| Literature DB >> 18172287 |
Abstract
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 beta(1)-integrin heterodimers and may modulate integrin binding affinity. This pathway may be a promising target for manipulation to inhibit metastatic cancer cell adhesion.Entities:
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Year: 2008 PMID: 18172287 DOI: 10.1158/0008-5472.CAN-07-2992
Source DB: PubMed Journal: Cancer Res ISSN: 0008-5472 Impact factor: 12.701