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ADP-Ribose and oxidative stress activate TRPM8 channel in prostate cancer and kidney cells

Ercan Baş1, Mustafa Nazıroğlu2,3, László Pecze4

  • 1Department of Urology, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey.

Scientific Reports
|March 13, 2019
PubMed

Insights

Oxidative stress activates the TRPM8 channel, increasing calcium and apoptosis in prostate cancer cells. This suggests TRPM8 activation is a potential therapeutic strategy for prostate cancer treatment.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • TRPM8 channel activation by oxidative stress may induce pro-apoptotic signals in cancer cells.
  • Understanding TRPM8's role in oxidative stress is crucial for cancer therapy development.

Purpose of the Study:

  • To evaluate TRPM8 activation's effect on apoptosis and oxidative stress in prostate cancer and kidney cells.
  • To investigate TRPM8-mediated calcium signaling in response to oxidative stress.

Main Methods:

  • Utilized prostate cancer (Du145M8) and human kidney (HEK293) cell lines, including TRPM8 knockout and transfected variants.
  • Measured intracellular calcium responses, apoptosis markers (Annexin V), mitochondrial membrane potential, ROS, and caspase activity.
  • Applied TRPM8 activators (cumene hydrogen peroxide, menthol, ADPR) and inhibitors (glutathione, specific blockers).

Main Results:

  • TRPM8 activation by oxidative stress (CHPx) and ADPR significantly increased intracellular calcium in Du145M8 and HEK293TM8 cells.
  • These responses were blocked by antioxidants and TRPM8 inhibitors.
  • Apoptosis, ROS, and caspase activity were elevated in TRPM8-expressing cells upon activation, but not in knockout or non-transfected cells.

Conclusions:

  • TRPM8 channel activation by oxidative stress and ADPR enhances apoptotic and oxidant effects in cancer cells.
  • Targeting TRPM8 activation presents a promising therapeutic strategy for prostate cancer treatment.

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