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Androgen-independent growth is induced by neuropeptides in human prostate cancer cell lines

J Jongsma1, M H Oomen, M A Noordzij

  • 1Department of Experimental Urology, Erasmus University, Rotterdam, The Netherlands. jongsma@uro.fgg.eur.nl

The Prostate
|December 1, 1999
PubMed
Abstract

Insights

Neuropeptides like gastrin-releasing peptide (GRP) stimulate androgen-independent prostate cancer growth in certain cell lines. Neuroendocrine (NE) cells may play a role in clinical prostate cancer progression.

Area of Science:

  • Oncology
  • Cell Biology
  • Endocrinology

Background:

  • Androgen-independent prostate cancer growth is a major challenge after androgen-ablation therapy.
  • Potential mechanisms include altered androgen receptor (AR) specificity, ligand-independent AR stimulation, or paracrine growth modulation by neuroendocrine (NE) cells.
  • Neuropeptides secreted by NE cells are implicated in prostate cancer progression.

Purpose of the Study:

  • To investigate the role of neuropeptides in androgen-independent prostate cancer growth.
  • To characterize the growth-modulating effects of specific neuropeptides (gastrin-releasing peptide (GRP), calcitonin (CT), serotonin (5-HT), and vasoactive intestinal peptide (VIP)) on various prostate cancer cell lines.
  • To determine the specificity and signaling pathways involved in neuropeptide-mediated growth.

Main Methods:

  • Established and characterized the androgen-independent FGC-DCC cell line from the androgen-dependent LNCaP cell line.
  • Utilized androgen-independent (DU-145, FGC-DCC, PC-3) and androgen-dependent (LNCaP, PC-346C) prostate cancer cell lines.
  • Assessed neuropeptide-induced growth modulation via (3)H-thymidine incorporation, tested specificity using anti-GRP antibody (2A11), and evaluated cAMP induction.

Main Results:

  • Neuropeptides stimulated androgen-independent growth in DU-145 and PC-346C cell lines.
  • Anti-GRP antibody 2A11 inhibited GRP-induced proliferation in DU-145, PC-346C, FGC-DCC, and PC-3 cells.
  • Cyclic adenosine monophosphate (cAMP) induction generally paralleled growth stimulation, with specific inhibitors showing differential effects.

Conclusions:

  • Gastrin-releasing peptide (GRP)-induced growth in DU-145 and PC-346C cells is specific and mediated by cAMP.
  • Androgen-independent growth of FGC-DCC cells involves Bcl-2 induction and potentially an autocrine, NE-like pathway.
  • Neuropeptides may promote the growth of non-NE prostate cancer cells, highlighting a potential role for NE cells in clinical prostate cancer progression.

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