Figure 1

Ginsenoside enhances the anti-proliferative effects of sunitinib in ccRCC cell lines and the xenograft model. (A) Cell viability was measured after 24 h of drug co-treatment with ginsenoside and sunitinib. Caki-1, 786-O, and A498 cells were treated with Rh2 (10 μM), Rg3 (10 μM), and sunitinib (10 μM) (**p < 0.01, ***p < 0.001). Perform at least three biological repeats (n = 3). (B) The Matrigel invasion assay showed that anti-invasiveness significantly decreased in ccRCC cell lines after co-treatment with ginsenoside and sunitinib. The representative images were obtained after 24 h of drug treatment. (n = 3). (C) Numbers of invading cells in each group (**p < 0.01, ***p < 0.001). (n = 3). (D,E) A498 cells were injected subcutaneously into balb/c nude mice (n = 5). We evaluated tumor volumes and sizes in four treatment groups: DMSO, Rh2 (10 mg/kg), sunitinib (10 mg/kg), and Rh2 + sunitinib. Mice received intraperitoneal injections of ginsenoside three times per week and sunitinib was given by oral administration every day. All groups were evaluated three times per week. The tumor weights were evaluated after 4 weeks of treatment (*p < 0.05, **p < 0.01). (F) Immunohistochemistry (IHC) staining for Ki-67 in A498 xenograft treated with Rh2/sunitinib. We quantified the Ki-67 positive areas identified in five mice tissues per group (*p < 0.05, ***p < 0.001). (200 × magnification).