Fig. 6
Apatinib inhibited esophageal cancer growth via the Akt/β-catenin pathway in vivo. a All xenograft models were sacrificed and photographed after treatment with vehicle or apatinib (10 and 30 mg/kg/day). n = 5 mice per group. b Tumor volume (expressed in mm3) of xenografts was monitored every 2 days. Day 1 represents the first day of apatinib treatment. P values were determined by one-way ANOVA with Tukey’s correction. **P < 0.01. c 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. d 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. e Xenograft tumors in the indicated groups were detected by immunofluorescence. Representative images of CD31 (green) and nuclei staining (DAPI, blue). Scale bar, 100 μm. f PCNA staining in the indicated groups was detected by IHC. Scale bar, 100 μm. 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 mRNA expression levels of Myc and Jun in tumor samples from the indicated groups were examined by qPCR. Data represent experiments in three independent tumors. P values were determined by one-way ANOVA with Tukey’s correction. **P < 0.01. i The protein levels of p-VEGFR2, p-Akt, β-catenin and CyclinD1 in tumor samples from the indicated groups were determined by western blotting