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RASSF1A and the Taxol Response in Ovarian Cancer

Susannah Kassler1, Howard Donninger, Michael J Birrer

  • 1J.G. Brown Cancer Center, University of Louisville, 417 CTR Building, 505 S. Hancock Street, Louisville, KY 40202, USA.

Molecular Biology International
|May 2, 2012
PubMed

Insights

Loss of the RASSF1A tumor suppressor gene correlates with Taxol resistance in ovarian cancer. Epigenetic therapy can restore RASSF1A expression, re-sensitizing tumors to Taxol treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • The RASSF1A tumor suppressor gene is frequently inactivated by promoter methylation in human cancers.
  • RASSF1A protein stabilizes microtubules, and its loss sensitizes cells to microtubule-destabilizing agents like Taxol.
  • Loss of RASSF1A expression correlates with Taxol resistance in ovarian cancer.

Purpose of the Study:

  • To investigate if RASSF1A levels determine Taxol response in ovarian cancer.
  • To explore if epigenetic therapy can reverse Taxol resistance in RASSF1A-negative ovarian tumors.

Main Methods:

  • Knockdown of RASSF1A expression in an ovarian cancer cell line.
  • Treatment with Taxol to assess apoptosis and cell survival.
  • Application of DNA Methyl Transferase inhibitors to restore RASSF1A expression and Taxol sensitivity.

Main Results:

  • RASSF1A knockdown inhibited Taxol-induced apoptosis and promoted cell survival.
  • Epigenetic therapy using DNA Methyl Transferase inhibitors restored RASSF1A expression.
  • Restored RASSF1A expression re-sensitized ovarian cancer cells to Taxol.

Conclusions:

  • RASSF1A plays a critical role in modulating tumor response to Taxol.
  • Epigenetic therapy is a potential strategy to overcome Taxol resistance in RASSF1A-deficient ovarian cancers.

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