m6A-centered Crosstalk Information

Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation

m6A Modification:
Crosstalk ID	M6ACROT05091				[1]
Non-coding RNA piR31115 METTL3 lncRNA miRNA circRNA Indirect Enhancement m⁶A modification YAP1 YAP1 IGF2BP2 : m⁶A sites
m6A Regulator	Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2)			READER	Regulator Info
m6A Target	Transcriptional coactivator YAP1 (YAP1)				Targert Gene
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type	Non-coding RNA (ncRNA)
Epigenetic Regulator	piR-31115			piRNA	View Details
Regulated Target	Methyltransferase-like protein 3 (METTL3)				View Details
Crosstalk Relationship	ncRNA → m6A			Enhancement
Crosstalk Mechanism	ncRNAs indirectly impacts m6A modification through downstream signaling pathways
Crosstalk Summary	Triple negative breast cancer cell derived piR 31115 promotes the proliferation and migration of endothelial cells via Methyltransferase-like protein 3 (METTL3) mediated m6A modification of Transcriptional coactivator YAP1 (YAP1).Concurrently, the IGF2BP2 plays a crucial role in stabilizing YAP1 protein expression.
Responsed Disease	Triple-negative breast cancer		ICD-11: 2C6Z		Disease Info
In-vitro Model	U2OS	Osteosarcoma	Homo sapiens		CVCL_0042
	WI-38 VA13 subline 2RA	N.A.	Homo sapiens		CVCL_2759
	CAL-27	Tongue squamous cell carcinoma	Homo sapiens		CVCL_1107
	HEK293T	Normal	Homo sapiens		CVCL_0063

References

Ref 1	Triple?negative breast cancer cell?derived piR?31115 promotes the proliferation and migration of endothelial cells via METTL3?mediated m6A modification of YAP1. Oncol Rep. 2025 Mar;53(3):34. doi: 10.3892/or.2025.8867. Epub 2025 Jan 17.