Src and FAK signalling controls adhesion fate and the epithelial-to-mesenchymal transition

Src kinase controls cellular adhesions, including cadherin-based intercellular adhesions and integrin-mediated cell–matrix adhesions. In epithelial cells, Src activation, or increased signalling from migratory growth factor receptors via Src, induces an adhesion switch that enhances dynamic cell–mat...

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Bibliographic Details
Published in:Current opinion in cell biology 2005-10, Vol.17 (5), p.542-547
Main Authors: Avizienyte, Egle, Frame, Margaret C
Format: Article
Language:English
Subjects:
Animals
Cadherins - physiology
Cell Adhesion - physiology
Cell Differentiation
Endocytosis - physiology
Epithelial Cells - cytology
Epithelial Cells - metabolism
Epithelial Cells - physiology
Humans
Integrins - physiology
Mesoderm - cytology
Mesoderm - metabolism
Mesoderm - physiology
Models, Biological
Neoplasms - metabolism
Signal Transduction - physiology
src-Family Kinases - metabolism
src-Family Kinases - physiology
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Summary:Src kinase controls cellular adhesions, including cadherin-based intercellular adhesions and integrin-mediated cell–matrix adhesions. In epithelial cells, Src activation, or increased signalling from migratory growth factor receptors via Src, induces an adhesion switch that enhances dynamic cell–matrix adhesions and migratory capacity while suppressing intercellular contact. Moreover, Src and the associated tyrosine kinase FAK are at the heart of the recently identified crosstalk between integrin- and cadherin-mediated adhesions of epithelial cells, particularly during the epithelial-to-mesenchymal transition.
ISSN:0955-0674
1879-0410
DOI:10.1016/j.ceb.2005.08.007