Fig. 7
Apatinib sensitized esophageal cancer to cisplatin by inhibiting the Akt/β-catenin pathway. a Cell proliferation inhibition of KYSE30 and TE1 cells was detected by a CCK-8 kit after cisplatin (0.3, 1 and 3 μM) treatment with or without apatinib (10 μM) for 24 h. P values were determined by Student’s t test. Data are representative of three independent experiments (mean and SEM). *P < 0.05, **P < 0.01. b KYSE30 and TE1 cells were treated with apatinib (10 μM) or/or cisplatin (1 μM) for 24 h. The protein levels of p-Akt and β-catenin were detected by western blotting. c All xenograft models were sacrificed and photographed after treatment with vehicle, low-dose apatinib (10 mg/kg/day), cisplatin (1 mg/kg/day) or low-dose apatinib plus cisplatin. n = 5 mice per group. d Tumor volume (expressed in mm3) of xenografts was monitored every 2 days. Day 1 represents the first day of treatment. P values were determined by one-way ANOVA with Tukey’s correction. *P < 0.05, **P < 0.01. e Tumors were weighed at the end of the experiment, and weight was expressed in gram. P values were determined by one-way ANOVA with Tukey’s correction. **P < 0.01. f The weight of the mouse was monitored every 2 days, and weight was expressed in gram. P values were determined by one-way ANOVA with Tukey’s correction. NS represents no significance. g Xenograft tumors in the indicated groups were detected by immunofluorescence. Representative images of TUNEL (green) and nuclei staining (DAPI, blue). Scale bar, 100 μm. h The protein levels of p-Akt and β-catenin in tumor samples from the indicated groups were determined by western blotting. i Schematic diagram of the molecular mechanism by which apatinib regulates the biological functions of esophageal cancer