Src signaling in cancer invasion

J Cell Physiol. 2010 Apr;223(1):14-26. doi: 10.1002/jcp.22011.

Abstract

Src is a non-receptor cytoplasmic tyrosine kinase which becomes activated following the stimulation of plasma membrane receptors including receptor tyrosine kinases and integrins, and is an indispensable player of multiple physiological homeostatic pathways. Once activated, Src is the starting point for several biochemical cascades that thereby propagate signals generated extracellularly along intracellular interconnected transduction pathways. Src transmits signals promoting cell survival and mitogenesis and, in addition, exerts a profound effect on the reorganization of the cytoskeleton and the adhesion systems that underpin cell migration and invasion. Because increased activity of Src is a frequent occurrence in many types of human cancer, and because there is evidence of a prominent role of Src in invasion and in other tumor progression-related events such as epithelial-mesenchymal transition (EMT) and development of metastasis, inhibitors targeting Src are being viewed as promising drugs for cancer therapy.

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Cell Adhesion
  • Cell Movement* / drug effects
  • Cell Transformation, Neoplastic / metabolism
  • Cell Transformation, Neoplastic / pathology
  • Cytoskeletal Proteins / metabolism
  • Enzyme Activation
  • Humans
  • Neoplasm Invasiveness
  • Neoplasms / drug therapy
  • Neoplasms / enzymology*
  • Neoplasms / pathology
  • Phosphorylation
  • Protein Conformation
  • Protein Kinase Inhibitors / pharmacology
  • Signal Transduction* / drug effects
  • Structure-Activity Relationship
  • Substrate Specificity
  • src-Family Kinases / antagonists & inhibitors
  • src-Family Kinases / chemistry
  • src-Family Kinases / metabolism*

Substances

  • Antineoplastic Agents
  • Cytoskeletal Proteins
  • Protein Kinase Inhibitors
  • src-Family Kinases