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An Intracellular Signal Pathway That Regulates Cancer Cell Adhesion in Response to Extracellular Forces

Surgical Service, John D. Dingell VA Medical Center and Departments of Surgery, Anesthesiology, Anatomy, and Cell Biology, Wayne State University Detroit, Michigan

Requests for reprints: Marc D. Basson, Surgical Service, John D. Dingell VA Medical Center, 4646 John R. Street, Detroit, MI 48201-1932. Phone: 313-576-3598; Fax: 313-576-1002; E-mail: marc.basson{at}va.gov.

Increasing evidence suggests that tumor cells can regulate their own adhesion via intracellular signals that modulate integrin binding affinity. Although the full pathway has not yet been elucidated, the effects of pressure seem likely to require cytoskeletal mechanosensing, Src, phosphatidylinositol 3-kinase, focal adhesion kinase, and Akt-1 activation. Ultimately, activated focal adhesion kinase accumulates at the membrane in association with β₁-integrin heterodimers and may modulate integrin binding affinity. This pathway may be a promising target for manipulation to inhibit metastatic cancer cell adhesion. [Cancer Res 2008;68(1):2–4]

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				E. Ciccimaro, S. K. Hanks, and I. A. Blair Quantification of Focal Adhesion Kinase Activation Loop Phosphorylation as a Biomarker of Src Activity Mol. Pharmacol., March 1, 2009; 75(3): 658 - 666. [Abstract] [Full Text] [PDF]