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. 2018 Apr 2;9(12):1013–1026. doi: 10.1007/s13238-018-0520-0

Figure 6.

Figure 6

HEC23-induced cell death is dependent on the STAT3-cathepsin pathway. (A) Quantifications of cell death induced by HEC-23 in the indicated types of carcinoma cells. (B) Quantification of cell death induced by HEC-23 together with or without cisplatin in HeLa cells. (C) Representative images (left) and flow cytometry quantification (right) of necrosis induced by HEC-23 (10 μmol/L, 12 h). (D) Quantification of cell death induced by HEC-23 (10 μmol/L, 24 h) in HeLa cells pre-treated with z-VAD (20 μmol/L) or 3-MA (1 μmol/L) for 30 min. (E) qPCR evaluation of the knockdown efficiency of siRIP1 and siRIP3. (F) Quantification of the viability of HeLa cells treated with HEC-23 and siRIP1, siRIP3 or both in the presence or absence of z-VAD. (G) Quantification of cell viability in siCtrl or siSTAT3 HeLa cells treated with HEC-23, CA-074-Me or IM-54. HeLa cells were transfected with siRNA for 48 h, followed by treatment with CA-074-Me (20 μmol/L) or IM-54 (2 μmol/L) for 30 min. The cells were then treated with HEC-23 for 24 h. MTT assays were performed to examine the viability of the cells. The concentration of HEC-23 was 10 μmol/L in all treatments. Data representing mean ± SEM were derived from 3 independent experiments. **P < 0.01, ***P < 0.001 (Scale bars, 10 μm)