The role of focal adhesion kinase in tumor initiation and progression
Year: 2009
Type: article
Abstract: Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase that acts as a primary regulator of focal adhesion signaling to regulate cell proliferation, survival and migration. While FAK is known to directly influence many fundamental adhesion and growth factor signaling pathways important in cancer and FAK is overexpressed in multiple human cancers studies addressing a causal role for FAK in tumor initiation and progression using transgenic models of human cancer had not been performed. Recently, using tissue-specific FAK-knockout in mouse models of human cancer, the consequences of FAK ablation in carcinoma were demonstrated by multiple independent research groups. Strong consensus evidence indicates that epithelial cells are able to transform in the absence of FAK, but do not undergo a malignant conversion to invasive carcinoma, and as such, metastasis is impaired. This is likely the consequence of decreased Src and p130Cas activation in concert with misregulated actin cytoskeleton dynamics and Rho GTPase signaling. Hence, FAK, as well as the FAK-regulating/regulated signaling network, are viable candidates for cancer metastasis therapies.
Source: Cell Adhesion & Migration
DOI: 10.4161/cam.3.4.9458
Authors: Paolo P. Provenzano, Patricia J. Keely
Language: English
Subfield: Immunology and Allergy
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,306
OpenAlex ID: W2048838314
