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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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ER_cofactor_specificity_arrays

ABSTRACT: The Estrogen Receptor cofactors SRC1 (NCOA1, KAT13A), SRC2 (NCOA2, GRIP1, TIF2, KAT13C) , SRC3 (NCOA3, AIB1, KAT13B, Rac3) , CBP and p300 are assessed for their genome-wide chromatin binding capacities in the breast cancer cell line MCF7. To determine the Estrogen Receptor dependency of interactions, experiments were performed in the absence of hormone and after Estradiol treatment. In addition, the data were compared with Estrogen Receptor ChIP-seq data from the same timepoint of Estradiol treatment.

ORGANISM(S): Homo sapiens

SUBMITTER: Gordon Brown

PROVIDER: E-MTAB-788 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Oestrogen receptor-co-factor-chromatin specificity in the transcriptional regulation of breast cancer.

Zwart Wilbert W Theodorou Vasiliki V Kok Marleen M Canisius Sander S Linn Sabine S Carroll Jason S JS

The EMBO journal 20111014 23

The complexity of oestrogen receptor α (ERα)-mediated transcription is becoming apparent, but global insight into the co-regulatory proteins that assist ERα transcription is incomplete. Here, we present the most comprehensive chromatin-binding landscape of ERα co-regulatory proteins to date. We map by ChIP-seq the essential p160 co-regulators (SRC1, SRC2 and SRC3), and the histone acetyl transferases p300 and CBP in MCF-7 breast cancer cells. We find a complex network of co-regulator binding, wi ...[more]

PMID: 22002538

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ChIP-Seq of human breast cancer cell lines MCF-7 in the absence of hormone and after Estradiol treatment with antibody against Estrogen Receptor cofactors SRC1, SRC2, SRC3, CBP and p300

Project description:The Estrogen Receptor cofactors SRC1 (NCOA1, KAT13A), SRC2 (NCOA2, GRIP1, TIF2, KAT13C) , SRC3 (NCOA3, AIB1, KAT13B, Rac3) , CBP and p300 are assessed for their genome-wide chromatin binding capacities in the breast cancer cell line MCF7. To determine the Estrogen Receptor dependency of interactions, experiments were performed in the absence of hormone and after Estradiol treatment. In addition, the data were compared with Estrogen Receptor ChIP-seq data from the same timepoint of Estradiol treatment.

2011-10-25 | E-MTAB-785 | biostudies-arrayexpress

ChIP-Seq of human breast cancer cell lines treated with estrogen and tamoxifen to investigate CTCF binding

Project description:CCCTC-binding factor (CTCF) is a conserved zinc finger transcription factor involved in chromatin looping. Recent evidence has shown a role for CTCF in ER biology. This experiment maps CTCF binding genome-wide in breast cancer cells and shows that CTCF binding does not change with estrogen or tamoxifen treatment. We find a small but reproducible proportion of CTCF binding events that overlap with both the nuclear receptor estrogen receptor and the forkhead protein FoxA1. These overlapping binding events are likely to be functional as they are biased towards estrogen-regulated genes. In addition, we identify cell-line specific CTCF binding events. These cell-line specific CTCF binding events are more likely to be associated with cell-line specific ER vinding events and are also more likely to be adjacent to genes that are expressed in that particular cell line. These data suggest a positive, pro-transcriptional role for CTCF in ER-mediated gene expression in breast cancer cells.

2011-12-07 | E-MTAB-740 | biostudies-arrayexpress

CTCF_ER_Arrays

2012-01-01 | E-MTAB-739 | biostudies-arrayexpress

Macrophage-to-endothelial Cell Crosstalk by 27-hydroxycholesterol Promotes Atherosclerosis in Male Mice

Project description:Human aortic endothelial cells were treated with vehicle (LUM1_S07615), estradiol (LUM1_S07617) or 27-hydroxycholesterol (LUM1_S07618), estrogen receptor alpha was immunoprecipitated, and the changes in the receptor interactome were interrogated.

2023-05-08 | MSV000091880 | MassIVE

Dynamics of protein expression reveals primary targets and secondary messengers of estrogen receptor signaling in MCF-7 breast cancer cells

Project description:Estrogen receptor-mediated proliferation of breast cancer cells is facilitated through expression of multiple primary target genes, products of which induce the secondary response to stimulation. To differentiate between the primary and secondary target genes of estrogen receptor signaling, we measured dynamics of protein expression induced by estradiol in MCF-7 breast cancer cells. Measurement of the global proteomic effects of estradiol by SILAC resulted in identification of 104 estradiol-regulated proteins, with only 41 corresponding genes having estrogen response elements (EREs). Selected reaction monitoring assays were used to validate 32 proteins and measure the dynamics of their expression within 72 hours upon estradiol stimulation and in the presence of 4-hydroxytamoxifen, thus confirming estrogen receptor-mediated signaling. Dynamics of protein expression revealed immediate early response proteins including TFF1 and CDK1 and delayed response proteins including CDK2 and NAB2. Presence or absence of EREs in the corresponding genes indicated early or delayed expression of proteins identified by SILAC. Finally, we measured accurate dynamics of estradiol-induced protein expression in the sub-network of primary and secondary targets of estrogen receptor. Interestingly, since NAB2 protein is also a repressor of EGR3-induced transcription, siRNA-mediated silencing of NAB2 resulted in the over-expression of some EGR3-induced proteins, such as ITGA2. To conclude, quantitative proteomics revealed secondary targets of estrogen receptor signaling potentially overlooked by genome-wide profiling of EREs and provided dynamics of protein expression in the network of transcription factors with a negative feedback loop.

