As expected, mRNA was up-regulated around fivefold by E2 (10?9 M) compared to vehicle treatment and 4OHT (10?6 M) which completely failed to induce the levels of mRNA (Figure 3A). of gene and recruitment of ER and SRC3 at the promoter of gene respectively. Molecular docking was used to delineate the binding modes of BP and BPA with the ER. PCR-based arrays were used to study the regulation of the apoptotic genes. Key Results BP and BPA induced the proliferation of breast cancer cells; however, unlike BPA, BP failed to induce apoptosis. BPA consistently acted as an agonist in our studies but BP exhibited mixed agonistic/antagonistic properties. Molecular docking revealed agonistic and antagonistic mode of binding for BPA and BP respectively. BPA treatment resembled E2 treatment in terms of PCR-based regulation of apoptotic genes whereas BP was similar to 4OHT treatment. Conclusions and Implications The chemical structure of ER ligand determines Hoechst 33342 analog 2 the agonistic or antagonistic biological responses by the virtue of their binding mode, conformation of the liganded-ER complex and the context of the cellular function. gene activation in the ER negative breast cancer cells stably transfected with either wild type ER or D351G mutated ER (MacGregor Schafer for 20 min at 4C. The supernatant were diluted 1 : 10 with ChIP dilution buffer. Normal rabbit IgG and Magna ChIP protein A magnetic bead (Upstate Cell Signaling Solutions, Temecula CA, Hoechst 33342 analog 2 USA) were used to immunoclear the supernatant followed by immunoprecipitation with antibodies against ER (1:1 mixture of cat# sc-543 and sc-7207; Santa Cruz Biotechnology Inc., Dallas, TX, USA) and steroid receptor coactivator-3 (SRC3) (cat# 13066; Santa Cruz Biotechnology, Inc.). Immunocomplexes were pulled down using protein A magnetic beads and a magnet. The beads bound to immunocomplexes were washed using different buffers as described previously (Maximov promoter (Maximov < 0.05 vs. vehicle treatment) (B) Dose-dependent effect of BP, BPA and E2 on apoptosis of MCF7 : 5C cells treated for 6 days as indicated. The black bar denotes the level of DNA in vehicle treated cells over a 6-day period. The growth is measured as amount of DNA present in each well. (*< 0.05 Hhex vs. vehicle treatment) (C) Dose dependent effect of BP and BPA on E2 (1 nM)-induced apoptosis in MCF7 : 5C cells, treated over a six day period. The growth is measured as amount of DNA present in each well. (*< 0.05 vs. 1 nM E2 treatment) (D) Effect of BP (10?6 M) and 4OHT (10?6 M) on BPA (10?6 M) induced apoptosis in MCF7 : 5C cells over 6-day period. (*< 0.05 vs. vehicle treatment; #< 0.05 vs. BPA treatment) The data are presented as percent of growth considering the vehicle treated cells as 100 percent. Each value is average of at least three replicates SD. Regulation of oestrogen-responsive gene trefoil factor 1(TFF1 or PS2) by BP and BPA We next investigated the transcriptional regulation of a well-characterized oestrogen-regulated gene, (gene were measured using RT-PCR. Two different concentrations (10?6 M and 10?5 M) were used for BP and BPA, because BPA is a weak oestrogen and we wanted to evaluate the concentration dependent regulation of these compounds. As expected, mRNA was up-regulated around fivefold by E2 (10?9 M) compared to vehicle treatment and 4OHT (10?6 M) which completely failed to induce the levels of mRNA (Figure 3A). On the other hand, BP treatment at 10?6 M concentration moderately (2 fold) up-regulated the mRNA levels and higher concentration (10?5 M) of BP failed to further increase the levels of (Figure 3A). Conversely, cells treated with BPA exhibited concentration dependent increase in up-regulation of the mRNA and the magnitude of up-regulation with high concentration (10?5 M) of BP was equivalent to the E2-mediated up-regulation of mRNA (Figure 3A). Open in a separate Hoechst 33342 analog 2 window Figure 3 Regulation of (gene followed by 45 min treatments of bisphenol (BP), bisphenol A (BPA) compared with 17-oestradiol (E2) and 4-hydroxy-tamoxifen (4OHT) in MCF7 cells. (A) MCF7 cells were treated with indicated treatments for 4 h and harvested for total RNA. Total RNA was reverse transcribed and assessed for gene expression levels using RT-PCR. gene was used as an internal control. All values are.
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