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Fig. 8 | Journal of Experimental & Clinical Cancer Research

Fig. 8

From: LCL161 increases paclitaxel-induced apoptosis by degrading cIAP1 and cIAP2 in NSCLC

Fig. 8

RIP1 is a critical mediator of LCL161-induced apoptosis. a A549 cells were treated for 48 h with 10 μM paclitaxel with/without 10 μM LCL161, and western blotting was performed for TRADD, TRAF2, RIP1, TNFR1, cIAP1 and cIAP2. b A549 cells were treated with 10 μM paclitaxel with/without 10 μM LCL161 for 48 h, and 5 μM proteasome inhibitor MG132 for 4 h before collecting the cells. Anti-RIP1 antibody was used to co-immunoprecipitate RIP1 and detected its interaction with TRADD, TRAF2 and cIAP. c A549 cells were treated for 48 h with 10 μM LCL161 and/or 10 μM paclitaxel in the presence of 20 mM Z-IETD-FMK. Caspase-8 was immunoprecipitated using an anti-caspase-8 antibody. The detection of RIP1 and FADD proteins was performed by western blot analysis. d A549 cells were transiently transfected with siRNA sequences against RIP1 for 48 h and then were treated with 10 μM LCL161 and/or 10 μM paclitaxel for another 48 h. RIP1 expression was analyzed by western blotting 48 h post-transfection. e Annexin V/PI staining was used to detect apoptosis, and the apoptotic rates are provided as mean ± SD; *P < 0.05; **P < 0.01; ***P < 0.001

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