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. 2015 Oct 2;6(34):35667–35683. doi: 10.18632/oncotarget.5523

Figure 4. ABT-737 induces Bax-dependent apoptotic cell death via Bim activation.

Figure 4

MC-3 and HN22 cells were treated with or without ABT-737 for 24 hr, total cellular protein was prepared, and the protein levels of total Bim were evaluated by Western blot analysis A. MC-3 and HN22 cells were treated with or without ABT-737 for 24 hr; afterwards, mitochondrial fractions were prepared, and the protein levels of total Bim were evaluated by Western blot analysis B. Immunocytochemistry revealed the mitochondrial translocation of Bim from the cytoplasm after ABT-737 treatment (20 μM in MC-3 cells and 22.5 μM in HN22 cells) for 24 hr. MitoTracker (red) staining labels mitochondria within each field C. MC-3 and HN22 cells were transfected with either control siRNA (siCon) or siRNA specific to Bim (siBim); afterwards, cells were treated with or without ABT-737. Western blot analysis was performed to evaluate the expression levels of Bim, active Bim (6A7) and cleaved-PARP D. β-actin was used as an internal control. The Cox4 exclusive mitochondria marker was used as a control for separating mitochondrial and cytosolic fractions. The results are shown as the mean ± SD from three independent experiments. *P < 0.05, **P < 0.01, and ***P < 0.001.