| Esophageal cancer（EC）is one of the least studied and deadliest cancers worldwide.It is ranked globally 8 th in the cause of death.It has been reported that the 5-year survival rate of esophageal cancer is 48.7%.EC recurrences occur frequently even after successful anti-cancer treatment due to presented in a locally advanced stage with a poor prognosis and survival,suggesting high aggressiveness with increased metastatic potential.Therefore,the treatment of esophageal cancer has always been a difficultproblem.Ginsenoside is a naturally compound which is found in the root of red ginseng.According to its optical rotation,Ginsenoside Rh2 can be divided into two enantiomers,（20S）G-Rh2 and（20R）G-Rh2.It is well known that（20S）G-Rh2 has excellent anti-tumor activity and can induced apoptosis in a variety of tumor cells including human leukemia cells,human cervical cancer cells,human ovarian cancer cells,human lung cancer cells,human liver cancer cells.In recent years,（20S）G-Rh2 is increasingly used for clinical cancer research,but the effect on esophageal cancer cells is still not clear.In the present study,we showed that the molecular mechanism of Ginsenoside Rh2 induced apoposis in the human esophageal cancer cells.This paper described the Ginsenoside Rh2induced apoptosis and mechanism of esophageal cancer cells.From the research,we found,（20S）G-Rh2 significantly inhibited the proliferation of human esophageal cancer ECA109 and TE-13 cells,and the inhibition was dose-effect relationship.The IC500 values of the two cells were:2.9mg/mL,3.7mg/mL.We determined that（20S）G-Rh2 inhibited esophageal cancer cell lines ECA109 and TE-13 growth by inducing apoptosis through cell morphology analysis,flow cytometry,detection of apoptosis marker Caspase-3 enzyme activity,and analysis of PARP fragmentation.（20S）G-Rh2inducedapoptosisthroughmitochondria-mediated endogenous pathway in esophageal cancer cell ECA109,TE-13.G-Rh2inducedthetranslocationofcytosolicBaxtothe mitochondria,mitochondrial cytochrome c released,and subsequent Caspase-9 activation.At the same time,Smac is released,binds to the anti-apoptotic protein c-IAP1 and trigger degradation of c-IAP1,thereby amplifying the apoptotic signal.（20S）G-Rh2 can also induced apoptosis in TE-13 esophageal cancer cells through a membrane death receptor-mediated extracellular pathway.In addition,We detected that Caspase-8 enzyme was activated in TE-13 cells and the expression of related death receptors Fas and DR5 was up-regulated at mRNA and protein levels.Therefore,（20S）G-Rh2 can also induce apoptosis by activating Caspase-8-mediated exogenous apoptosis signaling pathway. |
