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Reduction of Ventral Prostate Weight by Finasteride Is Associated with Suppression of Insulin-like Growth Factor I (IGF-I) and IGF-I Receptor Genes and with an Increase in IGF Binding Protein 3¹

Lady Davis Research Institute of the Jewish General Hospital and Departments of Surgery and Medicine, McGill University, Montreal, Quebec, Canada H3T 1E2

Finasteride, a competitive and specific inhibitor of 5-reductase, is widely used in the treatment of symptomatic benign prostatic hyperplasia. We demonstrate here that finasteride, when administered in an in vivo experimental system, caused ventral prostate regression. Intraprostatic dihydrotestosterone levels decreased, whereas testosterone levels increased in a dose-dependent manner following finasteride treatment. Finasteride also inhibited the expression of insulin-like growth factor (IGF)-I and IGF-I receptor genes in the ventral prostate. Finasteride significantly increased IGF binding protein-3 and slightly decreased IGF binding protein-2, -4, and -5 gene expression. Because IGFs are potent mitogens for prostate epithelial cells, this newly described activity of finasteride may contribute to its antiproliferative properties, particularly with regard to the inhibition of prostate growth seen clinically and in animal models.

¹ This work was supported by Grant 778 from the Cancer Research Society and a grant from the Fonds de la Research en Sante du Quebec (to H. H.).

² To whom requests for reprints should be addressed, at Lady Davis Research Institute, McGill University, 3755 Cote Ste Catherine Road, Montreal, Quebec, H3T 1E2 Canada. Phone: (514) 340-8260, extension 5263; Fax: (514) 340-7502.

Received 10/24/97. Accepted 12/ 2/97.

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