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Atorvastatin inhibited Rho-associated kinase 1 (ROCK1) and focal adhesion kinase (FAK) mediated adhesion and

Satyanarayana Rentala1, Ramakrishna Chintala, Manohar Guda

  • 1Department of Biotechnology, GITAM University, Visakhapatnam, Andhra Pradesh, India.

Biochemical and Biophysical Research Communications
|November 2, 2013
PubMed

Insights

Atorvastatin, a statin, inhibits prostate cancer cell adhesion and differentiation by affecting integrins, Rho-dependent kinase (ROCK), and focal adhesion kinase (FAK) signaling pathways.

Area of Science:

  • Oncology
  • Pharmacology
  • Cell Biology

Background:

  • Prostate cancer is a significant global health concern and a leading cause of cancer-related deaths in men.
  • Atorvastatin, a 3-hydroxy-3-methyl-glutarylcoenzyme-A (HMG-CoA) reductase inhibitor, has demonstrated potential anticancer activity in prostate cancer cell lines.

Purpose of the Study:

  • To investigate the effects of atorvastatin on the cell adhesion and differentiation of CD133(+)CD44(+) prostate cancer stem cells.
  • To elucidate the underlying molecular mechanisms involving integrins, Rho-dependent kinase (ROCK), and focal adhesion kinase (FAK) signaling pathways.

Main Methods:

  • CD133(+)CD44(+) cells from prostate cancer biopsies and peripheral blood were treated with varying concentrations of atorvastatin.
  • Cell adhesion assays, Western blot analysis for adhesion receptors (integrins) and signaling proteins (ROCK, FAK), and blocking studies with specific inhibitors and antibodies were performed.

Main Results:

  • Atorvastatin dose-dependently inhibited cell attachment to endothelial cells and reduced differentiation.
  • The drug decreased the expression of integrins α1 and β1, and reduced phosphorylated MYPT1 and FAK.
  • Atorvastatin significantly suppressed ROCK1 and FAK-mediated differentiation, confirmed by antibody treatments.

Conclusions:

  • Atorvastatin exhibits beneficial effects on prostate cancer cells by modulating cell adhesion molecules and differentiation markers.
  • These effects are likely mediated through the Rho-dependent kinase (ROCK) and focal adhesion kinase (FAK) signaling pathways.
  • The findings suggest potential novel therapeutic strategies for prostate cancer utilizing atorvastatin.
Keywords:
Differentiation and signaling cascadeFAKIntegrinProstate cancer stem cellROCK1

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