FAK regulates biological processes important for the pathogenesis of cancer.
Since its initial discovery as a substrate and binding partner for the Src oncogene, a role for the focal adhesion kinase (FAK) in cancer has been speculated. In this review the clinical evidence correlating FAK overexpression with cancer and the experimental evidence demonstrating that FAK can control some phenotypes associated with cancer will be discussed. In addition, the emerging theme of interactions between the FAK and growth factor signaling pathways will be described. The evidence presented in this review provides a compelling case for a role for FAK in the pathology of human cancer.
Gabarra-Niecko
Veronica
V
Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Schaller
Michael D
MD
Dunty
Jill M
JM
D000818:Animals; D002448:Cell Adhesion; D045744:Cell Line, Tumor; D051417:Focal Adhesion Kinase 1; D051416:Focal Adhesion Protein-Tyrosine Kinases; D006801:Humans; D008954:Models, Biological; D009362:Neoplasm Metastasis; D009369:Neoplasms / Q000473:pathology*; D010641:Phenotype; D011505:Protein-Tyrosine Kinases / Q000378:metabolism / Q000502:physiology*; D015398:Signal Transduction; D019061:src-Family Kinases / Q000378:metabolism*
D011505:Protein-Tyrosine Kinases; D051417:Focal Adhesion Kinase 1; D051416:Focal Adhesion Protein-Tyrosine Kinases; C496050:PTK2 protein, human; D019061:src-Family Kinases