Molecular Mechanisms of Prostate Cancer Progression
Abstract
In studies to define the mechanisms involved in the progression of immortal, non-tumorigenic prostate cells to a tumorigenic state, we have found that molecular chaperones are elevated along with telomerase activity. Elevated chaperone function results in an increase in telomerase assembly. In order to determine the importance of the chaperone increaser we are investigating, both genetically and pharmacologically, whether ectopic chaperone expression results in transformation and if chaperones are targets for prostate cancer therapy. Individual chaperones have been over-expressed in non-tumorigenic prostate cells and are currently being tested for their ability to upregulate telomerase and other chaperone targets, as well as to influence tumorigenic growth (soft agar and nude mouse assays). In addition, treatment of malignant prostate cancer cell lines with radicicol, a specific hsp9O inhibitor, provides for a decline in telomerase activity and a decrease in overall telomerase length, suggesting that chaperone inhibition provides an indirect means to block telomerase activation and is a plausible therapeutic option for prostate cancer treatment.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jan 01, 2003
- Accession Number
- ADA415249
Entities
People
- Lynn W. Elmore
- Shawn E. Holt
Organizations
- Virginia Commonwealth University