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Preparation of Mitochondria from Ovarian Cancer Tissues and Control Ovarian Tissues for Quantitative Proteomics Analysis
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Mutation or loss of p53 differentially modifies TGFβ action in ovarian cancer

Eoghainín Ó hAinmhire1, Suzanne M Quartuccio1, Whay Cheng1

  • 1Department of Medicinal Chemistry and Pharmacognosy, Center for Pharmaceutical Biotechnology, University of Illinois at Chicago, Chicago, Illinois, United States of America.

Plos One
|March 4, 2014
PubMed

Insights

Transforming Growth Factor Beta (TGFβ) impacts ovarian cancer. Wild-type p53 inhibits cancer cell growth with TGFβ, while mutant or absent p53 allows proliferation and migration, affecting invasion markers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gynecologic Oncology

Background:

  • Ovarian cancer is a leading cause of gynecologic cancer deaths in the US.
  • The p53 tumor suppressor is frequently mutated (96%) in high-grade serous ovarian carcinomas.
  • Dysregulation of the Transforming Growth Factor Beta (TGFβ) pathway is implicated in various cancers, including ovarian.

Purpose of the Study:

  • To investigate the role of p53 (wild-type, mutant, or null) in mediating ovarian cancer cell response to TGFβ signaling.
  • To examine the effects of TGFβ on ovarian surface epithelium and fallopian tube epithelium.
  • To understand how p53 status influences TGFβ-induced proliferation, migration, and expression of invasion-related genes.

Main Methods:

  • Utilized ovarian cancer cell lines with varying p53 expression (wild-type, mutant, null).
  • Assessed cell proliferation and migration in response to TGFβ treatment.
  • Analyzed protein expression of DKK1 and TMEPAI, key genes in ovarian cancer metastasis.

Main Results:

  • Only ovarian cancer cells with wild-type p53 exhibited TGFβ-induced growth inhibition.
  • TGFβ stimulated migration in p53-null cells, an effect not seen in cells with mutant p53.
  • Knockdown of wild-type p53 increased TGFβ-induced migration.
  • p53-null and p53-knockdown cells showed increased DKK1 and TMEPAI expression; mutant p53 cells had lower induction.

Conclusions:

  • Loss or mutation of p53 enables continued proliferation of ovarian cancer cells despite TGFβ signaling.
  • Mutant p53 expression in ovarian cancer cells reduces TGFβ-induced migration and lowers levels of pro-invasive genes DKK1 and TMEPAI.
  • p53 status critically modulates ovarian cancer cell response to TGFβ, impacting proliferation, migration, and metastatic potential.

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