The FDX1 methylation regulatory mechanism in the malignant phenotype of glioma.

To explore the regulatory mechanism of FDX1 methylation in malignant phenotype of glioma. We screened pathway through bioinformatic analysis, proceeded RIP and cell models to verify the regulation of RNAs and mitophagy. We chose Clone and Transwell assay to evaluate the malignant phenotype of glioma cells. MMP was detected by flow cytometry and mitochondrial morphology was observed by TEM. We constructed animal models to study the sensibility of glioma cells to cuproptosis. We successfully obtained the signal pathway. Cell model detection showed C-MYC could upregulate FDX1 through YTHDF1 axis. The detection of mitophagy showed C-MYC could inhibit mitophagy in glioma cells by YTHDF1/FDX1 axis. Functional experiments revealed C-MYC could enhance glioma cell proliferation and invasion via YTHDF1/FDX1 axis. In vivo experiment showed glioma cells were highly sensitive to cuproptosis. We concluded C-MYC could upregulate FDX1 by YTHDF1-mediated m6A methylation, thus promoting the malignant phenotype in glioma cells.