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Apoptosis and chemoresistance in human ovarian cancer: is Xiap a determinant?

J Li1, H Sasaki, Y L Sheng

  • 1Department of Obstetrics and Gynaecology and Department of Cellular and Molecular Medicine, University of Ottawa, Loeb Health Research Institute, The Ottawa Hospital (Civic Campus), Canada.

Biological Signals and Receptors
|May 16, 2000
PubMed

Insights

Cisplatin chemotherapy triggers apoptosis in ovarian cancer by altering cell death and survival gene expression. Targeting Xiap (X-linked inhibitor of apoptosis protein) may overcome chemoresistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cisplatin is a key chemotherapy agent for epithelial ovarian cancer (EOC).
  • Chemoresistance remains a significant challenge in EOC treatment.
  • The balance between cell death and cell survival genes influences treatment response.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying cisplatin-induced apoptosis in EOC cells.
  • To identify key regulatory genes involved in chemoresistance.
  • To explore Xiap as a potential therapeutic target for overcoming cisplatin resistance.

Main Methods:

  • Analysis of gene expression changes in EOC cells treated with cisplatin.
  • Focus on the roles of Xiap (X-linked inhibitor of apoptosis protein), Fas/FasL, caspase-3, MDM2, and FAK.
  • Exploration of gene therapy strategies involving Xiap antisense and P53.

Main Results:

  • Cisplatin treatment suppresses Xiap expression and upregulates the Fas/FasL system in EOC cells.
  • These changes activate caspase-3 and lead to cleavage of MDM2 and FAK.
  • Imbalance in these gene expressions favors chemoresistance.

Conclusions:

  • Suppressed Xiap and activated Fas/FasL are crucial in cisplatin-induced apoptosis.
  • Xiap dysregulation contributes to chemoresistance in EOC.
  • Targeting Xiap, potentially with P53 modulation, offers a novel therapeutic strategy for chemoresistant ovarian cancer.

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