Antitumor effects of beta-amyrin in Hep-G2 liver carcinoma cells are mediated via apoptosis induction, cell cycle disruption and activation of JNK and P38 signalling pathways.

OBJECTIVE

Liver cancer is one of the major causes of cancer related deaths throughout the world and the fifth most common type of malignancy in men and eighth in women. Beta-amyrin has been reported to exhibit significant pharmacological properties and in the present study we examined the anticancer and apoptotic effects of beta-amyrin against Hep-G2 liver cancer cells.

METHODS

The antiproliferative activity of beta-amyrin was determined by MTT assay. Apoptosis was assessed by DAPI staining and DNA damage was checked by the comet assay. The cell cycle analysis was carried out by flow cytometry and protein expression was examined by western blotting.

RESULTS

Beta-amyrin exhibited significant anticancer activity against Hep-G2 cancer with IC50 values of 25 μM. The anticancer effects were attributed to induction of apoptosis and G2/M cycle arrest in a dose-dependent manner. Moreover, beta-amyrin could also activate the p38 and JNK signalling pathways.

CONCLUSIONS

Based on the results of the current study, we propose that beta-amyrin may prove an important lead molecule for the treatment of liver cancer.