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. 2016 Aug 24;7(41):67129–67141. doi: 10.18632/oncotarget.11562

Figure 3. H2-18-induced cell death is RIP1-dependent programmed necrosis.

Figure 3

A. The effect of pan caspase inhibitor Z-VAD-FMK and autophagy inhibitor bafilomycin A1 on H2-18-induced cell death in HCC-1954 cells. Data are shown as means ± SD. *, P<0.05; **, P<0.01; ***, P<0.001; Student's unpaired t test. B. Immunoblots assessing the key components in caspase signaling in HCC-1954 cells treated with control IgG, trastuzumab, pertuzumab, pertuzumab plus trastuzumab, and H2-18. Lysates of HCC-1954 cell treated with NaN3 were used as positive control. C. Immunoblots examining Bcl-2 family in HCC-1954 cells treated with control IgG, trastuzumab, pertuzumab, pertuzumab plus trastuzumab, and H2-18. D. TEM images of HCC-1954 cells treated with control IgG, trastuzumab, pertuzumab, pertuzumab plus trastuzumab, and H2-18 for 48 hours. Representative images are shown. H2-18-treated HCC-1954 cells exhibited shedding of villi(➨), disruption of the plasma membrane(→), extensive cytoplasmic vacillation (▲), and intact nuclei (N). E. The effect of Nec-1 on H2-18-induced cell death in HCC-1954 cells. Every experiment was repeated 3 times. Data are shown as means ± SD. *, P<0.05; **, P<0.01; ***, P<0.001; ANOVA.