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S10 phosphorylation of p27 mediates atRA induced growth arrest in ovarian carcinoma cell lines

Maria Radu1, Dianne R Soprano, Kenneth J Soprano

  • 1Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania, USA.

Journal of Cellular Physiology
|July 11, 2008
PubMed

Insights

All trans retinoic acid (atRA) inhibits ovarian cancer cell growth by increasing p27 protein phosphorylation. This specific modification is crucial for atRA

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • All trans retinoic acid (atRA) is known to inhibit ovarian carcinoma cell growth.
  • p27 is a cyclin-dependent kinase inhibitor whose levels are elevated by atRA.

Purpose of the Study:

  • To investigate the role of p27 phosphorylation at the S10 residue in mediating atRA-induced growth arrest in ovarian cancer cells.
  • To compare the effects of atRA on sensitive (CAOV3) versus resistant (SKOV3) cell lines.

Main Methods:

  • Treatment of CAOV3 and SKOV3 cells with atRA.
  • Analysis of p27, phospho-p27 (S10), and skp2 protein levels.
  • Use of an S10-non-phosphorylatable p27 mutant (A10-p27) to assess dominant-negative effects.

Main Results:

  • atRA treatment increased S10 phospho-p27 levels in CAOV3 cells, accompanied by decreased skp2 levels.
  • Resistant SKOV3 cells did not show these changes.
  • The A10-p27 mutant impaired atRA's effects on p27/CDK interactions, CDK activity, and S-phase gene expression, conferring resistance.

Conclusions:

  • Phosphorylation of p27 at S10 is a critical mechanism for all trans retinoic acid-induced growth arrest in ovarian cancer.
  • Targeting p27 phosphorylation could be a strategy to overcome resistance to atRA in ovarian carcinoma.

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