FAK in cancer: mechanistic findings and clinical applications

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


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Focal Adhesion Kinase 1 / antagonists & inhibitors*
  • Focal Adhesion Kinase 1 / metabolism*
  • Humans
  • Molecular Targeted Therapy / methods
  • Neoplasm Invasiveness
  • Neoplasms / metabolism*
  • Neoplasms / pathology
  • Protein Kinase Inhibitors / pharmacology*
  • Signal Transduction
  • Small Molecule Libraries / pharmacology
  • Stromal Cells / enzymology*
  • Tumor Microenvironment


  • Protein Kinase Inhibitors
  • Small Molecule Libraries
  • Focal Adhesion Kinase 1
  • PTK2 protein, human