MIR155 ADAR Methylation : modification sites
m6A Regulator	YTH domain-containing family protein 3 (YTHDF3)			READER	Regulator Info
m6A Target	Growth arrest specific 5 (GAS5)				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 155 (MIR155)				View Details
Crosstalk Relationship	m6A → A-to-I			Inhibition
Crosstalk Mechanism	m6A modification indirectly impacts RNA modification through downstream signaling pathways
Crosstalk Summary	YTHDF3 interacts with Growth arrest specific 5 (GAS5), increasing its m6A level and inhibiting its physical interaction with MicroRNA 155 (MIR155), which was regulated by ADAR1-mediated A-to-I modification.
In-vitro Model	HCT 116	Colon carcinoma	Homo sapiens		CVCL_0291
	RKO	Colon carcinoma	Homo sapiens		CVCL_0504
	HN4	Clear cell renal cell carcinoma	Homo sapiens		CVCL_IS30
	CAL-27	Tongue squamous cell carcinoma	Homo sapiens		CVCL_1107

References

Ref 1	Long noncoding RNA GAS5 inhibits progression of colorectal cancer by interacting with and triggering YAP phosphorylation and degradation and is negatively regulated by the m(6)A reader YTHDF3. Mol Cancer. 2019 Oct 16;18(1):143. doi: 10.1186/s12943-019-1079-y.
Ref 2	ADAR1 promotes the epithelial-to-mesenchymal transition and stem-like cell phenotype of oral cancer by facilitating oncogenic microRNA maturation. J Exp Clin Cancer Res. 2019 Jul 17;38(1):315. doi: 10.1186/s13046-019-1300-2.
Ref 3	LncRNA GAS5 participates in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155. BMC Pulm Med. 2021 Nov 11;21(1):362. doi: 10.1186/s12890-021-01724-y.