Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05338
[1]
Non-coding RNA miR-27a-3p FTO  lncRNA       miRNA   circRNA Direct Inhibition m6A modification FOXO3 FOXO3 FTO Demethylation : m6A sites
m6A Modification:
m6A Regulator Fat mass and obesity-associated protein (FTO) ERASER
m6A Target Forkhead box protein O3 (FOXO3)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator hsa-miR-27a-3p microRNA View Details
Regulated Target FTO alpha-ketoglutarate dependent dioxygenase (FTO) View Details
Crosstalk Relationship ncRNA  →  m6A Inhibition
Crosstalk Mechanism ncRNAs directly impacts m6A modification through modulating the expression level of m6A regulator
Crosstalk Summary miR-27a-3p inhibits the expression of FTO via direct binding to FTO. FTO overexpression promotes the nuclear translocation of Forkhead box protein O3 (FOXO3) and upregulates the expression levels of the FOXO3a downstream targets BIM, BNIP3, BCL-6, and PUMA, possibly by interacting with FOXO3a.
Responsed Disease Glioblastoma multiforme ICD-11: XH0MB1
In-vivo Model GBM cells were infected with lentivirus overexpressing FTO (Lv-FTO) or control lentivirus (Lv-NC), followed by subcutaneous injection with 2.5×105 cells in a total volume of 200 μl into the right dorsal-lateral flanks of mice.
References
Ref 1 The miR-27a-3p/FTO axis modifies hypoxia-induced malignant behaviors of glioma cells. Acta Biochim Biophys Sin (Shanghai). 2023 Jan 25;55(1):103-116. doi: 10.3724/abbs.2023002.