ABSTRACT
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 farmcultivated ginseng extract (FGE), MGE more strongly inhibited cell migration and formation of capillarylike network within noncytotoxic ranges in SVEC410 cells. In addition, MGE dosedependently suppressed Transwell cell migration of the cells. Moreover, MGE reduced the phosphorylation and expression of VEGFR2 as well as the phosphorylation of FAK, Src, Akt and ERK, the intermediate proteins in the VEGFR2 signaling cascade, in the cells. As expected, MGE dramatically decreased hemoglobin content in Matrigel plugs in mice. In conclusion, MGE possesses stronger antiangiogenic properties than FGE in vascular endothelial cells. Such effect of MGE is correlated with inhibition of activation of the VEGFR2 signaling pathway. Therefore, the novel features of MGE may be helpful for understanding its anticancer mechanism for the treatment of cancer patients.
