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The DEK Oncoprotein Functions in Ovarian Cancer Growth and Survival

Kari E Hacker1, Danielle E Bolland1, Lijun Tan1

  • 1Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Michigan Medical Center, Ann Arbor, MI 48109.

Neoplasia (New York, N.Y.)
|November 10, 2018
PubMed

Insights

Targeting the DEK oncoprotein shows promise for epithelial ovarian cancer therapy. Reducing DEK levels slows tumor growth, induces cell death, and enhances chemotherapy effectiveness in preclinical models.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Alterations in DNA damage repair are crucial in ovarian cancer development.
  • The DEK oncoprotein is involved in DNA double-strand break repair.
  • Targeting DNA damage response pathways offers therapeutic opportunities.

Purpose of the Study:

  • To investigate the role of the DEK oncoprotein in epithelial ovarian cancer.
  • To determine if DEK is a viable therapeutic target for ovarian cancer.

Main Methods:

  • DEK expression levels were analyzed in primary tumors and cell lines.
  • RNA interference (siRNA and shRNA) was used to deplete DEK in ovarian cancer cells.
  • Cell growth, apoptosis, and DNA damage were assessed upon DEK knockdown.
  • In vivo studies were conducted using a mouse xenograft model.

Main Results:

  • DEK is overexpressed in epithelial ovarian cancers and cell lines.
  • DEK depletion in vitro reduced cell growth, induced apoptosis, and caused DNA damage.
  • The effects of DEK depletion were amplified by concurrent chemotherapy.
  • DEK knockdown in vivo resulted in slower tumor growth and smaller tumors.

Conclusions:

  • DEK overexpression contributes to epithelial ovarian cancer progression.
  • Targeting DEK and its associated pathways is a promising therapeutic strategy for ovarian cancer.
  • DEK inhibition may enhance the efficacy of conventional chemotherapy.

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