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FAK in cancer: mechanistic findings and clinical applications
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FAK in cancer: mechanistic findings and clinical applications
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Journal Article
FAK in cancer: mechanistic findings and clinical applications
2014
Overview
Key Points
Focal adhesion kinase (FAK) is a non-receptor protein tyrosine kinase that drives tumour growth and metastasis through kinase-dependent and kinase-independent pathways.
FAK promotes metastasis by regulating processes involved in tumour cell motility and invasion, including control of focal adhesion and cytoskeletal dynamics, as well as the regulation of matrix metalloproteinase (MMP) surface expression.
Tumour growth is enhanced through pro-proliferative and anti-apoptotic functions of FAK.
FAK is connected to cancer stem cell and progenitor cell maintenance through kinase-dependent and kinase-independent functions. FAK signals contribute to the malignant outgrowth of these cells.
FAK favours tumour progression via the regulation of signalling pathways within cells of the tumour microenvironment, such as endothelial cells, haematopoietic cells, platelets, macrophages and fibroblasts.
FAK activity promotes endothelial cell migration, proliferation and survival, and it stimulates tumour angiogenesis. FAK-mediated regulation of endothelial cell permeability can influence tumour metastasis.
FAK expression and activity in tumour and endothelial cells is frequently upregulated and correlated with a poor patient prognosis.
Several molecules that target FAK kinase activity or its kinase-independent scaffolding function are under investigation in preclinical trials. Promising drug candidates in Phase I or II clinical trials are small molecule ATP-competitive inhibitors.
Focal adhesion kinase (FAK) can promote tumour growth and metastasis through various kinase-dependent and kinase-independent pathways. This Review discusses the roles of FAK in tumour cells and cells of the microenvironment, as well as the progress that is being made in the clinical development of FAK inhibitors.
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.
Publisher
Nature Publishing Group UK,Nature Publishing Group
