These studies may aid in providing a better understanding of the relationships amongst phytoestrogens, ER alpha, AhR and p53 in breast cancer cells.
Book Title: Phytoestrogens and Breast Cancer
Author:Amelita L. Sanchez
Published on 2012 by
ISBN: /
Total Page: 230
Book Category:Breast
Book is About: Breast Cancer
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Breast cancer is the most diagnosed cancer amongst women. Approximately 230,480 new cases of breast cancer and 39,520 expected deaths due to breast cancer were predicted in 2011. Our laboratory has previously reported regulation of p53 by exogenous 17 beta-estradiol (E2) in T47D breast cancer cells. The proposed mechanism of action of these findings is via the estrogen receptor alpha (ER alpha). While these results provide a salient foundation in elucidating ways to combat hormone-dependent breast cancer, continuous development of novel hormonal therapies is crucial. Phytoestrogens (PEs), have gained interest in the scientific community as potential alternatives to current therapies, due to their structural similarity to E2 and demonstrated estrogenic and anti-estrogenic activities in mammalian systems. A novel dietary compound, 3, 3', 4',7-tetrahydroxyflavone (fisetin) has been reported to inhibit proliferation of cancer cells, including cancers of the colon, prostrate and breast and has potential correlations with p53 and ER alpha. Studies have suggested that PEs have binding affinities for ER alpha and also for the aryl hydrocarbon receptor (AhR), which may potentiate a possible mechanism of action. Therefore, I have examined effects of fisetin on cancer cell proliferation, protein and mRNA expression levels of p53, ER alpha, and AhR in T47D cells. The cells were treated at various time intervals with 20-70 mu M of fisetin, 10nM E2, 1 mu M ICI 182, 780 or a protease inhibitor (MG-132) in varying experimental designs. Cells were treated with fisetin, extracted, quantified and proteins separated on SDS-PAGE and subjected to Western blot analysis. Cell proliferation assays were employed as a cancer cell functional analysis. Increasing concentrations of fisetin caused a 6-8 fold decrease in T47D cell number. Western blot analysis revealed an up-regulation of p53 at low concentrations and down-regulation in p53 at higher concentrations of fisetin. A biphasic expression was observed in the level of ER alpha. Cells treated with fisetin at high concentrations altered AhR expression level. Various ligand treatments resulted in differential responses on mRNA levels of ESR1 and TP53 genes. These studies may aid in providing a better understanding of the relationships amongst phytoestrogens, ER alpha, AhR and p53 in breast cancer cells.
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