Mountain ginseng (Panax ginseng) has been used for cancer patient therapy in Northeast Asia. Although it is well known that cancer cells are able to induce angiogenesis, the effect of mountain ginseng on angiogenesis is still unknown. In the present study, we investigated whether ethanolic extract of mountain ginseng (MGE) could inhibit angiogenesis in in vitro and in vivo models. In comparison with farm‑cultivated ginseng extract (FGE), MGE more strongly inhibited cell migration and formation of capillary‑like network within non‑cytotoxic ranges in SVEC4‑10 cells. In addition, MGE dose‑dependently suppressed Transwell cell migration of the cells. Moreover, MGE reduced the phosphorylation and expression of VEGF‑R2 as well as the phosphorylation of FAK, Src, Akt and ERK, the intermediate proteins in the VEGF‑R2 signaling cascade, in the cells. As expected, MGE dramatically decreased hemoglobin content in Matrigel plugs in mice. In conclusion, MGE possesses stronger anti‑angiogenic properties than FGE in vascular endothelial cells. Such effect of MGE is correlated with inhibition of activation of the VEGF‑R2 signaling pathway. Therefore, the novel features of MGE may be helpful for understanding its anticancer mechanism for the treatment of cancer patients.
Keywords: SVEC4‑10 cells; VEGF‑R2; angiogenesis; ginsenosides; mountain ginseng.