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Updated: Jun 22, 2026
An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
Published on: August 13, 2019
Effect of selective estrogen receptor modulators on cell proliferation and estrogen receptor activities in normal
H Nomura1, H Kawashima, S Masaki
1Department of Urology, Osaka City University Graduate School of Medicine, Asahimachi, Abenoku, Osaka, Japan.
Abstract:
We examined the effect of E(2) and selective estrogen receptor modulators (SERMs) on the proliferation and estrogen receptor (ER) activities in normal human prostate cells. SERMs such as toremifene, raloxifene and tamoxifen suppressed the proliferation of prostate epithelial and stromal cells whereas anti-androgens did not. In prostate stromal cells, the transactivation activities of ER were enhanced by adding E(2) and reduced remarkably by toremifene. The results indicate that the ER-mediated pathway plays a central role in the growth of normal prostate cells.
Insights
Selective estrogen receptor modulators (SERMs) inhibit normal human prostate cell growth. Estrogen receptor (ER) activity is central to prostate cell proliferation, with SERMs like toremifene showing significant suppressive effects.
Area of Science:
- Endocrinology
- Cell Biology
- Prostate Cancer Research
Background:
- Estrogen receptor (ER) signaling is implicated in prostate cell function.
- The role of ER and selective estrogen receptor modulators (SERMs) in normal prostate cells requires further elucidation.
Purpose of the Study:
- To investigate the impact of estradiol (E(2)) and SERMs on normal human prostate cell proliferation.
- To assess the effect of E(2) and SERMs on estrogen receptor (ER) activity in prostate cells.
Main Methods:
- Treatment of normal human prostate epithelial and stromal cells with E(2) and various SERMs (toremifene, raloxifene, tamoxifen).
- Assessment of cell proliferation rates.
- Measurement of ER transactivation activities in prostate stromal cells.
Main Results:
- SERMs, including toremifene, raloxifene, and tamoxifen, significantly suppressed prostate epithelial and stromal cell proliferation.
- Anti-androgens did not affect prostate cell proliferation.
- Estradiol (E(2)) enhanced ER transactivation in prostate stromal cells, while toremifene markedly reduced it.
Conclusions:
- The estrogen receptor (ER)-mediated pathway is a critical regulator of normal prostate cell growth.
- SERMs demonstrate potential as agents to control prostate cell proliferation through ER modulation.
