Expression of focal adhesion kinase in normal and pathologic human prostate tissues
Article first published online: 19 SEP 2002
Copyright © 2002 Wiley-Liss, Inc.
Volume 53, Issue 2, pages 124–132, 1 October 2002
How to Cite
Rovin, J. D., Frierson, H. F., Ledinh, W., Parsons, J. T. and Adams, R. B. (2002), Expression of focal adhesion kinase in normal and pathologic human prostate tissues. Prostate, 53: 124–132. doi: 10.1002/pros.10114
- Issue published online: 19 SEP 2002
- Article first published online: 19 SEP 2002
- Manuscript Accepted: 21 MAR 2002
- Manuscript Received: 25 OCT 2001
- The Warren and Clara Cole Scholarship of the American College of Surgeons
- The CaPCURE Foundation
- The National Cancer Institute. Grant Numbers: CA74298, CA76465
- adhesion, kinase
Focal adhesion kinase (FAK) regulates multiple cellular processes including growth, differentiation, adhesion, motility, and apoptosis. In tumor cells, including prostate adenocarcinoma, FAK overexpression has been linked to cancer progression.
By using immunohistochemistry, FAK expression was investigated in human prostate specimens.
FAK was expressed predominantly in the basal layer of normal prostate epithelium but not in secretory epithelium. FAK was expressed at similar levels in all stages of prostate tumorigenesis, including preinvasive carcinoma and metastatic disease. Elevated FAK expression was observed at the earliest stages of transformation and expression continued during cancer progression.
Given the established role for FAK in the regulation of integrin signaling, we suggest that the sustained elevated levels of FAK expression during prostate tumor cell progression is consistent with a role for FAK in the development and maintenance of prostate carcinoma. Prostate 53: 124–132, 2002. © 2002 Wiley-Liss, Inc.