Ginseng
saponins exert various important pharmacological effects with regard to the control of many diseases, including
cancer. In this study, the anticancer effect of
ginsenosides on human
cancer cells was investigated and compared. Among the tested compounds,
ginsenoside-Rh2 displays the highest inhibitory effect on cell viability in HepG2 cells.
Ginsenoside-Rh2, a ginseng
saponin isolated from the root of Panax ginseng, has been suggested to have potential as an
anticancer agent, but the underlying mechanisms remain elusive. In the present study, we have shown that
cancer cells have differential sensitivity to ginsenoside-Rh2-induced apoptosis, raising questions regarding the specific mechanisms responsible for the discrepant sensitivity to
ginsenoside-Rh2. In this study, we demonstrate that
AMP-activated protein kinase (AMPK) is a survival factor under
ginsenoside-Rh2 treatment in
cancer cells.
Cancer cells with acute responsiveness of AMPK display a relative resistance to
ginsenoside-Rh2, but cotreatment with AMPK inhibitor resulted in a marked increase of ginsenoside-Rh2-induced apoptosis. We also observed that
p38 MAPK (
mitogen-activated protein kinase) acts as another survival factor under
ginsenoside-Rh2 treatment, but there was no signaling crosstalk between AMPK and
p38 MAPK, suggesting that combination with inhibitor of AMPK or
p38 MAPK can augment the anticancer potential of
ginsenoside Rh2.