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All-trans retinoic acid induces DU145 cell cycle arrest through Cdk5 activation

Eugene Lin1, Mei-Chih Chen, Chih-Yang Huang

  • 1Department of Life Sciences, National Chung Hsing University, Taichung, Taiwan.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|May 24, 2014
PubMed
Abstract

Insights

All-trans retinoic acid (ATRA) inhibits prostate cancer cell growth by activating cyclin-dependent kinase 5 (Cdk5) and p27. This study explores ATRA

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • All-trans retinoic acid (ATRA), the active form of vitamin A, is known to induce growth arrest in various cancer cells.
  • Cyclin-dependent kinase 5 (Cdk5) activity is modulated by ATRA, and Cdk5 has been implicated in prostate cancer cell fate.
  • Previous research suggests Cdk5 plays a role in the biological behavior of prostate cancer cells.

Purpose of the Study:

  • To investigate the role of Cdk5 in ATRA-induced growth arrest of the castration-resistant prostate cancer cell line DU145.
  • To determine if ATRA up-regulates the Cdk inhibitor protein, p27, in a Cdk5-dependent manner.
  • To elucidate the molecular mechanisms underlying ATRA's anti-proliferative effects in prostate cancer.

Main Methods:

  • DU145 cells were treated with ATRA.
  • Assessed cell proliferation, cell cycle distribution, and protein expression of Cdk5 and p27.
  • Examined protein localization of Cdk5/p27 using immunocytochemistry.
  • Utilized a Cdk5 inhibitor and siRNA for Cdk5 knockdown to assess functional roles.

Main Results:

  • ATRA treatment significantly inhibited DU145 cell proliferation.
  • ATRA significantly increased p27 expression, mediated by Cdk5 up-regulation.
  • Cdk5 inhibition reversed ATRA-induced G1 phase arrest and proliferation inhibition.
  • ATRA treatment led to increased nuclear localization of p27, which was reduced by Cdk5 inhibition.

Conclusions:

  • ATRA induces growth inhibition in castration-resistant prostate cancer cells by activating the Cdk5/p27 pathway.
  • This finding enhances understanding of prostate cancer treatment strategies.
  • Potential implications for nutritional interventions in prostate cancer patient management.

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