Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00642
[1], [2], [3]
m6A modification MIR18A MIR18A METTL3 Methylation : m6A sites Indirect Enhancement RNA modification PTEN PTEN TET1 Demethylation : modification sites
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target hsa-mir-18a
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type RNA modification (RNAMod)  >> 5-methylcytidine (m5C)
Epigenetic Regulator Methylcytosine dioxygenase TET1 (TET1) ERASER View Details
Regulated Target Mutated in multiple advanced cancers 1 (PTEN) View Details
Crosstalk Relationship m6A  →  m5C Enhancement
Crosstalk Mechanism m6A modification indirectly impacts RNA modification through downstream signaling pathways
Crosstalk Summary METTL3 interacts with hsa-mir-18a, decreasing its m6A level and promoting its physical interaction with Mutated in multiple advanced cancers 1 (PTEN), which was regulated by TET1-mediated m5C modification.
In-vitro Model
Hep 3B2.1-7 Childhood hepatocellular carcinoma Homo sapiens CVCL_0326
Hep-G2 Hepatoblastoma Homo sapiens CVCL_0027
MKN45 Gastric adenocarcinoma Homo sapiens CVCL_0434
References
Ref 1 Exosomal miR-21 regulates the TETs/PTENp1/PTEN pathway to promote hepatocellular carcinoma growth. Mol Cancer. 2019 Oct 27;18(1):148. doi: 10.1186/s12943-019-1075-2.
Ref 2 N(6)-methyladenosine-dependent pri-miR-17-92 maturation suppresses PTEN/TMEM127 and promotes sensitivity to everolimus in gastric cancer. Cell Death Dis. 2020 Oct 9;11(10):836. doi: 10.1038/s41419-020-03049-w.
Ref 3 Long Noncoding RNA WDFY3-AS2 Represses the Progression of Esophageal Cancer through miR-18a/PTEN Axis. J Oncol. 2021 Jun 5;2021:9951010. doi: 10.1155/2021/9951010. eCollection 2021.