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

Figure 4. Mcl-1 does not inhibit CIS through up-regulation of anti-oxidant molecules.

Figure 4

(A) HCT116 p53−/− shControl or shMcl-1 cells were pretreated with inhibitor of catalase (3-AT); SOD (2-MT) or GPx (MSA) with or without doxorubicin. ROS levels were assessed with Amplex Red at the indicated time points. (B and C) Quantitative analysis of CIS in HCT116 p53−/− shMcl-1 cells as assessed by PML and γ-H2AX nuclear body formation (B) and Ki67 staining (C). (D–F) Reactive oxygen species inhibitors block CIS. HCT116 p53−/− shcontrol or shMcl-1 cells were pretreated with or without N-acetylcysteine (NAC) or diphenyleneiodonium (DPI) in the presence or absence of doxorubicin for 24 hours. (D) Effects of NAC and DPI on the ROS generation. (E and F) Quantitative analysis of CIS with or without ROS-generating inhibitors as assessed by PML and γ-H2AX nuclear body formation (E) and Ki67 staining (F). Significant differences are compared with untreated control versus doxorubicin treated as well as untreated versus doxorubicin plus inhibitors (*p ≤ 0.05). Error bars represent ± S.D.