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Nat Rev Cancer. 2014 Sep;14(9):598-610. doi: 10.1038/nrc3792. Epub 2014 Aug 7.

FAK in cancer: mechanistic findings and clinical applications.

Author information

1
University of California San Diego, Moores Cancer Center, Department of Reproductive Medicine, 3855 Health Sciences Dr., MC0803, La Jolla, California 92093 USA.

Abstract

Focal adhesion kinase (FAK) is a cytoplasmic protein tyrosine kinase that is overexpressed and activated in several advanced-stage solid cancers. FAK promotes tumour progression and metastasis through effects on cancer cells, as well as stromal cells of the tumour microenvironment. The kinase-dependent and kinase-independent functions of FAK control cell movement, invasion, survival, gene expression and cancer stem cell self-renewal. Small molecule FAK inhibitors decrease tumour growth and metastasis in several preclinical models and have initial clinical activity in patients with limited adverse events. In this Review, we discuss FAK signalling effects on both tumour and stromal cell biology that provide rationale and support for future therapeutic opportunities.

PMID:
25098269
PMCID:
PMC4365862
DOI:
10.1038/nrc3792
[Indexed for MEDLINE]
Free PMC Article

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