Relaxin/RXFP1 signaling in prostate cancer progression

Ann N Y Acad Sci. 2009 Apr;1160:379-80. doi: 10.1111/j.1749-6632.2008.03793.x.

Abstract

We found that relaxin peptide expression is significantly elevated in recurrent human prostate cancer. Stimulation with relaxin increased migration, invasiveness, proliferation, and adhesion of LNCaP and PC3 cells in vitro. Opposite effects on cellular phenotype were observed after suppression of endogenous relaxin/RXFP1 expression or signaling. We showed an accelerated progression of prostate cancer in TRAMP males with transgenic relaxin overexpression and a longer survival of TRAMP, RXFP1-deficient males. Suppression of RXFP1 expression in PC3 xenografts in nude mice by intratumoral injections of short interfering RNA resulted in decreased tumor size, cell proliferation, and metastasis rate.

MeSH terms

  • Animals
  • Cell Adhesion / drug effects
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Proliferation / drug effects
  • Disease Progression*
  • Humans
  • Male
  • Mice
  • Mice, Nude
  • Mice, Transgenic
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / pathology
  • RNA Interference
  • Receptors, G-Protein-Coupled / genetics
  • Receptors, G-Protein-Coupled / physiology*
  • Receptors, Peptide / genetics
  • Receptors, Peptide / physiology*
  • Relaxin / genetics
  • Relaxin / pharmacology
  • Relaxin / physiology*
  • Signal Transduction*

Substances

  • RXFP1 protein, human
  • Receptors, G-Protein-Coupled
  • Receptors, Peptide
  • Relaxin