Induction of apoptosis in prostate cancer by ginsenoside Rh2
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Tony Tong-Lin Wu1,2,3, Yat-Ching Tong4, I-Hung Chen4, Ho-Shan Niu5, Yingxiao Li6 and Juei-Tang Cheng1,6
1Institute of Medical Sciences, Chang Jung Christian University, Tainan, Taiwan
2Division of Urology, Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
3Department of Urology, School of Medicine, National Yang Ming University, Taipei, Taiwan
4Department of Urology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan
5Department of Nursing, Tzu Chi University of Science and Technology, Hualien, Taiwan
6Department of Medical Research, Chi-Mei Medical Center, Tainan, Taiwan
Juei-Tang Cheng, email: [email protected]
Ho-Shan Niu, email: [email protected]
Keywords: prostate cancer; apoptosis; ginsenoside Rh2; peroxisome proliferator-activated receptor
Received: July 21, 2017 Accepted: January 22, 2018 Published: January 27, 2018
The therapeutic action of ginsenoside Rh2 on several cancer models has been reported. This study aimed to evaluate its apoptotic effect on prostate cancer and the underlying mechanism. Cultured DU145 cells were treated with Rh2 (5 × 10–5 to 1 × 10–4 M), peroxisome proliferator-activated receptor-delta (PPAR-delta) antagonist GSK0660 (1 × 10–6 to 5 × 10–6 M); or small interfering RNA (siRNA) of PPAR-delta. The treatment effects were evaluated with cell viability assay, life/death staining and flow cytometry for apoptosis. Immunostaining was used for reactive oxygen species (ROS) and superoxide detection. Western blot analysis for PPAR-delta and signal transducer and activator of transcription 3 (STAT3) protein expression were performed. The results showed that Rh2 significantly decreased DU145 cell survival and increased cell apoptosis. ROS and superoxide induction, PPAR-delta up-regulation and phosphorylated STAT3 (p-STAT3) down-regulation by Rh2 were demonstrated. GSK0660 partially but significantly inhibited the Rh2-induced apoptosis and restored cell viability. Treatment with siRNA reversed the Rh2-induced apoptosis as well as changes in PPAR-delta and p-STAT3 expression. In conclusion, our findings have demonstrated that ginsenoside Rh2 induces prostate cancer DU145 cells apoptosis through up-regulation of PPAR-delta expression which is associated with p-STAT3 up-regulation and ROS/superoxide induction. Rh2 may be potentially useful in the treatment of prostate cancer.
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