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Increase of human prostate cancer cell (DU145) apoptosis by telmisartan through PPAR-delta pathway

Tony Tong-Lin Wu1, Ho-Shan Niu2, Li-Jen Chen2

  • 1Division of Urology, Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung City, Taiwan; Department of Urology, School of Medicine, National Yang Ming University, Taipei, Taiwan.

European Journal of Pharmacology
|February 9, 2016
PubMed

Insights

Telmisartan reduces prostate cancer cell survival by up-regulating peroxisome proliferator-activated receptor-delta (PPAR-delta). Inhibiting PPAR-delta reverses this effect, suggesting it as a potential therapeutic target for prostate cancer.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Prostate cancer remains a significant health concern, necessitating novel therapeutic strategies.
  • Understanding the molecular mechanisms underlying cancer cell survival is crucial for developing targeted treatments.

Purpose of the Study:

  • To investigate the effect of telmisartan on prostate cancer DU145 cell survival.
  • To elucidate the role of the peroxisome proliferator-activated receptor-delta (PPAR-delta) pathway in telmisartan-induced apoptosis.

Main Methods:

  • DU145 prostate cancer cells were treated with telmisartan, a PPAR-delta antagonist (GSK0660), or PPAR-delta siRNA.
  • Cell viability, apoptosis, cell cycle, and PPAR-delta protein expression were assessed using cell viability assays, flow cytometry, and Western blot analysis.

Main Results:

  • Telmisartan dose-dependently reduced DU145 cell survival and induced cell cycle arrest.
  • GSK0660 and PPAR-delta siRNA partially reversed telmisartan's effects, indicating PPAR-delta's involvement.
  • Telmisartan significantly increased PPAR-delta protein expression in DU145 cells.

Conclusions:

  • Telmisartan induces apoptosis in prostate cancer DU145 cells via up-regulation of the PPAR-delta pathway.
  • Targeting the PPAR-delta pathway may offer a potential therapeutic approach for prostate cancer treatment.
Keywords:
ApoptosisPeroxisome proliferator-activated receptorProstate cancerTelmisartan

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