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Cell cycle genes as targets of retinoid induced ovarian tumor cell growth suppression

D Zhang1, S Vuocolo, V Masciullo

  • 1Department of Microbiology & Immunology, Temple University School of Medicine, 3400 North Broad Street, Philadelphia, Pennsylvania, PA 19140, USA.

Oncogene
|December 26, 2001
PubMed

Insights

All-trans-retinoic acid (RA) affects ovarian carcinoma cell growth by altering cell cycle gene expression. RA-sensitive cells show increased levels of tumor suppressors and cell cycle inhibitors, suggesting pocket protein pathways are key targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Ovarian carcinoma is a significant health concern.
  • Understanding the mechanisms of retinoid action in cancer is crucial for developing new therapies.

Purpose of the Study:

  • To investigate the effect of all-trans-retinoic acid (RA) on cell cycle gene expression in RA-sensitive and RA-resistant ovarian carcinoma cell lines.
  • To identify key molecular targets of RA in suppressing ovarian cancer cell growth.

Main Methods:

  • Gene expression analysis using multiprobe RNAse protection assays.
  • Protein level analysis via Western blotting and in vitro kinase assays.
  • Assessment of protein-protein interactions, including p27-cyclin E and RB-2/p130-E2F4 complexes.

Main Results:

  • RA-sensitive cells (CA-OV3) exhibited higher expression of p53, p27, p21, and p16 compared to RA-resistant cells (SK-OV3).
  • RA treatment decreased hyperphosphorylated Retinoblastoma protein (RB) and RB-2/p130, while increasing hypophosphorylated forms.
  • RA treatment elevated cyclin-dependent kinase (CDK) inhibitor p27 expression and reduced CDK 2, 4, and 6 activity.

Conclusions:

  • Pocket protein pathways are critical targets for retinoid-mediated suppression of ovarian carcinoma cell growth.
  • Differential expression of cell cycle regulators and their interactions underlies retinoid sensitivity in ovarian cancer.

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