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EBP1, an ErbB3-binding protein, is decreased in prostate cancer and implicated in hormone resistance

Yuexing Zhang1, Douglas Linn, Zhenqiu Liu

  • 1Greenebaum Cancer Center, University of Maryland School of Medicine, 655 West Baltimore Street, Baltimore, MD 21201, USA.

Molecular Cancer Therapeutics
|October 15, 2008
PubMed

Insights

ErbB3-binding protein 1 (EBP1) downregulation promotes hormone-refractory prostate cancer. Restoring EBP1 inhibits androgen receptor and ErbB3 signaling, reducing tumor growth and offering a new therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Aberrant androgen receptor (AR) activation by ErbB2/ErbB3 drives hormone resistance in prostate cancer.
  • ErbB3-binding protein 1 (EBP1) functions as an AR corepressor and is decreased in hormone-refractory prostate cancer models.

Purpose of the Study:

  • To investigate the role of EBP1 expression in human prostate cancer.
  • To determine the therapeutic potential of EBP1 in hormone-refractory prostate cancer.

Main Methods:

  • Studied EBP1 mRNA and protein levels in prostate cancer tissues versus benign prostate tissue.
  • Restored EBP1 expression in hormone-refractory LNCaP C81 cells and assessed phenotypic changes and AR target gene expression.
  • Investigated the effect of EBP1 on heregulin (HRG)-stimulated growth and AKT phosphorylation.
  • Utilized short hairpin RNA to abrogate EBP1 expression in hormone-dependent LNCaP cells.
  • Evaluated the impact of EBP1 on tumor growth in mouse xenograft models.

Main Results:

  • EBP1 gene and protein expression were significantly decreased in prostate cancer tissues compared to benign tissues.
  • Restoring EBP1 in LNCaP C81 cells ameliorated the androgen-independent phenotype and reduced AR target gene expression.
  • EBP1 restoration abolished HRG-stimulated growth and AKT phosphorylation in hormone-refractory cells.
  • Abrogating EBP1 in hormone-dependent LNCaP cells promoted HRG-stimulated growth.
  • EBP1 restoration decreased xenograft tumor growth, while EBP1 abrogation enhanced tumor growth.

Conclusions:

  • EBP1 plays a crucial role in inhibiting both AR- and HRG-stimulated growth in prostate cancer.
  • Decreased EBP1 expression contributes to the development of hormone-refractory prostate cancer.
  • Restoring EBP1 represents a potential novel therapeutic strategy for androgen-refractory prostate cancer.

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