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Open AccessReview

Phytoestrogen Biological Actions on Mammalian Reproductive System and Cancer Growth

by 1 and Qing MU 2,*
1
Department of Biology, University of Ottawa, Gendron Hall, 30 Marie Curie, K1N 6N5, Ottawa, ON, Canada
2
School of Pharmacy, Fudan University, 826 Zhangheng Road, 201203, Pudong, Shanghai, China
*
Author to whom correspondence should be addressed.
Sci. Pharm. 2011, 79(1), 1-20; https://doi.org/10.3797/scipharm.1007-15
Received: 20 July 2010 / Accepted: 31 December 2010 / Published: 31 December 2010
Phytoestrogens are a family of diverse polyphenolic compounds derived from nature plant that structurally or functionally mimic circulating estrogen in the mammalian reproductive system. They induce estrogenic and anti-estrogenic effects in the brain-pituitary-gonad axis (a principal endocrine system involving in reproductive regulation) and peripheral reproductive organs. The dichotomy of phytoestrogen-mediated actions elucidates that they play the biological activities via complex mechanisms and belong to various chemical classes. In comparison with their unobvious physiological functions in normal reproductive tissues, there are increasing investigations showing that phytoestrogen induces significant inhibitory effects on the growth of breast and ovarian cancers through different signaling pathways. This review summarized the results of the previous studies regarding principal signaling transductions for mediating the growth of the ovarian and breast cancers. Phytoestrogen potentially modulates the signaling molecules via: (1) blocking the nuclear and membrane estrogen receptors (ER), (2) interfering with the growth factor receptor, (3) inhibiting the G protein-coupled receptor in ER-deficient cells, (4) activating apoptosis and nullifying anti-apoptotic signals.
Keywords: Phytoestrogen; Estrogen Receptor; Breast Cancer; Ovarian Cancer Phytoestrogen; Estrogen Receptor; Breast Cancer; Ovarian Cancer
MDPI and ACS Style

ZHAO, E.; MU, Q. Phytoestrogen Biological Actions on Mammalian Reproductive System and Cancer Growth. Sci. Pharm. 2011, 79, 1-20.

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