Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00623
[1], [2], [3]
m6A modification hsa-miR-34a hsa-miR-34a METTL14 Methylation : m6A sites Indirect Enhancement RNA modification ATG5 ATG5 FTO Demethylation : modification sites
m6A Modification:
m6A Regulator Methyltransferase-like 14 (METTL14) WRITER
m6A Target hsa-miR-34a
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 Autophagy protein 5 (ATG5) View Details
Crosstalk Relationship m6A  →  m6Am Enhancement
Crosstalk Mechanism m6A modification indirectly impacts RNA modification through downstream signaling pathways
Crosstalk Summary METTL14 interacts with hsa-miR-34a, decreasing its m6A level and promoting its physical interaction with Autophagy protein 5 (ATG5), which was regulated by FTO-mediated m6Am modification.
In-vitro Model
A2780 Ovarian endometrioid adenocarcinoma Homo sapiens CVCL_0134
SK-OV-3 Ovarian serous cystadenocarcinoma Homo sapiens CVCL_0532
References
Ref 1 FTO accelerates ovarian cancer cell growth by promoting proliferation, inhibiting apoptosis, and activating autophagy. Pathol Res Pract. 2020 Sep;216(9):153042. doi: 10.1016/j.prp.2020.153042. Epub 2020 Jun 20.
Ref 2 N6-Methyladenosine Induced miR-34a-5p Promotes TNF-alpha-Induced Nucleus Pulposus Cell Senescence by Targeting SIRT1. Front Cell Dev Biol. 2021 Mar 5;9:642437. doi: 10.3389/fcell.2021.642437. eCollection 2021.
Ref 3 miR-34a inhibits progression of neuroblastoma by targeting autophagy-related gene 5. Eur J Pharmacol. 2019 May 5;850:53-63. doi: 10.1016/j.ejphar.2019.01.071. Epub 2019 Feb 1.