Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00474
[1], [2], [3]
m6A modification NEAT1 NEAT1 METTL14 Methylation : m6A sites Indirect Inhibition RNA modification MIR181A1 MIR181A1 ADAR Methylation : modification sites
m6A Modification:
m6A Regulator Methyltransferase-like 14 (METTL14) WRITER
m6A Target Nuclear paraspeckle assembly transcript 1 (NEAT1)
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 MicroRNA 181a-1 (MIR181A1) View Details
Crosstalk Relationship m6A  →  A-to-I Inhibition
Crosstalk Mechanism m6A modification indirectly impacts RNA modification through downstream signaling pathways
Crosstalk Summary METTL14 interacts with Nuclear paraspeckle assembly transcript 1 (NEAT1), increasing its m6A level and inhibiting its physical interaction with MicroRNA 181a-1 (MIR181A1), which was regulated by ADAR1-mediated A-to-I modification.
In-vitro Model
769-P Renal cell carcinoma Homo sapiens CVCL_1050
786-O Renal cell carcinoma Homo sapiens CVCL_1051
CAL-27 Tongue squamous cell carcinoma Homo sapiens CVCL_1107
HN4 Clear cell renal cell carcinoma Homo sapiens CVCL_IS30
References
Ref 1 Methyltransferase-like 14 suppresses growth and metastasis of renal cell carcinoma by decreasing long noncoding RNA NEAT1. Cancer Sci. 2022 Feb;113(2):446-458. doi: 10.1111/cas.15212. Epub 2021 Dec 16.
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 Long Noncoding RNA Nuclear Enriched Abundant Transcript 1 (NEAT1) Regulates Proliferation, Apoptosis, and Inflammation of Chondrocytes via the miR-181a/Glycerol-3-Phosphate Dehydrogenase 1-Like (GPD1L) Axis. Med Sci Monit. 2019 Oct 28;25:8084-8094. doi: 10.12659/MSM.918416.