Signal Transduction Pathway in Maspin-Induced Tumor Suppression of Prostate Cancer
Abstract
The purpose of this project was to identify a maspin receptor, and to investigate the signal transduction in maspin-induced cancer suppression. Human prostasin was examined as a candidate for maspin receptor. Our major progress is in the following areas. First, prostasin expression is found down-regulated in prostate cancer. Second, PC-3 cells transfected with a human prostasin cDNA displayed a significantly reduced level of invasiveness (50-80% inhibition). Third, the prostasin-transfected PC-3 cells have an increased maspin expression, suggesting a concerted tumor suppression mechanism between these two proteins. Fourth, prostasin expression in LNCaP cells can be up-regulated by dihydrotestosterone, suggesting a possibility that prostasin's down-regulation in prostate cancer is not due to gene damage. Fifth, a human maspin-expressing fruit-fly strain has been established, as well as a strain that expresses human hepsin, a second candidate for maspin receptor. Overall, we have tested the initial hypothesis at or exceeding the pace intended. Several unexpected findings were made regarding the behaviors of human prostasin, and the stage is set for the follow-through investigation on how maspin and prostasin work synergistically to suppress prostate cancer. A prostate cancer therapy and methods of diagnosis are being developed as part of the extended goal of our research.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 1999
- Accession Number
- ADB262052
Entities
People
- Karl X. Chai
Organizations
- University of Central Florida