Fig. 2: ABT-263 induces apoptosis and enhances radiation-induced apoptosis in HCT116 as well as non-selected and hypoxia-selected NCI-H460 cells.
From: Bcl-2/Bcl-xL inhibitor ABT-263 overcomes hypoxia-driven radioresistence and improves radiotherapy
Cells were treated with indicated concentrations of ABT-263, irradiated with 10 Gy (IR), or both in normoxia (Nx, 20% O2) or in severe hypoxia (Hx, <0.2% O2). Apoptosis levels of (A) HCT116, (B) non-selected NCI-H460 and (C) hypoxia-selected NCI-H460 cells were determined by flow cytometric analysis of DNA fragmentation (Sub G1 fraction) 48 h after respective treatment in normoxic or hypoxic condition. Data are shown as mean of three independent experiments ± SD. *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001. *, **, *** above bars: comparing treatment with ABT-263 to non-treated respective controls (0 µM ABT-263). Same data sets were used in left and middle graphs to show apoptosis in normoxic cells. Similarly, same data sets were used in left and right graphs to show apoptosis in hypoxic cells. D Whole-cell lysates were made 48 h after respective treatment and protein levels of cleaved caspase 3, PARP, cleaved PARP, and Bax were assessed by Western blot analysis. β-actin was used as loading control for whole-cell lysates. Figures show representative results.
