Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05942
[1]
m6A modification FAM225A FAM225A METTL3 Methylation : m6A sites Direct Enhancement Non-coding RNA FAM225A miR-590-3p  lncRNA       miRNA   circRNA
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target Family with sequence similarity 225 member A (FAM225A)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator Family with sequence similarity 225 member A (FAM225A) LncRNA View Details
Regulated Target hsa-miR-590-3p View Details
Crosstalk Relationship m6A  →  ncRNA Enhancement
Crosstalk Mechanism m6A regulators directly modulate the functionality of ncRNAs through specific targeting ncRNA
Crosstalk Summary Silencing METTL3 decreases Family with sequence similarity 225 member A (FAM225A) RNA stability, which serves as the ceRNA for sponging both hsa-miR-590-3p and miR-1275, increasing the levels of their target integrin beta3 (ITGB3), finally stimulating FAK/PI3K/Akt signaling. miR-590-3p has been reported as a tumor suppressor in cholangiocarcinoma and hepatocellular carcinoma and miR-1275 can inhibit NPC cell growth and suppress hepatocellular carcinoma cell proliferation.
Responsed Disease Cholangiocarcinoma ICD-11: XH7M15
Pathway Response PI3K-Akt signaling pathway hsa04151
Cell Process mRNA stability
Cell proliferation
Cell invasion
References
Ref 1 The functions of N6-methyladenosine modification in lncRNAs. Genes Dis. 2020 Mar 19;7(4):598-605. doi: 10.1016/j.gendis.2020.03.005. eCollection 2020 Dec.