The Tumor Biology of Focal Adhesion Kinase

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Cellscience Reviews Vol.3 No.1
ISSN 1742-8130

The Tumor Biology of Focal Adhesion Kinase

Elena Kurenova ^1*, Vita Golubovskaya ^1*, & William Cance ^1,2

¹ Department of Surgery, ² Department Biochemistry and Molecular Biology, University of Florida, Gainesville, FL.
^* These authors contributed equally to the work.

Focal adhesion kinase (FAK) is an intracellular protein-tyrosine kinase that is localized to contact points between cells and their extracellular matrix and plays a key role in protecting cells from apoptosis. It is implicated in cell migration, adhesion and cell cycle control. Overexpression of FAK is a common event in numerous tumors, and we have demonstrated that FAK upregulation occurred in early stages of tumorigenesis. We have also shown that FAK overexpression suppressed apoptosis, thus providing a survival signal to human cancer cells, and attenuation of FAK caused detachment and apoptosis in breast cancer cells. Furthermore, our data has recently shown that FAK can directly interact with the serine-threonine kinase, Receptor Interacting Protein (RIP), the tyrosine kinase Vascular Endothelial Growth Factor Recptor 3 (VEGFR3) and the transcription factor/tumor suppressor p53. We hypothesize that interactions between FAK and these types of signaling molecule are critical components for suppressing apoptosis in tumor cells and the disruption of these interactions will lead to tumor cell death. Understanding FAK biology during tumorigenesis and its physical interactions with other protein partners and their downstream signaling pathways will be essential in developing novel cancer therapeutics.

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