Fig. 7: Schematic representation of BCL-XL and MCL-1-mediated protection against apoptosis in medulloblastoma cells. | Cell Death & Disease

Fig. 7: Schematic representation of BCL-XL and MCL-1-mediated protection against apoptosis in medulloblastoma cells.

From: The identification of BCL-XL and MCL-1 as key anti-apoptotic proteins in medulloblastoma that mediate distinct roles in chemotherapy resistance

Fig. 7

Under basal conditions, BCL-XL sequesters pro-apoptotic proteins BAK, PUMA and BIM. Treatment with cisplatin or WEHI-539 changes the interactions of pro-apoptotic proteins. Cisplatin treatment promotes BCL-XL mediated sequestration of these proteins, as well as BAX sequestration. The addition of WEHI-539 to cisplatin treatment results in the release of pro-apoptotic proteins and restoration of apoptotic signalling, leading to significant cell death. WEHI-539 treatment alone, on the other hand, does not result in apoptosis, and rather increases MCL-1 dependence, demonstrating that co-treatment with BCL-XL and MCL-1 inhibitors is required for BH3 mimetic mediated apoptosis in medulloblastoma cells. Created with BioRender.com.

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