Tyrosine kinase signalling in breast cancer: epidermal growth factor receptor and c-Src interactions in breast cancer

Breast Cancer Res. 2000;2(3):203-10. doi: 10.1186/bcr55. Epub 2000 Mar 7.


Both the non-receptor tyrosine kinase, c-Src, and members of the epidermal growth factor (EGF) receptor family are overexpressed in high percentages of human breast cancers. Because these molecules are plasma membrane-associated and involved in mitogenesis, it has been speculated that they function in concert with one another to promote breast cancer development and progression. Evidence to date supports a model wherein c-Src potentiates the survival, proliferation and tumorigenesis of EGF receptor family members, in part by associating with them. Phosphorylation of the EGF receptor by c-SRC is also critical for mitogenic signaling initiated by the EGF receptor itself, as well as by several G-protein coupled receptors (GPCRs), a cytokine receptor, and the estrogen receptor. Thus, c-Src appears to have pleiotropic effects on cancer cells by modulating the action of multiple growth-promoting receptors.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Breast / metabolism
  • Breast Neoplasms / metabolism*
  • ErbB Receptors / genetics
  • ErbB Receptors / metabolism*
  • Female
  • Gene Expression Regulation, Neoplastic
  • Genes, erbB-2
  • Humans
  • Phosphorylation
  • Protein-Tyrosine Kinases / metabolism*
  • Receptors, Estrogen / genetics
  • Signal Transduction*
  • Trans-Activators / metabolism*
  • src-Family Kinases / metabolism*


  • Receptors, Estrogen
  • Trans-Activators
  • ErbB Receptors
  • Protein-Tyrosine Kinases
  • src-Family Kinases