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. 2017 Mar 7;8(17):28154–28168. doi: 10.18632/oncotarget.15962

Figure 1. DDR components are important in Mcl-1-regulated senescence.

Figure 1

HCT116 p53−/− cells stably transfected with either a shControl (CIS resistant, Mcl-1 proficient) or shMcl-1 (CIS sensitive, Mcl-1 deficient), were treated with 100 ng/ml doxorubicin or left untreated in the presence or absence of caffeine (ATM/ATR inhibitor) or KU-55933 (ATM specific inhibitor). (A and B) Western blot detection of ATM-1981P, ATR-S428P Chk1-S345P, and Chk2-T68P under chemotherapy conditions. β-Actin (Actin) was used as a loading control. (C–G) Quantitative analysis of CIS in HCT116p53−/− shControl or shMcl-1 cells as assessed by β-gal activity (C), PML (D and E), and γ-H2AX nuclear body (F and G) formation in the presence or absence of the indicated ATM/ATR inhibitors. *P < 0.05, comparing those given DDR inhibitors + doxorubicin to doxorubicin alone. (H) The effects of DDR factor inhibitors on ROS generation. Cells were treated as in Figure A and B, and change in intracellular ROS production was determined using the Amplex Red reagent as described in the Material and Methods. Error bars represent ± S.D. Graphical data are inclusive of at least three independent experiments.