Mechanism of antitumor effect of a novel bFGF binding peptide on human colon cancer cells

Cancer Sci. 2010 May;101(5):1212-8. doi: 10.1111/j.1349-7006.2010.01501.x. Epub 2010 Jan 19.

Abstract

Colon cancer is a leading cause of morbidity and mortality in Western countries. Basic fibroblast growth factor (bFGF) was up-regulated in patients with colon cancer and was considered as a potential therapeutic target. In this study, we first demonstrated that a novel bFGF-binding peptide (named P7) inhibited proliferation of several colon cancer cell lines including HT-29, LoVo, and Caco2 cells stimulated by bFGF. Further investigations with HT-29 cells indicated that P7 arrested the cell cycle at the G0/G1 phase of bFGF-stimulated cells, reduced the levels of phospho-Erk1/Erk2 induced by bFGF, and caused significant changes in the expression of proteins related to proliferation, cell cycle, and cancer. Our results suggested that the bFGF-binding peptide has a potential antitumor effect on colon cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Carrier Proteins / pharmacology*
  • Cell Cycle / drug effects
  • Colonic Neoplasms / drug therapy*
  • Colonic Neoplasms / pathology
  • Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors
  • Fibroblast Growth Factor 2 / antagonists & inhibitors*
  • Fibroblast Growth Factor 2 / metabolism
  • HT29 Cells
  • Humans
  • Proteomics
  • Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

Substances

  • Antineoplastic Agents
  • Carrier Proteins
  • Fibroblast Growth Factor 2
  • Extracellular Signal-Regulated MAP Kinases