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Androgen Regulation of JM-27 Is Associated With the Diseased Prostate

RAJIV DHIR^,

SUN LU

GREGORIO PIROZZI

KULKARNI PRAKASH

ROBERT H. GETZENBERG^*,,

From the Departments of ^* Urology and Pathology, and University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, Pennsylvania; and Gene Logic Inc, Gaithersburg, Maryland.

Correspondence to: Dr Robert H. Getzenberg, Department of Urology Research Laboratories, University of Pittsburgh, Shadyside Medical Center G-40, 5200 Centre Avenue, Pittsburgh, PA 15232.

Despite intense research efforts, the etiology of prostatic hyperplasia associated with both benign prostatic hyperplasia (BPH) and prostate cancer remains poorly understood. Our previous studies using array technology identified JM-27 as a transcript that is dramatically up-regulated in the prostates of patients with symptomatic BPH and in normal, adjacent prostatic regions of patients with prostate cancer. In the present study, using an extended sample set, we show a correlation between the messenger RNA and protein expression of JM-27. To investigate the possible functions of this gene, its expression in the rat prostate was examined by immunoblot analysis using a polyclonal antibody specific to human JM-27. This antibody reacts with 2 rat polypeptides of 17 kd and 27 kd in size. Whereas the 27-kd form of the JM-27 protein found in human prostate is selectively expressed in the dorsolateral lobes of the rat prostate, the 17-kd form is expressed only in the ventral lobe. Expression of both forms of this protein appears to be androgen-regulated. There is a time-dependent decrease in expression of the protein products in the ventral and dorsolateral lobes of the rat prostate after castration. Administration of exogenous testosterone in castrated animals maintains protein expression in both lobes. Androgens are believed to play a central role in prostate growth and development, and therefore, it is tempting to speculate that JM-27, an androgen-regulated gene, may be involved in prostatic growth regulation. Further studies are underway to evaluate such a function for JM-27 in prostatic diseases.

     Key words: Benign prostatic hyperplasia, prostate cancer, genes, gene expression