Reactive oxygen species (ROS) are chemical species that alter redox status, and are responsible for inducing
carcinogenesis. The purpose of the present study was to assess the effects of the
glutathione S transferase-activated
nitric oxide donor prodrug, JS-K, on ROS accumulation and on proliferation and apoptosis in human
prostate cancer cells. Cell proliferation and apoptosis, ROS accumulation and the activation of the mitochondrial signaling pathway were measured. The results demonstrated that JS-K may inhibit
prostate cancer cell growth in a dose- and time-dependent manner, and induce ROS accumulation and apoptosis in a dose-dependent manner. With increasing concentrations of JS-K, expression of
pro-apoptotic proteins increased, but Bcl-2 expression decreased. Additionally, the
antioxidant N-acetylcysteine reversed JS-K-induced cell apoptosis; conversely, the
pro-oxidant glutathione disulfide exacerbated JS-K-induced apoptosis. In conclusion, the data suggest that JS-K induces
prostate cancer cell apoptosis by increasing ROS levels.