JS-K promotes apoptosis by inducing ROS production in human prostate cancer cells

Qiu,Mingning; Chen,Lieqian; Tan,Guobin; Ke,Longzhi; Zhang,Sai; Chen,Hege; Liu,Jianjun

doi:10.3892/ol.2016.5535

JS-K promotes apoptosis by inducing ROS production in human prostate cancer cells

Authors:
- Mingning Qiu
- Lieqian Chen
- Guobin Tan
- Longzhi Ke
- Sai Zhang
- Hege Chen
- Jianjun Liu
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Affiliations: Laboratory of Urology, Guangdong Medical University, Zhanjiang, Guangdong 524001, P.R. China
Published online on: December 27, 2016 https://doi.org/10.3892/ol.2016.5535
Pages: 1137-1142
Copyright: © Qiu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

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.

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