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Current evidence suggests that the reactive oxygen species (ROS) derived from redox (reductionoxidation) imbalance in the TME may contribute to genomic damage, promoting DNA mutations and activating oncogenes 105 , and also affect intracellular signal transduction of multiple cellular pathways, thus conferring specific conditions for initiation and malignant progression of many human tumors, including gliomas 105,106,107,108,109

In vitro-cultured HCT116 cells were treated with mdivi-1 to inhibit DRP1 expression, which resulted in severe chromosome dislocation during mitosis [93]

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