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Growth factors in steroid-responsive prostatic tumor cells
D Dondi1, R M Moretti, M M Marelli
1Department of Endocrinology, University of Milano, Italy.
Steroids
|April 1, 1996
Summary
Luteinizing hormone-releasing hormone (LHRH) agonists inhibit prostate cancer cell growth by interfering with epidermal growth factor (EGF) signaling pathways. LHRH does not affect androgen receptor expression but blocks EGF-induced c-fos expression in prostate tumor cells.
Area of Science:
- Oncology
- Endocrinology
- Molecular Biology
Background:
- Androgens are known to stimulate prostate cancer growth.
- A luteinizing hormone-releasing hormone (LHRH)-like system inhibits cell proliferation in human androgen-dependent prostate tumor cell lines (LNCaP).
Purpose of the Study:
- To investigate if LHRH inhibits prostate cancer cell proliferation by interfering with testosterone (T) and epidermal growth factor (EGF).
- To clarify the mechanisms by which LHRH affects T and EGF signaling in LNCaP cells.
Main Methods:
- LNCaP cells were treated with an LHRH agonist (LHRH-A).
- Effects on androgen receptor mRNA expression were evaluated after T stimulation.
- EGF receptor concentration and EGF-induced intracellular signaling (c-fos expression, EGF receptor tyrosine phosphorylation) were assessed.
Main Results:
- LHRH-A counteracted the proliferative action of T but did not affect androgen receptor mRNA expression.
- LHRH-A inhibited the mitogenic action of EGF and reduced EGF receptor concentration.
- LHRH-A blocked EGF-induced c-fos proto-oncogene expression but did not alter EGF-induced tyrosine phosphorylation of the EGF receptor.
Conclusions:
- LHRH may inhibit cell proliferation in androgen-dependent prostate tumors by interfering with specific mechanisms of EGF signaling.
- LHRH's interaction with testosterone-activated pathways in prostate tumors requires further investigation.