Farnesol induces apoptosis of DU145 prostate cancer cells through the PI3K/Akt and MAPK pathways

Abstract

The aim of this study was to investigate the effect of farnesol on the induction of apoptosis in DU145 prostate cancer cells. 3-(4,5-Dimethylthiazol-2- yl)-2,5-diphenyl tetrazolium bromide assay showed that cell proliferation decreased significantly in a dose- and time-dependent manner. 4′,6-Diamidino-2-phenylindole staining showed that chromatin condensation in cells treated with 60 μM of farnesol was markedly higher than in the control groups. Farnesol increased the expression of p53, p-c-Jun N-terminal kinase, cleaved-caspase-3, Bax, and cleaved-caspase-9, but decreased the expression of p-phosphatidylinositol-3-kinase (PI3K), p-Akt, p-p38, Bcl-2, and p-extracellular signal-regulated protein kinase, in a dose-dependent manner. The apoptotic cell ratio increased in a dose-dependent manner. The tumor growth inhibitory effect of farnesol was investigated in a mouse model. Compared to the control group, tumor volume decreased significantly in the group administered 50 mg/kg farnesol. Apoptosis was frequently detected in this same group by terminal deoxynucleotidyl transferase dUTP nick-end labeling assay. The results indicated that farnesol induced apoptosis of DU145 prostate cancer cells through the PI3K/Akt and mitogen-activated protein kinase signaling pathways.