Effect of estradiol, zearalenone and apigenin on ER-positive breast cancer cells MCF-7
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PROVIDER: PRJNA489503 | ENA |
REPOSITORIES: ENA
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Project description:To understand the molecular effect of E2 and the dietary compound zearalenone and apigenin on MCF-7 proliferation. Results provide insight into the pathway involved by these dietary compounds on MCF-7 proliferation.
2020-07-07 | GSE119552 | GEO
Project description:Human estrogen-responsive breast cancer cell line MCF-7 TET Off (MCF-7 wt) were used to produce stable clones expressing ER-beta tagged with TAP-tag respectively at the C-term and at the N-term (C-TAP-ER-beta and N-TAP-ER-beta) or expressing ER-alpha tagged (C-TAP-ER-alpha) as previously described.(C-TAP-ER-beta, N-TAP-ER-beta, C-TAP-ER-alpha) were treated with 10nM of17-beta-estradiol, or vehicle (ETOH). miRNA expression was analyzed on total RNA extracted before or after 6, 12, 24, and 72 hours hormonal stimulation. Total RNA was fluorescently labelled, amplified in triplicate, to be, than, pooled for the Hybridization.Each pool, were hybridized for 18 hours on Illumina v2 MicroRNA Expression BeadChips, and after scanning, analysis was performed with GenomeStudio v.2010.1 software, for quality control and miRNA expression analysis.
2011-07-29 | E-TABM-1055 | biostudies-arrayexpress
Project description:Comparing the expression profiles of the genes in response to estrogen or 17b-estradiol (E2) and a mycotoxin, zearalenone (ZEA), and its analogues. Keywords: Gene expression profiling
2010-03-11 | GSE15249 | GEO
Project description:Goal: study the impact of estrogen receptor (ER) ligands on ER binding to chromatin in MCF-7 cells Methods: ER Chromatin Immunoprecipitation and Sequencing (ChIP-seq) Results: All tested ligands increase binding of ER onto DNA in MCF-7 breast cells. These ligands thus promote an association between ER and DNA, irrespective of their mode of action: selective ER modulator (SERM) 4-OH tamoxifen, and selective ER degraders (SERD) fulvestrant and GDC-0927.
2019-07-25 | GSE117941 | GEO
Project description:Estrogens have been shown to elicit anti-cancer effects against estrogen receptor alpha (ER)-positive breast cancer. We sought to determine the underlying mechanism of therapeutic response. Response to 17b-estradiol was assessed in ER+ breast cancer models with resistance to estrogen deprivation: WHIM16 patient-derived xenografts, C7-2-HI and C4-HI murine mammary adenocarcinomas, and long-term estrogen-deprived MCF-7 cells. As another means to reactivate ER, the anti-estrogen fulvestrant was withdrawn from fulvestrant-resistant MCF-7 cells. Transcriptional, growth, apoptosis, and molecular alterations in response to ER reactivation were measured. 17b-estradiol treatment and fulvestrant withdrawal induced transcriptional activation of ER, and cells adapted to estrogen deprivation or fulvestrant were hypersensitive to 17b-estradiol. ER transcriptional response was followed by an unfolded protein response and apoptosis. Such apoptosis was dependent upon the unfolded protein response, p53, and JNK signaling. Anti-cancer effects were most evident in models exhibiting genomic amplification of the gene encoding ER (ESR1), suggesting that engagement of ER at high levels is cytotoxic. These data indicate that long-term adaptation to estrogen deprivation or ER inhibition alters sensitivity to ER reactivation. In such adapted cells, 17b-estradiol treatment and anti-estrogen withdrawal hyperactivate ER, which drives an unfolded protein response activation and subsequent growth inhibition and apoptosis. 17b-estradiol treatment should be considered as an alternative therapy for anti-estrogen-resistant disease, particularly in patients with tumors harboring ESR1 amplification or overexpression. Furthermore, therapeutic strategies that enhance an unfolded protein response may enhance the therapeutic effects of ER reactivation.
2019-08-19 | GSE121631 | GEO
Project description:Comparing the expression profiles of the genes in response to estrogen or 17b-estradiol (E2) and a mycotoxin, zearalenone (ZEA), and its analogues. Keywords: Gene expression profiling Two-condition experiment, E2- or ZEA-treated vs. control cells. 2 to 3 biological replicates, independently grown and harvested. Two to three replicates per array.
2010-09-09 | E-GEOD-15249 | biostudies-arrayexpress
Project description:Estrogens have been shown to elicit anti-cancer effects against estrogen receptor alpha (ER)-positive breast cancer. We sought to determine the underlying mechanism of therapeutic response. Response to 17b-estradiol was assessed in ER+ breast cancer models with resistance to estrogen deprivation: WHIM16 patient-derived xenografts, C7-2-HI and C4-HI murine mammary adenocarcinomas, and long-term estrogen-deprived MCF-7 cells. As another means to reactivate ER, the anti-estrogen fulvestrant was withdrawn from fulvestrant-resistant MCF-7 cells. Transcriptional, growth, apoptosis, and molecular alterations in response to ER reactivation were measured. 17b-estradiol treatment and fulvestrant withdrawal induced transcriptional activation of ER, and cells adapted to estrogen deprivation or fulvestrant were hypersensitive to 17b-estradiol. ER transcriptional response was followed by an unfolded protein response and apoptosis. Such apoptosis was dependent upon the unfolded protein response, p53, and JNK signaling. Anti-cancer effects were most evident in models exhibiting genomic amplification of the gene encoding ER (ESR1), suggesting that engagement of ER at high levels is cytotoxic. These data indicate that long-term adaptation to estrogen deprivation or ER inhibition alters sensitivity to ER reactivation. In such adapted cells, 17b-estradiol treatment and anti-estrogen withdrawal hyperactivate ER, which drives an unfolded protein response activation and subsequent growth inhibition and apoptosis. 17b-estradiol treatment should be considered as an alternative therapy for anti-estrogen-resistant disease, particularly in patients with tumors harboring ESR1 amplification or overexpression. Furthermore, therapeutic strategies that enhance an unfolded protein response may enhance the therapeutic effects of ER reactivation.
2019-08-19 | GSE121379 | GEO
Project description:Lysozyme-GFP ER-HoxA9 cells were cultured in the presence of estradiol (active ER-HoxA9) or in the absence of estradiol (inactive ER-HoxA9). Samples were taken at 10 time points over a 120 hour time course of myeloid differentiation to examine those gene expression changes that accompany differentiation upon the release of HoxA9 differentiation arrest.
2016-10-01 | GSE84874 | GEO
Project description:Identification of Estrogen Receptor alpha (ERa) binding sites by ChIP-seq in MCF-7 breast cancer cells following an estrogen treatment. This study describes molecular effects of estradiol treatment and subsequent regulation by ER for a single gene/locus. A public ER chipseq (available in SRA as ERR011973), in addition to our own data, guided us to regulatory regions were ER was binding that were then analyzed in detail using "manual" ChIP. MCF-7 cells were treated for 1 h either 10 nm estradiol (E2) or vehicle (ethanol) and subjected to ChIP using antibodies against ERa or IgG.
2012-12-17 | E-GEOD-34759 | biostudies-arrayexpress
Project description:Three human ER+ breast cancer cell lines--MCF-7, T47-D, BT-474--grown with or without estradiol (E2). Keywords: Cell Line Comparison
2006-01-15 | GSE3529 | GEO