Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00070
[1], [2]
RNA modification METTL3 METTL3 NSUN6 Methylation : modification sites Direct Enhancement m6A modification SOCS2 SOCS2 METTL3 Methylation : m6A sites
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target Suppressor of cytokine signaling 2 (SOCS2)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type RNA modification (RNAMod)  >> 5-methylcytidine (m5C)
Epigenetic Regulator tRNA (cytosine(72)-C(5))-methyltransferase NSUN6 (NSUN6) WRITER View Details
Regulated Target Methyltransferase-like protein 3 (METTL3) View Details
Crosstalk Relationship m5C  →  m6A Enhancement
Crosstalk Mechanism RNA modification directly impacts m6A modification through modulating the expression level of m6A regulator
Crosstalk Summary NSUN6 upregulates the expression of oncogenic METTL3 and catalyzes its m5C modification in COAD cells. Overexpression of METTL3 significantly relieved the cell cycle inhibition of COAD caused by NSUN6 deficiency.An increased level of METTL3 may maintain the tumorigenicity of colon cancer cells by suppressing Suppressor of cytokine signaling 2 (SOCS2).
Responsed Disease Colon cancer ICD-11: 2B90
Cell Process Colon adenocarcinoma
In-vitro Model
HCT 116 Colon carcinoma Homo sapiens CVCL_0291
HCT 8 Colon adenocarcinoma Homo sapiens CVCL_2478
SW480 Colon adenocarcinoma Homo sapiens CVCL_0546
NCM460 Normal Homo sapiens CVCL_0460
References
Ref 1 NSUN6 mediates 5-methylcytosine modification of METTL3 and promotes colon adenocarcinoma progression. J Biochem Mol Toxicol. 2024 Jun;38(6):e23749. doi: 10.1002/jbt.23749.
Ref 2 Long non?coding RNA growth arrest?specific 5 (GAS5) acts as a tumor suppressor by promoting autophagy in breast cancer. Mol Med Rep. 2020 Sep;22(3):2460-2468. doi: 10.3892/mmr.2020.11334. Epub 2020 Jul 10.