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Anticancer Res ; 32(4): 1181-91, 2012 Apr.
Article in English | MEDLINE | ID: mdl-22493348

ABSTRACT

AIM: The aim of the present study was to identify the mechanism by which genistein and 17ß-estradiol inhibit proliferation of MDA-MB-231 breast cancer cells. MATERIALS AND METHODS: The expression of cell signaling proteins involved in cell apoptosis, proliferation, and survival (BCL-2 associated X protein, BAX; B-cell lymphoma 2, BCL-2; extracellular signal regulated kinase, pERK1/2; and protein kinase B, pAKT) were examined by western blotting, and tested whether these effects correlated with cell proliferation and apoptosis. RESULTS: Compared to the control, 1 µM genistein plus 1 nM 17ß-estradiol significantly increased apoptosis, and the BAX/BCL-2 ratio, with a concomitant decrease in ERK1/2 phosphorylation. High concentrations of genistein (100 µM) both in the presence and absence of 17ß-estradiol also increased apoptosis; however, these changes were not correlated with the BAX/BCL-2 ratio or with phosphorylation of ERK1/2. CONCLUSION: These results suggest that different concentrations of genistein elicit cell responses through different signaling mechanisms. These results are especially relevant in premenopausal women with breast cancer who are on a soy diet.


Subject(s)
Breast Neoplasms/pathology , Cell Proliferation/drug effects , Estradiol/pharmacology , Extracellular Signal-Regulated MAP Kinases/metabolism , Genistein/pharmacology , bcl-2-Associated X Protein/metabolism , Blotting, Western , Breast Neoplasms/enzymology , Breast Neoplasms/metabolism , Cell Line, Tumor , Female , Humans , Signal Transduction
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