Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05433
[1]
m6A modification hsa-miR-25-3p hsa-miR-25-3p METTL3 Methylation : m6A sites Direct Enhancement Non-coding RNA miR-25-3p PTEN  lncRNA       miRNA   circRNA
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target hsa-miR-25-3p
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator hsa-miR-25-3p microRNA View Details
Regulated Target Mutated in multiple advanced cancers 1 (PTEN) View Details
Crosstalk Relationship m6A  →  ncRNA Enhancement
Crosstalk Mechanism m6A regulators directly modulate the functionality of ncRNAs through specific targeting ncRNA
Crosstalk Summary METTL3 involves in the pathogenesis of diabetic retinopathy (DR). Both METTL3 mRNA and hsa-miR-25-3p were low-expressed in the peripheral venous blood samples of diabetes mellitus (DM) patients compared to normal volunteers, and high-glucose inhibited METTL3 and miR-25-3p expressions in RPE cells. Overexpression of METTL3 attenuates high-glucose induced RPE cell pyroptosis by regulating miR-25-3p/Mutated in multiple advanced cancers 1 (PTEN)/Akt signaling cascade through DGCR8.
Responsed Disease Diabetes ICD-11: 5A10-5A14
Pathway Response PI3K-Akt signaling pathway hsa04151
Cell Process Cell viability
Cell apoptosis
References
Ref 1 Overexpression of METTL3 attenuates high-glucose induced RPE cell pyroptosis by regulating miR-25-3p/PTEN/Akt signaling cascade through DGCR8. Aging (Albany NY). 2020 May 4;12(9):8137-8150. doi: 10.18632/aging.103130. Epub 2020 May 4.