2014-09-01 | Florian J. Sulzmaier, Christine Jean and David D. Schlaepfer
The article "FAK in cancer: mechanistic findings and clinical applications" by Florian J. Sulzmaier, Christine Jean, and David D. Schlaepfer, published in *Nature Reviews Cancer*, discusses the role of focal adhesion kinase (FAK) in cancer progression and metastasis. FAK is a cytoplasmic protein tyrosine kinase that is overexpressed and activated in several advanced-stage solid cancers. The authors highlight how FAK promotes tumor progression and metastasis through both kinase-dependent and kinase-independent mechanisms, affecting cell movement, invasion, survival, gene expression, and cancer stem cell self-renewal. Small molecule FAK inhibitors have shown initial clinical activity in reducing tumor growth and metastasis, with limited adverse events. The review covers the regulatory mechanisms of FAK, its interactions with integrins and other signaling pathways, and its roles in the tumor microenvironment, including endothelial cells, neutrophils, macrophages, and fibroblasts. The authors also discuss the potential of FAK inhibitors as chemotherapeutics, emphasizing the need to consider the overlapping functions of FAK and PYK2, another related protein tyrosine kinase.The article "FAK in cancer: mechanistic findings and clinical applications" by Florian J. Sulzmaier, Christine Jean, and David D. Schlaepfer, published in *Nature Reviews Cancer*, discusses the role of focal adhesion kinase (FAK) in cancer progression and metastasis. FAK is a cytoplasmic protein tyrosine kinase that is overexpressed and activated in several advanced-stage solid cancers. The authors highlight how FAK promotes tumor progression and metastasis through both kinase-dependent and kinase-independent mechanisms, affecting cell movement, invasion, survival, gene expression, and cancer stem cell self-renewal. Small molecule FAK inhibitors have shown initial clinical activity in reducing tumor growth and metastasis, with limited adverse events. The review covers the regulatory mechanisms of FAK, its interactions with integrins and other signaling pathways, and its roles in the tumor microenvironment, including endothelial cells, neutrophils, macrophages, and fibroblasts. The authors also discuss the potential of FAK inhibitors as chemotherapeutics, emphasizing the need to consider the overlapping functions of FAK and PYK2, another related protein tyrosine kinase.