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Figure 1 | Molecular Cancer

Figure 1

From: Epigenetic reactivation of estrogen receptor-α (ERα) by genistein enhances hormonal therapy sensitivity in ERα-negative breast cancer

Figure 1

GE and TSA synergistically induced ERα re-expression in ERα-negative MDA-MB-231 breast cancer cells. A) Graphic presentation of dose- and time- dependent ERα expression by GE treatment. MDA-MB-231 cells were plated in 6-well plates in triplicate and exposed to various concentrations of GE for up to 3 days. B) ERα expression changes by the combined treatment of GE with 5-aza (left) and TSA (right). The MDA-MB-231 cells were treated with or without either 25 μM GE or 2 μM 5-aza and 100 ng/ml TSA alone or together for 3 days. Control cells were grown in parallel with the treated cells but received vehicle DMSO. Quantitative real-time PCR was performed to measure relative transcription of ERα. C) Cellular viability in response to E2 and tamoxifen (TAM). D) The expression of PGR, an ERα target gene, in response to E2 and tamoxifen. GE and/or TSA-pretreated MDA-MB-231 cells were treated with or without 10 nM of E2 or 1 μM TAM for 1 days. MCF-7 cells served as a positive control. Cells were harvested at the indicated time periods and assessed for cellular viability and PGR expression, respectively. Cellular viability was measured by MTT assay and PGR expression was detected by quantitative real-time PCR. Data are in triplicate from three independent experiments and were normalized to GAPDH and calibrated to levels in the relevant control samples. Bars, SD; *, P < 0.05, * * P < 0.001, significantly different from control; £, P < 0.05, significantly different from GE (Figure 1B); †, P < 0.05, significantly different from 5-aza or TSA (Figure 1B). E) The ERα protein levels were determined by western-blot analysis. MCF-7 cells served as a positive control. GAPDH antibody was used to ensure equal loading. Representative photograph from an experiment was repeated three times.

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