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Hormonal regulation of beta2-adrenergic receptor level in prostate cancer

Håkon Ramberg1, Turid Eide, Kurt Allen Krobert

  • 1Faculty Division Aker University Hospital, University of Oslo, Oslo Urological University Clinic, Aker University Hospital, Oslo, Norway.

The Prostate
|May 6, 2008
PubMed
Abstract

Insights

Beta-2 adrenergic receptor (beta(2)-AR) levels change during prostate cancer progression. Beta(2)-AR is down-regulated by androgen deprivation therapy but increased by T3 in cancer cells.

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Androgen deprivation therapy is standard for prostate cancer but can lead to hormone-refractory prostate cancer (HRCAP).
  • Ligand-independent activation of the androgen receptor is implicated in HRCAP.
  • The beta(2)-adrenergic receptor (beta(2)-AR) is a known activator of the androgen receptor.

Purpose of the Study:

  • To investigate the role and regulation of beta(2)-AR in prostate cancer.
  • To examine beta(2)-AR expression in relation to androgen sensitivity and therapy.

Main Methods:

  • Analysis of prostatic cell lines using cDNA microarrays, RT-PCR, radioligand binding, cAMP assays, and transfection.
  • Immunohistochemistry and Affymetrix microarrays on clinical prostate specimens.
  • Assessment of beta(2)-AR expression under various conditions, including androgen deprivation and T3 treatment.

Main Results:

  • Beta(2)-AR mRNA and protein were down-regulated in hormone-sensitive prostate cancer cells upon androgen deprivation or bicalutamide treatment.
  • Androgen-independent cell lines showed modest up-regulation of beta(2)-AR compared to hormone-sensitive cells.
  • Triiodothyronine (T3) increased beta(2)-AR levels, an effect inhibited by bicalutamide. Beta(2)-AR expression was higher in malignant prostate tissues and down-regulated by androgen ablation therapy.

Conclusions:

  • Beta(2)-AR levels are modulated by androgen status and T3 in prostate cancer cells.
  • Androgen ablation therapy in patients leads to reduced beta(2)-AR expression.
  • Beta(2)-AR may play a role in prostate cancer progression and response to therapy.

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