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Adv Cancer Res. 2008;101:45-61. doi: 10.1016/S0065-230X(08)00403-X.

FAK expression regulation and therapeutic potential.

Author information

  • 1State Key Laboratory of Pharmaceutical Biotechnology, College of life Science, Nanjing University, Nanjing, PR China.

Abstract

Focal adhesion kinase (FAK) is a non-receptor protein tyrosine kinase that localizes to cellular focal adhesions or cell contacts within the extracellular matrix. FAK is activated by a variety of cell surface receptors and transmits signals to a range of targets. FAK participates in growth factor receptor-mediated signaling pathways and plays essential roles in cell survival, proliferation, migration, and invasion. In the present chapter, the mechanisms of FAK activation, the modulation of FAK function by phosphorylation, and the mechanisms regulating FAK expression are reviewed. Overexpression of FAK is widely observed in numerous tumor types, and is used as a marker for invasion and metastasis. FAK could be therapeutically targeted at various levels, such as at the level of FAK gene transcription by regulating its transcription factor(s) with siRNA, at the FAK mRNA level with FAK siRNA, or at the protein level. At the protein level, FAK's localization to focal adhesions could be disrupted by expression of dominant-negative FAK-Related Non-Kinase or its focal adhesion targeting domain, and its kinase activity could be inhibited by FIP200, the FAK kinase domain-interacting protein and kinase-activity inhibitor. In recent years, small molecule inhibitors against FAK transcription and activation have been discovered, and these will provide additional approaches for potential tumor therapies.

PMID:
19055942
[PubMed - indexed for MEDLINE]
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