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A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
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Prolonging androgen sensitivity in prostate cancer - a role for COX inhibitors?

Andrew Richards1, Kevin McGeechan, Marzieh Niknam

  • 1Department of Urology, Royal Prince Alfred Hospital, Australia. office@drandrewrichards.com.au

ANZ Journal of Surgery
|November 10, 2009
PubMed
Abstract

Insights

Cyclooxygenase-2 (COX-2) inhibitors do not extend androgen sensitivity in advanced prostate cancer. This study found no significant difference in time to androgen independence or tumor growth when COX-2 inhibitors were used with castration.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Advanced prostate cancer initially responds to androgen deprivation but inevitably becomes androgen independent.
  • Prolonging the period of androgen sensitivity is a critical clinical objective.
  • Cyclooxygenase-2 (COX-2) inhibitors are investigated for their potential to extend androgen sensitivity.

Purpose of the Study:

  • To evaluate the efficacy of cyclooxygenase-2 (COX-2) inhibitors in prolonging androgen sensitivity in prostate cancer.
  • To determine if COX-2 inhibition can delay the progression to androgen independence.

Main Methods:

  • Immunohistochemistry was used to assess COX-2 expression in human prostate tissues (benign, malignant, androgen-dependent, androgen-independent).
  • A xenograft model of prostate cancer in nude mice was used, involving castration and treatment with a COX-2 inhibitor or vehicle.
  • Key endpoints included time to androgen independence (AIPC), tumor growth rate, and prostate-specific antigen (PSA) rise rate.

Main Results:

  • COX-2 protein was upregulated in prostate cancer and remained elevated after androgen ablation and in the androgen-independent state in human tissues.
  • In the LNCaP xenograft model, COX-2 expression varied, with some downregulation observed in AIPC.
  • Administration of a COX-2 inhibitor alongside castration did not significantly alter the time to AIPC, tumor growth rate, or PSA rise rate.

Conclusions:

  • The findings do not support the use of COX-2 inhibitors as a strategy to prolong androgen responsiveness in prostate cancer.
  • Further research may be needed to explore alternative therapeutic targets for overcoming androgen independence.

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