The combination effects of phytoestrogens on cell proliferation, cell cycle progression and estrogen receptor alpha
Journal
Journal of Food and Drug Analysis
Journal Volume
13
Journal Issue
1
Pages
30-37
Date Issued
2005
Author(s)
Abstract
Phytoestrogens are plant chemicals that have been related to the occurrence of human breast cancers and other estrogen-dependent cancers. This study was designed to examine the potential combinational effects and estrogenic activity of phytoestrogens in MCF-7 human breast cancer cells. Results showed that the phytoestrogens biochanin A and daidzein inhibited the proliferation of MCF-7 cells in a dose-dependent manner. Both biochanin A and daidzein delayed the progression of the cell cycle from the G2/M phase to the G1 phase at growth inhibitory concentrations. Treatment with biochanin A down-regulated the level of estrogen receptor-alpha (ER-α) mRNA, but this down-regulation was not affected by the presence of the antiestrogen ICI182,780. When cells were treated with biochanin A at a growth inhibitory concentration of 40 μg/mL, co-administration of daidzein resulted in an enhanced inhibitory effect on the MCF-7 cell growth. In addition, neither the growth inhibition, nor the delayed cell cycle progression induced by biochanin A was affected by the addition of antiestrogen. These results suggest that the growth regulatory effects of phytoestrogens may be associated with cell cycle progression, and the underlying mechanism involves at least in part the modulation of a non-classical ER-α signal pathway.
Subjects
Estrogen receptor; Fertility; Phytoestrogen
SDGs
Other Subjects
biochanin A; daidzein; estrogen receptor alpha; fulvestrant; messenger RNA; phytoestrogen; analysis of variance; article; breast cancer; cell culture; cell cycle; cell cycle G1 phase; cell cycle G2 phase; cell growth; cell proliferation; cell strain MCF 7; concentration response; controlled study; down regulation; drug effect; growth inhibition; human; human cell; reverse transcription polymerase chain reaction; signal transduction; Mink cell focus-forming virus
Type
journal article