Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00553
[1], [2], [3]
RNA modification MIR122 MIR122 ADARB1 Methylation : modification sites Indirect Inhibition m6A modification SOX6 SOX6 METTL3 Methylation : m6A sites
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target Transcription factor SOX-6 (SOX6)
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 Double-stranded RNA-specific editase 1 (ADARB1) WRITER View Details
Regulated Target MicroRNA 122 (MIR122) View Details
Crosstalk Relationship A-to-I  →  m6A Inhibition
Crosstalk Mechanism RNA modification indirectly impacts m6A modification through downstream signaling pathways
Crosstalk Summary ADARB1 interacts with MicroRNA 122 (MIR122), increasing it's A-to-I level and inhibiting its physical interaction with Transcription factor SOX-6 (SOX6), which was regulated by METTL3-mediated m6A modification.
In-vitro Model
SK-ChA-1 Cholangiocarcinoma Homo sapiens CVCL_6952
Huh-7 Adult hepatocellular carcinoma Homo sapiens CVCL_0336
References
Ref 1 The m6A writers regulated by the IL-6/STAT3 inflammatory pathway facilitate cancer cell stemness in cholangiocarcinoma. Cancer Biol Med. 2021 Aug 4;19(3):343-57. doi: 10.20892/j.issn.2095-3941.2020.0661. Online ahead of print.
Ref 2 ADAR2-mediated editing of miR-214 and miR-122 precursor and antisense RNA transcripts in liver cancers. PLoS One. 2013 Dec 27;8(12):e81922. doi: 10.1371/journal.pone.0081922. eCollection 2013.
Ref 3 Circular RNA Pleiotrophin promotes carcinogenesis in glioma via regulation of microRNA-122/SRY-box transcription factor 6 axis. Eur J Cancer Prev. 2020 Mar;29(2):165-173. doi: 10.1097/CEJ.0000000000000535.