The expression patterns of 17b-estradiol responsive genes in wt MCF7, OHT resistant MCF7 and ICI resistant MCF7
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE5840 | GEO | 2007/09/14
SECONDARY ACCESSION(S): PRJNA97237
REPOSITORIES: GEO
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Project description:Compare the expression pattern of 17b-estradiol responsive genes in parent, OHT-resistant and ICI-resistant breast cancer cells. Experiment Overall Design: Data for 4 replicate experiments performed with biologically independent samples. Experiment Overall Design: KN01M001v0 DMSO (control) wt MCF7 -> GSM136152 Experiment Overall Design: KN01H002v0 DMSO (control) wt MCF7 -> GSM136148 Experiment Overall Design: KN01H003v0 DMSO (control) wt MCF7 -> GSM136150 Experiment Overall Design: KN01H004v0 DMSO (control) wt MCF7 -> GSM136152 Experiment Overall Design: KN01M005v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136153 Experiment Overall Design: KN01H006v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136154 Experiment Overall Design: KN01H007v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136155 Experiment Overall Design: KN01H008v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136156
2008-06-14 | E-GEOD-5840 | biostudies-arrayexpress
Project description:Compare the expression pattern of 17b-estradiol responsive genes in parent, OHT-resistant and ICI-resistant breast cancer cells. Experiment Overall Design: Data for 4 replicate experiments performed with biologically independent samples. Experiment Overall Design: KN01M001v0 DMSO (control) wt MCF7 -> GSM136152 Experiment Overall Design: KN01H002v0 DMSO (control) wt MCF7 -> GSM136148 Experiment Overall Design: KN01H003v0 DMSO (control) wt MCF7 -> GSM136150 Experiment Overall Design: KN01H004v0 DMSO (control) wt MCF7 -> GSM136152 Experiment Overall Design: KN01M005v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136153 Experiment Overall Design: KN01H006v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136154 Experiment Overall Design: KN01H007v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136155 Experiment Overall Design: KN01H008v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136156
| S-ECPF-GEOD-5840 | biostudies-other
Project description:MCF7 breast cancer cell lines: drug-resistant (OHT and ICI) cell lines vs. drug-sensitive (wild type) cell lines. Assessment of association between gene expression and methylation.
2011-10-05 | GSE25519 | GEO
Project description:MCF7 breast cancer cell lines: drug-resistant (OHT and ICI) cell lines vs. drug-sensitive (wild type) cell lines. Assessment of association between gene expression and methylation. Two comparisons: OHT-resistant vs. wild type, and ICI-resistant vs. wild type. OHT: 4-hydroxytamoxifen ICI: fulvestrant ((ICI 182780) This submission represents the methylation component of the study.
2011-10-04 | E-GEOD-25519 | 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:The expression patterns of 17b-estradiol responsive genes in wt MCF7, OHT resistant MCF7 and ICI resistant MCF7
| PRJNA97237 | ENA
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:Purpose: Study the temporal effect of OHT on gene expression in MCF7 cells using mRNA-seq. Methods: MCF7 cells were treated with 100nM OHT for 2h, 6h and 24h or 24h with vehicle alone (ethanol). Six biological replicates of each time point were included in the analysis. For the library preparation the Illumina TruSeq Stranded mRNA Library Prep Kit High Throughput was used and 2 lanes of SE50 were run on HiSeq 4000. Results: We identify 27,520 genes of which 1,187 were significantly regulated in response to OHT in at least one time point. This included transcriptional repression of cell cycle genes as well as a number of known ERα target genes. Conclusions: We demonstrate a transcriptional response to OHT in MCF7 cells, with ERa target genes and genes linked to cell cycle progression being repressed.
2018-10-12 | GSE104872 | GEO
Project description:The objective of the study was to investigate the effect of proteasome inhibition on glucocorticoid and estrogen receptor regulated gene expression. Experiment Overall Design: MCF-7 cells were treated with proteasome inhibitor (MG132), dexamethasone, 17b-estradiol or MG132 plus dexamethasone or MG132 plus 7b-estardiol. Control cells were not treated. RNA was collected from 2 biological experiments.
2008-06-20 | E-GEOD-8383 | biostudies-arrayexpress
Project description:Cutibacterium acnes 17B Genome sequencing
| PRJNA162693 | ENA