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¹ Bioactive Materials Key Lab of Ministry of Education, Institute for Molecular, Biology, Nankai University, Tianjin 300071, China
² Department of Medical Oncology, Harvard Medical School, Dana Farber Cancer Institute, Boston, 02115 Massachusetts, USA
³ Department of Urology, Innsbruck Medical University, Anichstrasse 35, A-6020 Innsbruck, Austria
⁴ Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611-3010, USA

(Correspondence should be addressed to J Zhang; Email: zhangju{at}nankai.edu.cn)

Estradiol (E2) level in stroma of benign prostatic hyperplasia (BPH) increases with age, and this increase was associated with an elevated expression of aromatase in prostatic stromal cells (PrSCs). Here, we showed that conditioned medium (CM) of BPH-1 (a benign hyperplastic prostatic epithelial cell line), but not of prostate cancer cell lines (LNCaP, DU-145, and PC-3), stimulates aromatase expression in PrSCs. Cyclooxygenase-2 (COX-2) mRNA level in BPH-1, as well as prostaglandin E2 (PGE2) concentration in BPH-1 CM, was significantly higher than that of prostate cancer cell lines. CM of BPH-1 treated with NS-398 (a specific inhibitor of COX-2) failed to stimulate aromatase expression in PrSCs. And PGE2 can stimulate aromatase expression in PrSCs. Our data suggested that BPH-1 induced aromatase expression in PrSCs through the production of PGE2 in a paracrine mechanism.