Figure 7: Blunting autophagosome formation and cathepsin activity protects cells from IMB-6G-induced cell death. | Scientific Reports

Figure 7: Blunting autophagosome formation and cathepsin activity protects cells from IMB-6G-induced cell death.

From: Lysosomal dysfunction and autophagy blockade contribute to IMB-6G-induced apoptosis in pancreatic cancer cells

Figure 7

MiaPaCa-2 and HupT-3 cells were transfected with control siRNA or siAtg5, followed by IMB-6G (5 μM) treatment for 24 h. (a) Apoptotic cell death was measured by flow cytometry. Values are expressed as the mean ± SD, #p < 0.01 compared with IMB-6G-untreated siCtrl group, **p < 0.01 compared with IMB-6G-treated siCtrl group. (b) Cleaved PARP1/caspase3, LC3-II, and ATG5 were detected by immunoblotting. (c) MiaPaCa-2 and HupT-3 cells were treated with CA-074Me (CTSB specific inhibitor) or E-64 (CTSB and CTSL inhibitor), followed by IMB-6G (5 μM) treatment for 24 h, the apoptotic cell death was measured by flow cytometry. Data are mean ± SD of 3 independent experiments, #p < 0.01 compared with DMSO-treated group, *p < 0.05, **p < 0.01 compared with IMB-6G-treated group. (d) The proposed pathway of IMB-6G-induced autophagy-dependent apoptosis in pancreatic cancer cells. IMB-6G-activated autophagosome formation is an upstream event that may trigger LMP. IMB-6G-induced LMP causes lysosomal release of cathepsin and eventually triggers apoptosis.

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