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Resveratrol, a natural product derived from grape, exhibits antiestrogenic activity and inhibits the growth of human breast cancer cells
Author(s) -
Lu Runqing,
Serrero Ginette
Publication year - 1999
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199906)179:3<297::aid-jcp7>3.0.co;2-p
Subject(s) - resveratrol , estrogen receptor , mcf 7 , cell growth , phytoalexin , endocrinology , cancer cell , growth factor , estrogen , medicine , chemistry , receptor , biology , pharmacology , cancer , biochemistry , human breast , breast cancer
Resveratrol is a natural phytoalexin compound found in grapes and other food products. In this study, the effect of resveratrol on the growth of human breast cancer cells was examined. Results show that resveratrol inhibits the growth of estrogen receptor(ER)‐positive MCF‐7 cells in a dose‐dependent fashion. Detailed studies with MCF‐7 cells demonstrate that resveratrol antagonized the growth‐promoting effect of 17‐β‐estradiol (E 2 ) in a dose‐dependent fashion at both the cellular (cell growth) and the molecular (gene activation) levels. At 5 × 10 −6 M, resveratrol abolished the growth‐stimulatory effect mediated by concentrations of E 2 up to 10 −9 M. The antiestrogenic effect of resveratrol could be observed at a concentration of 10 −6 M and above. The antiestrogenic effect of resveratrol was also demonstrated at the molecular level. Resveratrol in a dose‐dependent fashion antagonized the stimulation by E 2 of progesterone receptor gene expression in MCF‐7 cells. Moreover, expression of transforming growth factor‐α and insulin‐like growth factor I receptor mRNA was inhibited while the expression of transforming growth factor β2 mRNA was significantly elevated in MCF‐7 cells cultivated in the presence of resveratrol (10 −5 M). In summary, our results show that resveratrol, a partial ER agonist itself, acts as an ER antagonist in the presence of estrogen leading to inhibition of human breast cancer cells. J. Cell. Physiol. 179:297–304, 1999. © 1999 Wiley‐Liss, Inc.