Control of Adhesion-Dependent Cell Survival by Focal Adhesion Kinase

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...

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Bibliographic Details
Published in:The Journal of cell biology 1996-08, Vol.134 (3), p.793-799
Main Authors: Frisch, Steven M., Vuori, Kristiina, Ruoslahti, Erkki, Chan-Hui, Po-Ying
Format: Article
Language:English
Subjects:
Animals
Antibodies
Apoptosis
Apoptosis - physiology
Biochemistry
Calcium-Calmodulin-Dependent Protein Kinases - metabolism
CD2 Antigens - genetics
Cell adhesion
Cell Adhesion - physiology
Cell Adhesion Molecules - analysis
Cell Adhesion Molecules - genetics
Cell Adhesion Molecules - physiology
Cell Line
Cell lines
Cell Survival
Cell Transformation, Neoplastic
Cells
Cellular biology
COS cells
Cytoskeletal Proteins - metabolism
Dogs
Enzyme Activation
Epithelial Cells
Fibroblasts
Focal Adhesion Kinase 1
Focal Adhesion Protein-Tyrosine Kinases
Focal adhesions
Kidney
Mice
Mice, Nude
Paxillin
Phosphoproteins - metabolism
Phosphorylation
Protein-Tyrosine Kinases - analysis
Protein-Tyrosine Kinases - genetics
Protein-Tyrosine Kinases - physiology
Proto-Oncogene Proteins - biosynthesis
Proto-Oncogene Proteins c-bcl-2
Rats
Recombinant Fusion Proteins - analysis
Recombinant Fusion Proteins - metabolism
T lymphocytes
Tumor cell line
Tyrosine - metabolism
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Description
Summary: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.
ISSN:0021-9525
1540-8140
DOI:10.1083/jcb.134.3.793