In vitro the behaviors of metastasis with suppression of VEGF in human bone metastatic LNCaP-derivative C4-2B prostate cancer cell line

J Exp Clin Cancer Res. 2012 May 1;31(1):40. doi: 10.1186/1756-9966-31-40.

Abstract

Background: Vascular endothelial growth factor (VEGF) is a signal protein produced by cells that stimulates vasculogenesis and angiogenesis. VEGF is believed to implicate poor prognosis in various cancers. The overexpression of VEGF may be an early step in the process of metastasis.

Methods: ELISA was used to investigate the levels of VEGF, bFGF and IL8 in human bone metastatic LNCaP-derivative C4-2B prostate cancer cell line and its parental cell line, LNCaP and to determine the effect of bevacizumab on reducing the level of VEGF. Cell proliferation assay, invasion assay and in vitro angiogenesis assay were performed under the condition with bevacizumab or control IgG.

Results: Human bone metastatic LNCaP-derivative C4-2B prostate cancer cell line expressed a higher level of VEGF than its parental primary prostate cancer cell line LNCaP. The effect of bevacizumab is dose-dependent and time-dependent: 100 μg/mL of bevacizumab and 3-day treatment was more effective than low-dose and lesser-day treatment for decreasing the level of VEGF. Bevacizumab is able to suppress cell proliferation, angiogenesis and invasion in human bone metastatic C4-2B prostatic cancer cell line.

Conclusions: The overexpression of VEGF can be inhibited by bevacizumab in human bone metastatic cancer cell line. The behaviors of metastasis involving proliferation, angiogenesis and invasion are suppressed by anti-VEGF therapy.

MeSH terms

  • Antibodies, Monoclonal, Humanized / administration & dosage*
  • Bevacizumab
  • Bone Neoplasms / secondary
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Fibroblast Growth Factors / metabolism
  • Gene Expression Regulation, Neoplastic / drug effects*
  • Humans
  • Interleukin-8 / metabolism
  • Male
  • Neoplasm Invasiveness / prevention & control
  • Neovascularization, Pathologic / drug therapy
  • Prostatic Neoplasms* / drug therapy
  • Prostatic Neoplasms* / pathology
  • Vascular Endothelial Growth Factor A* / genetics
  • Vascular Endothelial Growth Factor A* / immunology
  • Vascular Endothelial Growth Factor A* / metabolism

Substances

  • Antibodies, Monoclonal, Humanized
  • CXCL8 protein, human
  • Interleukin-8
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • Bevacizumab
  • Fibroblast Growth Factors