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. 2018 Jul 10;9(7):773. doi: 10.1038/s41419-018-0806-4

Fig. 8. The role of caspases in 26S depletion-mediated TNBC cell death.

Fig. 8

Differential cell death response of (a) naive MCF10A, (b) Ras-transformed MCF10A, and (c) cancer cell line MDA-MB-231 upon 26S depletion. Cells harboring doxycycline-inducible PSMD1 shRNA were either doxycycline treated to induce PSMD1 shRNA expression or left untreated. Cell cycle was analyzed by FACS after 4 days, and cell death level was quantified by measuring subG1 fraction. d Caspase-3 cleavage in MDA-MB-231 cells versus normal fibroblasts was analyzed by immunoblot after 4 days of PSMD1 shRNA induction. Asterisks mark the 17 and 19 kD caspase-3 cleavage products. e Caspase-3 cleavage in MCF10A Ras-transformed versus naive MCF10A cells was analyzed by immunoblot after 4 days of PSMD1 shRNA induction. Role of caspases in cell death mediated by 26S depletion was examined by using pan-caspases inhibitor QVD. Cells were induced to express PSMD1 shRNA by doxycycline in the presence or absence of 25 μMQVD, and protein expression (f) and viability (g) were analyzed after 4 days