Tyrosine kinase signalling in breast cancer: epidermal growth factor receptor and c-Src interactions in breast cancer.
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.
Department of Microbiology and Cancer Center, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908, USA.
J S
JS
Biscardi
R C
RC
Ishizawar
C M
CM
Silva
S J
SJ
Parsons
D001940:Breast / Q000378:metabolism; D001943:Breast Neoplasms / Q000378:metabolism*; D066246:ErbB Receptors / Q000235:genetics / Q000378:metabolism*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D018734:Genes, erbB-2; D006801:Humans; D010766:Phosphorylation; D011505:Protein-Tyrosine Kinases / Q000378:metabolism*; D011960:Receptors, Estrogen / Q000235:genetics; D015398:Signal Transduction; D015534:Trans-Activators / Q000378:metabolism*; D019061:src-Family Kinases / Q000378:metabolism*
D011960:Receptors, Estrogen; D015534:Trans-Activators; D066246:ErbB Receptors; D011505:Protein-Tyrosine Kinases; D019061:src-Family Kinases