CONTACT: JENNIFER CRONIN
2130 Medical Laboratories
Iowa City IA 52242
(319) 335-9917; fax (319) 335-8034
Release: Aug. 2, 1999
UI researchers identify prostate tumor suppressor
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
"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 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."