Journal
ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
Volume 11, Issue 7, Pages 607-616Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/187152011796817646
Keywords
Androgen-independence; FAK; focal adhesion kinase; prostate cancer; tyrosine kinase; prostate cancer
Categories
Funding
- Department of Defense [W81XWH-08-1-0026, W81XWH-09-1-0465]
- National Institutes of Health [CA094108, CA116430]
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available