Lost proteins could lead to new treatments for prostate cancer
Contact: Elizabeth Crown ecrownnorthwestern.edu 3125038928 Northwestern University Northwestern University researchers have discovered that a protein normally produced by the body to regulate the normal growth of the prostate is necessary because mice that lack this protein develop an enlarged prostate. The excessive growth of the prostate in these animals resembles human disease, benign prostatic hyperplasia. In an article in the June issue of Nature Medicine, lead authors Jennifer Doll Wheeler and Veronica, with their colleagues from the Feinberg School of Medicine at Northwestern University in Chicago and Umea published University in Sweden, presented their studies a protein called epitheliumderived pigment factor (PEDF).The observation of too many cells in the prostate
of mice PEDFnull has led researchers to examine PEDF in human prostate and prostate cancer, as well as in cultured cells of these tissues. PEDF was easily detected in healthy prostate tissue and normal prostate cells, but little or no PEDF was detected in most samples of prostate tissue being examined or isolated in prostate cancer cells cultured in the laboratory. Androgens, the male sex hormones that regulate growth of the prostate, has been shown to inhibit the production of PEDF.Because androgen ablation (removal) therapy is an important part of treatment for prostate cancer, the researchers measured the production of PEDF is androgen ablation in prostate cancer cells.They found that PEDF production seems to turn into cells of these tumors. An important role recently
defined for PEDF was its potent activity as an inhibitor of angiogenesis, the growth of new blood vessels, which is required for tumor growth. To determine if PEDF may affect cells in a tumor, in addition to the cells lining the blood vessels, the researchers examined the effects of purified PEDF on cultured prostate cancer cells. They found that PEDF caused an increase in the rate of death from prostate cancer cells Pages: [1] 2