Understanding the Roles of FAK in Cancer Inhibitors, Genetic Models, and New Insights

• Published in: The journal of histochemistry and cytochemistry Vol. 63; no. 2; pp. 114 - 128
• Main Authors: Yoon, Hyunho, Dehart, Joshua P., Murphy, James M., Lim, Ssang-Taek Steve
• Format: Journal Article
• Language: English
• Published: Los Angeles, CA SAGE Publications 01.02.2015
• Subjects: Animals; Cell Nucleus - enzymology; Disease Models, Animal; Epigenesis, Genetic; Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors; Focal Adhesion Protein-Tyrosine Kinases - chemistry; Focal Adhesion Protein-Tyrosine Kinases - genetics; Focal Adhesion Protein-Tyrosine Kinases - metabolism; Humans; Neoplasms - enzymology; Neoplasms - genetics; Neoplasms - pathology; Protein Kinase Inhibitors - pharmacology; FAK; cancer; genetic mouse model; metastasis; FAK inhibitors
• ISSN: 0022-1554; 1551-5044; 1551-5044
• DOI: 10.1369/0022155414561498

Focal adhesion kinase (FAK) is a protein tyrosine kinase that regulates cellular adhesion, motility, proliferation and survival in various types of cells. Interestingly, FAK is activated and/or overexpressed in advanced cancers, and promotes cancer progression and metastasis. For this reason, FAK became a potential therapeutic target in cancer, and small molecule FAK inhibitors have been developed and are being tested in clinical phase trials. These inhibitors have demonstrated to be effective by inducing tumor cell apoptosis in addition to reducing metastasis and angiogenesis. Furthermore, several genetic FAK mouse models have made advancements in understanding the specific role of FAK both in tumors and in the tumor environment. In this review, we discuss FAK inhibitors as well as genetic mouse models to provide mechanistic insights into FAK signaling and its potential in cancer therapy.