Skip to main content
. 2023 May 10;14:2691. doi: 10.1038/s41467-023-38318-7

Fig. 8. In vivo targeting of autophagy by TRPV1 inhibition renders tumors susceptible to cisplatin in a preclinical model.

Fig. 8

a CaSki CR cells were treated with cisplatin and AMG9810, as indicated. The frequency of apoptotic (active caspase 3+) cells was analyzed by flow cytometry. b The combination score was calculated based on changes in the percentage of apoptotic cells in cisplatin-treated tumor cells with or without AMG9810. Combination score = (% of active caspase 3+ tumor cells by cisplatin and AMG9810)/((% of active caspase 3+ tumor cells by cisplatin). c Schematic of the therapeutic regimen in mice implanted with CaSki CR cells. d tumor growth, e mass (at 19 d after challenge), and f survival of mice inoculated with CaSki CR cells treated with the indicated reagents. g The expression levels of LC3B, pEGFR, EGFR, pAKT, AKT, and MCL1 protein were confirmed by western blot analysis. β-actin was used as the internal loading control. Numbers below the blot images indicate the expression as measured by fold-change. h The frequency of apoptotic (active caspase 3+) cells was analyzed by flow cytometry in mice administrated DMSO or cisplatin, with or without AMG9810. For the in vivo experiments, five mice from each group were used. All experiments were performed in triplicate. The p values by two-way ANOVA (a, b, d) or one-way ANOVA (e, h) are indicated. The data represent the mean ± SD. Source data are provided as a Source Data file.