Potential antitumor effects of panaxatriol against DU-15 human prostate cancer cells is mediated via mitochondrial mediated apoptosis, inhibition of cell migration and sub-G1 cell cycle arrest.

Purpose: Prostate cancer is the most frequently diagnosed malignancy in men and the second major reason of cancer death in males. Currently, there are no viable options available for the treatment of advanced-stage prostate cancer. Against this backdrop, the present study aimed to study the anticancer effect of panaxatriol against prostate DU-15 cancer cells. Methods: MTT cell viability assay evaluated the effects of the drug on cell cytotoxicity, while clonogenic assay was used to assess the effects on colony formation in DU-15 cells. Apoptotic effects were evaluated by DAPI staining using fluorescence microscopy. Effects on reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were evaluated by flow cytometry using DCFH-DA and DiOC(6). Effects on cell cycle were measured by flow cytometry, while cell migration tendency of the cells was evaluated by in vitro wound healing assay. Results: The results indicated that panaxatriol exerts dose-dependent cytotoxic effects on prostate DU-15 cancer cells. The IC50 of panaxatriol was 30 mu M. Panaxatriol was found to exert its anticancer activity through induction of apoptosis. The apoptosis of DU-15 cancer cells was prompted by ROS-mediated alterations in mitochondrial membrane potential. Additionally, panaxatriol induced sub-G1 cell cycle arrest and suppressed the DU-15 cell migration ability in a concentration-dependent manner. Conclusion: Taken together, we strongly believe that panaxatriol may prove handy in the treatment and management of prostate cancer and deserves further research.