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. 2021 May 12;13(10):2317. doi: 10.3390/cancers13102317

Figure 5.

Figure 5

Proapoptotic mechanisms, which involve mitochondrial dysfunction, ER stress, and caspase activation, are suppressed in GBM. Dysregulation of mitochondrial homeostasis (often through oxidative imbalance) leads to the release of cytochrome c, a caspase activator. ER stress upregulates activating transcription factors; in turn, ATFs activate CHOP, p21, and proapoptotic proteins that enhance caspase activation. Active caspase 9 (along with Beclin-1) cleaves caspase 3, which enforces apoptosis and DNA fragmentation. In proliferating GBM cells, however, the anti-apoptotic protein Bcl-2 directly inhibits caspase 9, while mTOR inhibits Beclin-1.