Commentary: targeting colorectal cancer through molecular biology

Semin Oncol. 2005 Dec;32(6 Suppl 9):S37-9. doi: 10.1053/j.seminoncol.2005.06.012.


Multiple growth factor receptor pathways are deregulated in colon cancer, presenting potential targets for therapeutic intervention. In colon cancer cells, epithelial growth factor receptor activation is associated with the potential for deregulation of both angiogenesis and motility-related characteristics as cell cytoskeleton and cell-cell junction structure. Growth factor activation of receptors can result in increased cyclooxygenase-2 (COX-2) expression and consequent upregulation of prostaglandin E2; this, in turn, results in localization of urokinase proteolytic activity that promotes directional motility and invasiveness of cancer cells. Optimal therapeutic strategies to inhibit cancer cell motility, invasiveness, and angiogenesis may involve combinations of growth factor receptor inhibitors, COX-2 inhibitors, and urokinase inhibitors.

Publication types

  • Review

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • Blood Proteins / therapeutic use
  • Colorectal Neoplasms / drug therapy*
  • Colorectal Neoplasms / physiopathology
  • Cyclooxygenase 2 Inhibitors / therapeutic use
  • ErbB Receptors / antagonists & inhibitors
  • ErbB Receptors / drug effects
  • Growth Substances / physiology
  • Humans
  • Models, Biological*
  • Neoplasm Invasiveness / physiopathology
  • Neovascularization, Pathologic / drug therapy
  • Signal Transduction / drug effects
  • Signal Transduction / physiology*


  • Antineoplastic Agents
  • Blood Proteins
  • Cyclooxygenase 2 Inhibitors
  • Growth Substances
  • urokinase inhibitor
  • ErbB Receptors