Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00564
[1], [2], [3]
m6A modification GAS5 GAS5 YTHDF3 : m6A sites Indirect Inhibition RNA modification CDKN1C CDKN1C NSUN2 Methylation : modification sites
m6A Modification:
m6A Regulator YTH domain-containing family protein 3 (YTHDF3) READER
m6A Target Growth arrest specific 5 (GAS5)
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 Cyclin-dependent kinase inhibitor 1C (CDKN1C) View Details
Crosstalk Relationship m6A  →  m5C Inhibition
Crosstalk Mechanism m6A modification indirectly impacts RNA modification through downstream signaling pathways
Crosstalk Summary YTHDF3 interacts with Growth arrest specific 5 (GAS5), increasing its m6A level and inhibiting its physical interaction with Cyclin-dependent kinase inhibitor 1C (CDKN1C), which was regulated by NSUN2-mediated m5C modification.
In-vitro Model
SGC-7901 Gastric carcinoma Homo sapiens CVCL_0520
MGC-803 Gastric mucinous adenocarcinoma Homo sapiens CVCL_5334
HCT 116 Colon carcinoma Homo sapiens CVCL_0291
RKO Colon carcinoma Homo sapiens CVCL_0504
References
Ref 1 RNA methyltransferase NSUN2 promotes gastric cancer cell proliferation by repressing p57(Kip2) by an m(5)C-dependent manner. Cell Death Dis. 2020 Apr 24;11(4):270. doi: 10.1038/s41419-020-2487-z.
Ref 2 Long noncoding RNA GAS5 inhibits progression of colorectal cancer by interacting with and triggering YAP phosphorylation and degradation and is negatively regulated by the m(6)A reader YTHDF3. Mol Cancer. 2019 Oct 16;18(1):143. doi: 10.1186/s12943-019-1079-y.
Ref 3 Long non-coding RNA GAS5 accelerates oxidative stress in melanoma cells by rescuing EZH2-mediated CDKN1C downregulation. Cancer Cell Int. 2020 Apr 9;20:116. doi: 10.1186/s12935-020-01167-1. eCollection 2020.