Control of adhesion-dependent cell survival by focal adhesion kinase.

DOI PDF 被引用文献15件
  • S M Frisch
    Burnham Institute, La Jolla Cancer Research Center, California 92037, USA. sfrisch@ljcrf.edu
  • K Vuori
    Burnham Institute, La Jolla Cancer Research Center, California 92037, USA. sfrisch@ljcrf.edu
  • E Ruoslahti
    Burnham Institute, La Jolla Cancer Research Center, California 92037, USA. sfrisch@ljcrf.edu
  • P Y Chan-Hui
    Burnham Institute, La Jolla Cancer Research Center, California 92037, USA. sfrisch@ljcrf.edu

抄録

<jats:p>The interactions of integrins with extracellular matrix proteins can activate focal adhesion kinase (FAK) and suppress apoptosis in normal epithelial and endothelial cells; this subset of apoptosis has been termed "anoikis." Here, we demonstrate that FAK plays a role in the suppression of anoikis. Constitutively activated forms of FAK rescued two established epithelial cell lines from anoikis. Both the major autophosphorylation site (Y397) and a site critical to the kinase activity (K454) of FAK were required for this effect. Activated FAK also transformed MDCK cells, by the criteria of anchorage-independent growth and tumor formation in nude mice. We provide evidence that this transformation resulted primarily from the cells' resistance to anoikis rather than from the activation of growth factor response pathways. These results indicate that FAK can regulate anoikis and that the conferral of anoikis resistance may suffice to transform certain epithelial cells.</jats:p>

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