Fig. 6

YAP1 inhibitor suppresses CXCR7 induced tumor progression and metastasis. A Western blot analysis of the expression of DCLK1 or Vimentin normalized to β-actin in HCT116 and SW620 cells treated with CXCL12 (100 ng/ml) in the presence of AMD3100 (2 μM) and Verteporfin (3 µM) for 48 h. B Representative images of livers and lungs and H&E-stained sections of liver metastatic nodules in nude mice inoculated with HCT116^LV−CXCR7 and HCT116^Control cells via tail veins with or without the treatment of Verteporfin (10 mg/kg, n = 3 per group). The arrows point out the visible metastatic nodules of liver. C Representative images of colons from AOM/DSS-treated WT, Villin-CXCR7 mice and Villin-CXCR7 mice treated with Verteporfin (10 mg/kg). Average size of colon polyps was analyzed in different groups (n = 5). D RT-qPCR analysis of expression levels of miR-124-3p and miR-188-5p in colon cancer tissues from above-mentioned C57BL/6 mice. E Representative IHC staining of Vimentin in AOM/DSS-induced colon adenocarcinoma tissues from wild type C57BL/6 mice and Villin-CXCR7 mice administered with Verteporfin (10 mg/kg) or vehicle control via intraperitoneal injection daily. F Western blot analysis of DCLK1 and Vimentin expression in colon cancer tissues from these mice. GAPDH was used as loading control and statistical analysis was performed. *P < 0.05, **P < 0.01, ***P < 0.001