Abstract
To explore FDX1 methylation as a regulatory mechanism in the malignant phenotype of glioma, we screened for pathways involved through bioinformatic analysis, then proceeded with RIP and cell models to verify the regulation of RNAs and mitophagy. We chose Clone and Transwell assays to evaluate the malignant phenotype of glioma cells. MMP was detected by flow cytometry and mitochondrial morphology was observed by TEM. We also constructed animal models to study the sensitivity of glioma cells to cuproptosis. We successfully identified the signalling pathway: our cell model showed that C-MYC could upregulate FDX1 through YTHDF1 and inhibit mitophagy in glioma cells. Functional experiments revealed C-MYC could also enhance glioma cell proliferation and invasion via YTHDF1 and FDX1. In vivo experiments showed glioma cells were highly sensitive to cuproptosis. We concluded that C-MYC could upregulate FDX1 by m6A methylation, thus promoting the malignant phenotype in glioma cells.
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