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Volume 12, Issue 5 (September 2010) 12, 735–743; 10.1038/aja.2010.24

Antagonism of estrogen-mediated cell proliferation by raloxifene in prevention of ageing-related prostatic hyperplasia

Rui Yang1, Yu-Xia Ma1, Lin-Feng Chen2, Ying Zhou1, Zhan-Po Yang3, Yan Zhu4, Xiao-Ling Du1, Jian-Dang Shi1, Hong-Shun Ma3 and Ju Zhang1

1 Bioactive Materials Key Lab of Ministry of Education, Department of Biochemistry and Molecular Biology, College of
Life Sciences, Nankai University, Tianjin 300071, China
2 Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02445, USA
3 Department of Urology, Tianjin First Central Hospital, Tianjin 300192, China
4 Molecular Cardiology Research Institute, Tufts Medical Center, Tufts University School of Medicine, Boston, MA 02111, USA

Correspondence: Prof. Ju Zhang,zhangju@nankai.edu.cn and Prof. Jian-Dang Shi,shijd@nankai.edu.cn

Received 2 February 2010; Revised 15 March 2010; Accepted 29 March 2010; Published online 17 May 2010.


Estrogen has important roles in the initiation and development of benign prostatic hyperplasia (BPH). Regulators of the estrogen receptor (ER) are tissue- and cell-specific. We evaluated the effect of estrogen antagonist, raloxifene (Ral), on the prevention and treatment of BPH by investigating its effect on the proliferation of two different prostate cell lines: a stromal cell line, WPMY-1, and a benign prostatic hyperplasia epithelial cell line, BPH-1. We additionally evaluated its effect on prostatic hyperplasia induced by estrogen and androgen in a rat model. The effect of Ral on the prevention of prostatic hyperplasia was analyzed by haematoxylin and eosin staining and quantitative immunohistochemistry (IHC) for proliferating cell nuclear antigen and α-smooth muscle actin. In vitro and in vivo, tamoxifen (Tam), another anti-estrogen drug, and finasteride (Fin), a drug for the clinical treatment of BPH, served as efficacy controls. The in vitro data showed that neither Ral nor Tam alone affected the proliferation of WPMY-1 and BPH-1, but both antagonized the effect of oestradiol in promoting the proliferation of the two cells. Results from the IHC staining of the rat prostates indicated that, similar to Tam and Fin, Ral inhibited the proliferation of stromal cells in vivo. Interestingly, in contrast to Tam, both Ral and Fin inhibited the proliferation of epithelial cells. Furthemore, Ral treatment much strongly decreased the number of prostatic acini and the surrounding layers of smooth muscle cells than Fin (P < 0.05). Our data showed for the first time that Ral may have a role in the response of the rat prostate to selective ER modulators.


estrogen; prostatic hyperplasia; raloxifene; rats

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