The effect of bone-associated growth factors and cytokines on the growth of prostate cancer cells derived from soft tissue versus bone metastases in vitro

Int J Oncol. 2003 Apr;22(4):921-6.

Abstract

Prostate cancer metastasis to bone may be mediated by preferential proliferation of these cells in the bone's microenvironment. We hypothesize that this preferential proliferation is mediated by bone-associated growth factors (GFs) and cytokines. To test our hypothesis, human prostate cancer cells, derived from both soft tissue (LNCaP, DuCaP, DU145) and bone metastases (PC-3, VCaP, MDA-2a, MDA-2b), were treated with bone-associated GFs and cytokines (PDGF, IGF-1, TGF-beta, EGF, bFGF, TNF-alpha, IL-1, and IL-6) for 48 h, and their growth responses were compared. The responses of soft tissue-derived prostate cancer cell lines to bone GFs and cytokines were variable. LNCaP cell growth was stimulated by IGF-1 but was inhibited by TNF-alpha. DU145 cell growth was stimulated with EGF. Prostate cancer cell lines derived from bone metastases also responded variably to bone GFs and cytokines. IL-1 stimulated the growth of MDA-2a and 2b cell lines in a dose-dependent manner. PDGF and bFGF both demonstrated variable effects on bone-derived prostate cancer cell lines. TNF-alpha inhibited proliferation of the VCaP cells. These findings demonstrate that human prostate cancer cell lines derived from bone metastases may not respond preferentially to bone-associated GFs and cytokines.

MeSH terms

  • Bone Neoplasms / metabolism*
  • Bone Neoplasms / secondary
  • Cell Division
  • Cell Line, Tumor
  • Cytokines / metabolism*
  • Dose-Response Relationship, Drug
  • Growth Substances / metabolism*
  • Humans
  • Insulin-Like Growth Factor I / metabolism
  • Interleukin-1 / metabolism
  • Male
  • Neoplasm Metastasis
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / pathology*
  • Soft Tissue Neoplasms / metabolism*
  • Soft Tissue Neoplasms / secondary
  • Time Factors
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Cytokines
  • Growth Substances
  • Interleukin-1
  • Tumor Necrosis Factor-alpha
  • Insulin-Like Growth Factor I