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Epidermal growth factor receptor expression escapes androgen regulation in prostate cancer: a potential molecular

A M Traish1, A Morgentaler

  • 1Department of Biochemistry and Urology, Boston University School of Medicine, Boston, MA 02118, USA. atraish@bu.edu

British Journal of Cancer
|November 6, 2009
PubMed

Insights

Prostate cancer (PCa) can become resistant to androgen deprivation therapy. Loss of androgen regulation over epidermal growth factor receptor (EGFR) in PCa may drive this transition to androgen independence.

Area of Science:

  • Oncology
  • Molecular Biology
  • Urology

Background:

  • Androgen deprivation therapy (ADT) is a primary treatment for prostate cancer (PCa).
  • PCa often relapses into an androgen-refractory state, characterized by increased invasion and malignancy.
  • Androgens normally downregulate epidermal growth factor receptor (EGFR) in the prostate, but this regulation is lost in PCa.

Purpose of the Study:

  • To review the paradoxical relationship between androgen regulation of EGFR in normal prostate tissue versus PCa.
  • To explore how altered EGFR signaling contributes to the progression of PCa from androgen-dependent to androgen-independent states.

Main Methods:

  • Literature review of studies published from the mid-1980s to 2009.
  • Assessment of the relationship between androgens and EGFR function in normal prostate and PCa growth.
  • Analysis of findings from animal models, PCa cell lines, and human tumor specimens.

Main Results:

  • Androgens modulate prostate growth via cross-talk between androgen receptor (AR) and growth factor receptor pathways.
  • Loss of androgen-mediated EGFR downregulation in PCa correlates with increased tumor growth, invasion, and metastasis.
  • Altered EGFR signaling is implicated in the transition to androgen independence.

Conclusions:

  • The loss of androgen regulation of EGFR in PCa is a key factor in disease progression and treatment resistance.
  • A molecular switch controlling EGFR expression by androgens in normal prostate appears to be disrupted in PCa.
  • Understanding this mechanism has significant implications for the clinical management of prostate cancer.

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