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Updated: Aug 18, 2026
An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
Antiandrogen effects in models of androgen responsive cancer
1Department of Cellular and Molecular Biology, Southwest Foundation for Biomedical Research, San Antonio, TX 78284.
Abstract:
The ability of antiandrogens to antagonize androgen effects in androgen responsive tissues is well established. Antiandrogens may diminish in vivo or in vitro proliferation of some androgen responsive cancer cells without causing cessation of multiplication. These model studies are representative of clinical experience in treatment of human prostate cancer with antiandrogen therapy. Recent studies in the AXC/SSh rat prostate cancer model show that these cancer cells elaborate polypeptide growth factors which stimulate their proliferation. If growth factor production by these cells is androgen independent, this may provide an explanation for failure of androgen ablation or antiandrogen treatment to effectively halt prostate cancer cell proliferation.
Insights
Antiandrogens can slow prostate cancer growth but not stop it, as cancer cells may produce their own growth factors. This explains why androgen deprivation therapy sometimes fails.
Area of Science:
- Oncology
- Endocrinology
- Molecular Biology
Background:
- Antiandrogens are established to antagonize androgen effects in responsive tissues.
- Antiandrogens can reduce, but not eliminate, the proliferation of some androgen-responsive cancer cells.
- Clinical experience in prostate cancer treatment with antiandrogens shows variable efficacy.
Purpose of the Study:
- To investigate the mechanisms underlying the partial efficacy of antiandrogen therapy in prostate cancer.
- To explore the role of endogenous growth factors in androgen-independent cancer cell proliferation.
- To provide a potential explanation for treatment failures in prostate cancer management.
Main Methods:
- Utilized the AXC/SSh rat prostate cancer model for in vivo and in vitro studies.
- Investigated the proliferation of androgen-responsive cancer cells under antiandrogen treatment.
- Analyzed the production of polypeptide growth factors by prostate cancer cells.
Main Results:
- Antiandrogens demonstrated an ability to diminish cancer cell proliferation without complete cessation.
- Prostate cancer cells in the AXC/SSh rat model were found to elaborate polypeptide growth factors.
- These growth factors were shown to stimulate cancer cell proliferation.
Conclusions:
- The elaboration of polypeptide growth factors by prostate cancer cells may contribute to their proliferation.
- If growth factor production is androgen-independent, it could explain the failure of androgen ablation or antiandrogen therapy to halt cancer progression.
- This finding offers a potential molecular mechanism for therapeutic resistance in prostate cancer.
