Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00488
[1], [2], [3]
m6A modification H19 H19 METTL3 Methylation : m6A sites Indirect Enhancement RNA modification MIR22 MIR22 FTO Demethylation : modification sites
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target H19 imprinted maternally expressed transcript (H19)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type RNA modification (RNAMod)  >> N6,2'-O-dimethyladenosine (m6Am)
Epigenetic Regulator Fat mass and obesity-associated protein (FTO) ERASER View Details
Regulated Target hsa-mir-22 View Details
Crosstalk Relationship m6A  →  m6Am Enhancement
Crosstalk Mechanism m6A modification indirectly impacts RNA modification through downstream signaling pathways
Crosstalk Summary METTL3 interacts with H19 imprinted maternally expressed transcript (H19), decreasing its m6A level and promoting its physical interaction with hsa-mir-22, which was regulated by FTO-mediated m6Am modification.
In-vitro Model
MGG8 Glioblastoma Homo sapiens CVCL_D1H4
HEK293 Normal Homo sapiens CVCL_0045
References
Ref 1 N?-Methyladenosine Landscape of Glioma Stem-Like Cells: METTL3 Is Essential for the Expression of Actively Transcribed Genes and Sustenance of the Oncogenic Signaling. Genes (Basel). 2019 Feb 13;10(2):141. doi: 10.3390/genes10020141.
Ref 2 N6-adenosine methylation in MiRNAs. PLoS One. 2015 Feb 27;10(2):e0118438. doi: 10.1371/journal.pone.0118438. eCollection 2015.
Ref 3 Long non?coding RNA H19 regulates cell growth and metastasis via the miR?22?3p/Snail1 axis in gastric cancer. Int J Oncol. 2019 Jun;54(6):2157-2168. doi: 10.3892/ijo.2019.4773. Epub 2019 Apr 4.