Induction of apoptosis in prostate cancer by ginsenoside Rh2

Tony Tong Lin Wu, Yat-Ching Tong, I-Hung Chen, Ho Shan Niu, Yingxiao Li, Juei Tang Cheng

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish
Pages (from-to)11109-11118
Number of pages10
JournalOncotarget
Volume9
Issue number13
DOIs
Publication statusPublished - 2018 Jan 1

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PPAR delta
Prostatic Neoplasms
Apoptosis
Superoxides
STAT3 Transcription Factor
Reactive Oxygen Species
Cell Survival
Up-Regulation
Small Interfering RNA
STAT Transcription Factors
ginsenoside Rh2
Cultured Cells
Flow Cytometry
Down-Regulation
Western Blotting
Staining and Labeling

All Science Journal Classification (ASJC) codes

  • Oncology

Cite this

Wu, Tony Tong Lin ; Tong, Yat-Ching ; Chen, I-Hung ; Niu, Ho Shan ; Li, Yingxiao ; Cheng, Juei Tang. / Induction of apoptosis in prostate cancer by ginsenoside Rh2. In: Oncotarget. 2018 ; Vol. 9, No. 13. pp. 11109-11118.
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abstract = "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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Induction of apoptosis in prostate cancer by ginsenoside Rh2. / Wu, Tony Tong Lin; Tong, Yat-Ching; Chen, I-Hung; Niu, Ho Shan; Li, Yingxiao; Cheng, Juei Tang.

In: Oncotarget, Vol. 9, No. 13, 01.01.2018, p. 11109-11118.

Research output: Contribution to journalArticle

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