Biotransformed Soybean Extract Induces Cell Death of Estrogen-Dependent Breast Cancer Cells by Modulation of Apoptotic Proteins

The process of soybean biotransformation increases the quantity of isoflavones (daidzein and genistein), which besides being considered an alternative to estroprogestive hormone replacement therapy (HRT), are able of hindering the growth and development of tumor cells. We investigated the effects of...

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Published inNutrition and cancer Vol. 67; no. 4; pp. 612 - 619
Main Authors Stocco, Bianca, Toledo, Karina A, Fumagalli, Helen F, Bianchini, Francine J, Fortes, Vanessa S, Fonseca, Maria José V, Toloi, Maria Regina T
Format Journal Article
LanguageEnglish
Published United States Routledge 19.05.2015
Taylor & Francis Ltd
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Summary:The process of soybean biotransformation increases the quantity of isoflavones (daidzein and genistein), which besides being considered an alternative to estroprogestive hormone replacement therapy (HRT), are able of hindering the growth and development of tumor cells. We investigated the effects of soybean extract biotransformed by fungus on estrogen-dependent (MCF-7) and nondependent (SK-BR-3) breast cell lines. Cells were treated with different concentrations of biotransformed (BSE) and nonbiotransformed soybean extract (SE), or daidzein (D) and genistein (G) patterns isolated and in combination (D + G). Afterwards, we analyzed cell viability by MTT assay, phosphatidylserine exposure and cell permeability by flow cytometry; expression of apoptotic proteins by Western blotting. BSE promoted reduction in cell viability and increase in DNA degradation in both cell lines. In addition, we verified increase in cell permeability and in the expression of phosphatidylserine, as well as modulation in the expression of apoptotic proteins in MCF-7 cells. The cells did not show any signs of cell death when incubated with the controls (D, G, and D + G). Unknown components found in the BSE induce cell death by apoptosis and necrosis, mainly in MCF-7 cells. These processes depend on the activation of caspase-3 and involve an increase in the expression of proapoptotic molecules.
Bibliography:http://dx.doi.org/10.1080/01635581.2015.1015744
ISSN:1532-7914
0163-5581
1532-7914
DOI:10.1080/01635581.2015.1015744