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equol/cáncer de mama

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Soy foods are the richest sources of isoflavones, mainly daidzein and genistein. Soy isoflavones are structurally similar to the steroid hormone 17β-estradiol and may protect against breast cancer. S-(-)equol, a metabolite of the soy isoflavone daidzein, has a higher bioavailability and greater

[Equol induced apoptosis of human breast cancer MDA-MB-231 cell by inhibiting the expression of nuclear factor-kappaB].

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OBJECTIVE To study the inhibition effect of equol on MDA-MB-231 cells, a human breast cancer cell line with estrogen-independent receptor. METHODS Cultured MDA-MB-231 cells were treated with different contents of equol. The cell viability was assessed with MTT method. The apoptosis was detected by

Plasma equol concentration is not associated with breast cancer and fibrocystic breast conditions among women in Shanghai, China.

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Equol (a bacterial metabolite of the soy isoflavone daidzein) is produced by 30% to 50% of humans and may be associated with health outcomes. We hypothesized that plasma equol would be inversely associated with risks of fibrocystic breast conditions (FBC) and breast cancer (BC). Plasma from women in

[Effect of equol on breast tumors induced by 7, 12-dimethylbenz (α) anthracene in ovariectominzed rats].

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OBJECTIVE To study the effect of equol on the incidence of breast tumors induced by 7, 12-dimethylbenz(α) anthracene (DMBA) in ovariectomized rats. METHODS In the study, 48 female ovariectomized SD rats were randomly divided into 6 groups according to their weights: blank control group, fed on an

S-equol inhibits proliferation and promotes apoptosis of human breast cancer MCF-7 cells via regulating miR-10a-5p and PI3K/AKT pathway.

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S-equol is the exclusive enantiomeric form of the soy isoflavone metabolite produced by human intestinal bacterial flora, which has strong anti-cancer activity. Based on this, the purpose of this study was to investigate the anti-breast cancer mechanism of S-equol. We examined the effects of S-equol

Equol induced apoptosis via cell cycle arrest in human breast cancer MDA-MB-453 but not MCF-7 cells.

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To investigate the effects of equol on cell cycle distribution and apoptosis in human breast cancer cells, we first determined the antiproliferative effects of various concentrations of equol (1 nM to 100 µM) on MCF-7 and MDA-MB-453 cells at 24, 48 or 72 h of exposure. Equol significantly inhibited
The aim of this study was to determine whether the extracellular-signal-regulated kinase 1/2 (ERK1/2) pathway is involved in genistein- and equol-induced cell proliferation and estrogen receptor (ER) alpha transactivation. For MCF-7 human breast cells, low concentrations of genistein and equol

(±)-Equol does not interact with genistein on estrogen-dependent breast tumor growth.

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Equol (EQ) is a prominent microbial metabolite of the soy isoflavone, daidzein, with estrogen-like properties. The major soy isoflavone, genistein (GEN), stimulated growth of estrogen-dependent breast cancer (EDBC) cells in vitro and tumor growth in vivo but EQ did not. To understand possible

The chemopreventive action of equol enantiomers in a chemically induced animal model of breast cancer.

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We describe for the first time the chemopreventive effects of S-(-)equol and R-(+)equol, diastereoisomers with contrasting affinities for estrogen receptors (ERs). S-(-)equol, a ligand for ERbeta, is an intestinally derived metabolite formed by many humans and by rodents consuming diets containing

Equol induces apoptosis through cytochrome c-mediated caspases cascade in human breast cancer MDA-MB-453 cells.

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This study investigated the role of the caspase activation cascade in extrinsic and intrinsic apoptosis induced by equol in human breast cancer MDA-MB cells. First, the antiproliferative effect of equol was determined in cells treated with 1-100 microM equol for 24, 48, and 72h. Equol significantly

Stimulation of breast cancer cells in vitro by the environmental estrogen enterolactone and the phytoestrogen equol.

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The phenolic lignans enterolactone and enterodiol appear periodically in women's urine, dependent upon synthesis from plant-derived lignans by the intestinal microflora. The phytoestrogen equol is also present in women's urine, and is also derived from a vegetarian diet. Antiestrogenic or

The phytoestrogens daidzein and equol inhibit the drug transporter BCRP/ABCG2 in breast cancer cells: potential chemosensitizing effect.

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OBJECTIVE The soy isoflavone genistein has been described to up-regulate breast cancer resistance protein (BCRP) and, thus, enhance chemoresistance in breast cancer cells. The aim of this work was to assess the effect of long- and short-term incubation with daidzein, the second most abundant soy
Estrogens used in hormone replacement therapy regimens may increase the risk of developing breast cancer. Paradoxically, high consumption of plant-derived phytoestrogens, particularly soybean isoflavones, is associated with a low incidence of breast cancer. To explore the molecular basis for these

Equol enhances tamoxifen's anti-tumor activity by induction of caspase-mediated apoptosis in MCF-7 breast cancer cells.

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BACKGROUND Soy phytoestrogens, such as daidzein and its metabolite equol, have been proposed to be responsible for the low breast cancer rate in Asian women. Since the majority of estrogen receptor positive breast cancer patients are treated with tamoxifen, the basic objective of this study is to

Equol Enhances Apoptosis-inducing Activity of Genistein by Increasing Bax/Bcl-xL Expression Ratio in MCF-7 Human Breast Cancer Cells.

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Anticancer activities of soy isoflavones, such as genistein and equol, a bioactive metabolite of daidzein, have been extensively studied because of possible involvement in the prevention of breast cancer. However, their interactions still remain unclear. We investigated here whether cytotoxic
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