Focal Adhesion Kinase Controls Prostate Cancer Progression Via Intrinsic Kinase and Scaffolding Functions

Sheila      Figel; Irwin      H. Gelman

doi:10.2174/187152011796817646

Abstract

Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase which mediates integrin signaling from the sites of connection to the extracellular membrane known as focal adhesions. FAK mediates essential cellular processes including growth, proliferation, adhesion, migration, and survival through its functions as a molecular scaffold and as a kinase. FAK is frequently overexpressed and overactive in prostate cancer, which represents the second leading cause of cancer deaths in American men. Through the activation of major oncogenic pathways, FAK promotes the growth, survival, migration, metastasis, and androgen-independence of prostate tumors in vitro and in vivo. A full examination of FAK kinase function has never been completed despite many studies suggesting its importance and the development of kinase-specific therapeutic inhibitors. An expanded understanding of FAK kinase function is required to understand the role of FAK in prostate cancer progression, thereby aiding future development of novel inhibitory drugs and screening procedures.

Keywords: Androgen-independence, FAK, focal adhesion kinase, prostate cancer, tyrosine kinase, Focal Adhesion Targeting (FAT), fibronectin, phosphorylation, adherent cells