Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00610
[1], [2], [3], [4]
m6A modification MIR320A MIR320A METTL3 Methylation : m6A sites Indirect Inhibition RNA modification MALAT1 MALAT1 FTO Demethylation : modification sites
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target hsa-mir-320a
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 Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) View Details
Crosstalk Relationship m6Am  →  m6A Inhibition
Crosstalk Mechanism RNA modification indirectly impacts m6A modification through downstream signaling pathways
Crosstalk Summary FTO interacts with Metastasis associated lung adenocarcinoma transcript 1 (MALAT1), decreasing it's m6Am level and inhibiting its physical interaction with hsa-mir-320a, which was regulated by METTL3-mediated m6A modification.
In-vitro Model
253J Bladder carcinoma Homo sapiens CVCL_7935
HT-1197 Recurrent bladder carcinoma Homo sapiens CVCL_1291
HT-1376 Bladder carcinoma Homo sapiens CVCL_1292
References
Ref 1 FTO modifies the m6A level of MALAT and promotes bladder cancer progression. Clin Transl Med. 2021 Feb;11(2):e310. doi: 10.1002/ctm2.310.
Ref 2 The tumor-suppressive effects of alpha-ketoglutarate-dependent dioxygenase FTO via N6-methyladenosine RNA methylation on bladder cancer patients. Bioengineered. 2021 Dec;12(1):5323-5333. doi: 10.1080/21655979.2021.1964893.
Ref 3 m(6)A Methylation of Precursor-miR-320/RUNX2 Controls Osteogenic Potential of Bone Marrow-Derived Mesenchymal Stem Cells. Mol Ther Nucleic Acids. 2020 Mar 6;19:421-436. doi: 10.1016/j.omtn.2019.12.001. Epub 2019 Dec 12.
Ref 4 LncRNA MALAT1 inhibits hypoxia/reoxygenation-induced human umbilical vein endothelial cell injury via targeting the microRNA-320a/RAC1 axis. Biol Chem. 2020 Feb 25;401(3):349-360. doi: 10.1515/hsz-2019-0316.