Aug. 3, 1999 IOWA CITY, Iowa -- University of Iowa Health Care researchers may have found a way to prevent prostate cancer from spreading, according to research findings in the Aug. 1 issue of the journal Cancer Research.
The UI team, led by Mary J.C. Hendrix, Ph.D., professor and head of anatomy and cell biology; her graduate student, Jun Luo; and collaborator David M. Lubaroff, Ph.D., UI professor of urology, found that restoring a lost or decreased protein called E-cadherin hinders the ability of prostate cancer to spread.
"The results of this study provide a potential new therapeutic strategy for targeting invasive prostate cancer," said Hendrix, the associate director of basic research and deputy director for the UI Cancer Center.
"The correlation between the expression of the E-cadherin protein and the spreading of prostate cancer to distant sites may provide another weapon in the battle against this deadly disease," added Lubaroff, the associate director for research infrastructure for the UI Cancer Center.
Prostate cancer is the most commonly diagnosed cancer and is the second leading cause of cancer death in American men. Although most of the time the cancer is diagnosed and treated at early stages, some tumors do spread.
"The progression of the disease involves a number of steps, including discrete molecular changes," Hendrix explained. "It is crucial to identify the molecular changes and understand how they fit into the disease progression in order to develop better therapeutic approaches to manage prostate cancer."
Hendrix and her colleagues knew from previous studies that disruptions in the E-cadherin complex were commonly associated with many advanced forms of cancer. E-cadherin is an important intercellular adhesion molecule that helps to maintain the integrity of normal epithelial cells.
With data from laboratory experiments and clinical biopsies, UI researchers and other investigators elsewhere had suggested there was a correlation between the decreased E-cadherin and the ability of prostate cancer to spread. However, until this most recent UI study, there was no direct evidence to support the idea that genetic reintroduction of E-cadherin could suppress prostate cancer invasion.
Using prostate cancer cells from a rat model, the UI investigators restored missing or deficient E-cadherin in the cells. The results showed that the strategy drastically enhanced the ability of the prostate cancer cells to adhere to each other, thus restoring their epithelial integrity. The approach also suppressed the release of enzymes known to participate in cancer invasion through organs and tissues in the body.
The UI team is now involved in gene therapy studies to reintroduce E-cadherin into prostate cancer cells to inhibit the ability of these cells to invade and spread.
"The outcome of these studies could form the basis of the development of new clinical strategies for the treatment of prostate cancer," Hendrix said.
Richard D. Williams, M.D., UI professor and head of urology added: "This study is a prime example of the enormous potential that molecular biologic techniques have to change the behavior of cancer cells. When directly applied to patients, this discovery raises great hope of limiting the spread of prostate cancer within the body and thus improving survival."
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