Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00674
[1], [2], [3]
RNA modification H19 H19 NSUN2 Methylation : modification sites Indirect Enhancement m6A modification hsa-mir-19a hsa-mir-19a METTL3 Methylation : m6A sites
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target hsa-mir-19a
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type RNA modification (RNAMod)  >> 5-methylcytidine (m5C)
Epigenetic Regulator RNA cytosine C(5)-methyltransferase NSUN2 (NSUN2) WRITER View Details
Regulated Target H19 imprinted maternally expressed transcript (H19) View Details
Crosstalk Relationship m5C  →  m6A Enhancement
Crosstalk Mechanism RNA modification indirectly impacts m6A modification through downstream signaling pathways
Crosstalk Summary NSUN2 interacts with H19 imprinted maternally expressed transcript (H19), increasing its m5C level and promoting its physical interaction with hsa-mir-19a, which was regulated by METTL3-mediated m6A modification.
In-vitro Model
Hep-G2 Hepatoblastoma Homo sapiens CVCL_0027
MKN45 Gastric adenocarcinoma Homo sapiens CVCL_0434
References
Ref 1 Aberrant NSUN2-mediated m(5)C modification of H19 lncRNA is associated with poor differentiation of hepatocellular carcinoma. Oncogene. 2020 Nov;39(45):6906-6919. doi: 10.1038/s41388-020-01475-w. Epub 2020 Sep 25.
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 Blocking lncRNA H19-miR-19a-Id2 axis attenuates hypoxia/ischemia induced neuronal injury. Aging (Albany NY). 2019 Jun 5;11(11):3585-3600. doi: 10.18632/aging.101999.