Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00515
[1], [2], [3]
m6A modification MEG3 MEG3 METTL3 Methylation : m6A sites Indirect Inhibition RNA modification MIR18A MIR18A ADAR Methylation : modification sites
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target Maternally expressed 3 (MEG3)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type RNA modification (RNAMod)  >> Adenosine-to-Inosine editing (A-to-I)
Epigenetic Regulator Interferon-inducible protein 4 (ADAR1) WRITER View Details
Regulated Target hsa-mir-18a View Details
Crosstalk Relationship m6A  →  A-to-I Inhibition
Crosstalk Mechanism m6A modification indirectly impacts RNA modification through downstream signaling pathways
Crosstalk Summary METTL3 interacts with Maternally expressed 3 (MEG3), increasing its m6A level and inhibiting its physical interaction with hsa-mir-18a, which was regulated by ADAR1-mediated A-to-I modification.
In-vitro Model
Hep-G2 Hepatoblastoma Homo sapiens CVCL_0027
Huh-7 Adult hepatocellular carcinoma Homo sapiens CVCL_0336
CAL-27 Tongue squamous cell carcinoma Homo sapiens CVCL_1107
HN4 Clear cell renal cell carcinoma Homo sapiens CVCL_IS30
References
Ref 1 m6A-Induced LncRNA MEG3 Suppresses the Proliferation, Migration and Invasion of Hepatocellular Carcinoma Cell Through miR-544b/BTG2 Signaling. Onco Targets Ther. 2021 Jun 15;14:3745-3755. doi: 10.2147/OTT.S289198. eCollection 2021.
Ref 2 ADAR1 promotes the epithelial-to-mesenchymal transition and stem-like cell phenotype of oral cancer by facilitating oncogenic microRNA maturation. J Exp Clin Cancer Res. 2019 Jul 17;38(1):315. doi: 10.1186/s13046-019-1300-2.
Ref 3 Knockdown of Long Noncoding RNAs of Maternally Expressed 3 Alleviates Hyperoxia-Induced Lung Injury via Inhibiting Thioredoxin-Interacting Protein-Mediated Pyroptosis by Binding to miR-18a. Am J Pathol. 2020 May;190(5):994-1005. doi: 10.1016/j.ajpath.2019.12.013. Epub 2020 Feb 19.