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. 2014 Nov 3;111(46):16520–16525. doi: 10.1073/pnas.1415178111

Fig. 5.

Fig. 5.

BID is specifically activated by NSAIDs in cancer cells through the death receptor pathway. (A) Western blots of HCT116 cells treated with 120 µM sulindac sulfide or 500 µM indomethacin, with the arrowhead indicating tBID. (B) HCT116 cells were treated as in A, and analyzed for DR4, DR5, and FLIPs expression at indicated time points by Western blotting. (C) HCT116 cells were transfected with control scrambled or DR5 siRNA, and then treated with sulindac sulfide as in A. (Upper) Western blot analysis of indicated proteins at 36 h after treatment. (Lower) Apoptosis was analyzed by counting condensed/fragmented nuclei after nuclear staining at 24 h after treatment. (D) Parental and stable caspase 8 knockdown (Casp 8 KD) HCT116 cells were treated with sulindac sulfide as in A. (Upper) Western blot analysis of indicated proteins at 24 h after treatment. (Lower) Apoptosis was analyzed as in C at 24 h after treatment. (E) Indicated proteins were analyzed by Western blotting in NCM356 cells treated with sulindac sulfide as in A for 36 h. (F) BAX multimerization in NCM356 and HCT116 cells was analyzed as in Fig. 4C. Results in C and D were expressed as means + SD of three independent experiments. ***P < 0.001.