Figure 3.

Possible cellular and molecular mechanisms of ginsenosides aginst cancer. CDKs, cyclin-dependent kinases; MDM2, murine double minute-2; VEGF, vascular endothelial growth factor; bFGF, basic fibroblast growth factor; PDGF, platelet derived growth factor, MMP, matrix metalloproteinase; IAP, inhibitory apoptotic protein; TNF, tumor necrosis factor; NF-κB, nuclear factor κB; PI3K, Phosphatidylinositol 3-kinase; HIF-1, hypoxia-inducible factor-1; ERK, extracellular signal-regulated kinase; NRF2, nuclear factor (erythroid-derived 2)-like; AMPK, 5′ AMP-activated protein kinase; EGF, epithelial growth factor; ↑, upregulation; ↓, downregulation.