2016-04-14 | PXD002797 | Pride

Integrative genomics of gene regulation by estrogen receptors and and coregulators [ChIP-seq]

Project description:The closely related transcription factors (TFs), estrogen receptors ER? and ER?, regulate divergent gene expression programs and proliferative outcomes in breast cancer. Utilizing MCF-7 breast cancer cells with ER?, ER?, or both receptors as a model system to define the basis of differing response specification by related TFs, we show that these TFs and their key coregulators, SRC3 and RIP140, generate overlapping as well as unique chromatin-binding and transcription-regulating modules. Cistrome and transcriptome analyses and use of clustering algorithms delineated 11 clusters representing different chromatin-bound receptor and coregulator assemblies that could be functionally associated through enrichment analysis with distinct patterns of gene regulation and preferential coregulator usage, RIP140 with ER? and SRC3 with ER?. The receptors modified each other’s transcriptional effect, and ER? countered the proliferative drive of ER? through several novel mechanisms associated with specific binding site clusters. Our findings delineate distinct TF-coregulator assemblies that function as control nodes specifying precise patterns of gene regulation, proliferation, and metabolism, as exemplified by two of the most important nuclear hormone receptors in human breast cancer. Examination of Estrogen Receptors alpha and beta and their coregulators SRC3 and RIP140 in different cell types

2013-07-05 | E-GEOD-42348 | biostudies-arrayexpress

TLE1 mediates estrogen receptor binding

Project description:Estrogen receptor (ER) binds to distal enhancers within the genome and requires additional factors, such as the Forkhead protein FoxA1, for mediating chromatin interactions. We now show that the human Groucho protein, Transducin-like enhancer protein 1 (TLE1), positively assists some ER-chromatin interactions, a role that is distinct from its general role as a transcriptional repressor. We show that specific silencing of TLE1 inhibits the ability of ER to bind to a subset of ER binding sites within the genome, a phenomenon that results in perturbations in phospho-RNA Pol II recruitment. Furthermore, TLE1 is essential for effective ER-mediated cell division. We have discovered a distinct role for TLE1, as a necessary transcriptional component of the ER complex, where it facilitates ER-chromatin interactions.

2012-11-14 | E-MTAB-1368 | biostudies-arrayexpress

RNA-seq of human breast cancer cell lines MCF7 and CAMA1 treated with Fulvestrant, AZD9496 and AZD9833/camizestrant, with and without estradiol

Project description:Oral selective estrogen receptor degraders (SERDs) could become the backbone endocrine therapy (ET) for estrogen receptor-positive (ER+) breast cancer, as they achieve greater inhibition of ER-driven cancers than current ETs and overcome key resistance mechanisms. This dataset was aimed at exploring the preclinical effects of the next-generation oral SERD camizestrant (AZD9833) on MCF7 and CAMA1 cell lines. Cells were treated with 1 nM estradiol and 100 nM fulvestrant, AZD9496, or camizestrant for 24 hours, with three replicates per condition and non-estradiol-treated controls.

2023-09-11 | E-MTAB-13113 | biostudies-arrayexpress

Gene expression profiles elicited by estradiol and endoxifen in MCF7 parental and ER-beta expressing breast cancer cells

Project description:We have previously demonstrated that endoxifen is the most important tamoxifen metabolite responsible for eliciting the anti-estrogenic effects of this drug in breast cancer cells expressing estrogen receptor-alpha. However, the relevance of estrogen receptor-beta in mediating endoxifen action has yet to be explored. Therefore, the goals of this study were to determine the differences in the global gene expression profiles elicited by estradiol treatment and endoxifen between parental MCF7 breast cancer cells (expressing estrogen receptor alpha only) and MCF7 cells stably expressing estrogen receptor beta. Total RNA was isolated from parental or estrogen-receptor beta expressing MCF7 cells following 24 hour treatments with either ethanol vehicle, 1nM 17-beta-estradiol or 1nM estradiol plus 40nM endoxifen. All studies were conducted in biological replicates of 2.

2011-02-18 | E-GEOD-27375 | biostudies-arrayexpress

Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer. [cell models RNA-seq]

Project description:Transcriptomic changes and estrogen and progesterone receptor binding in multiple ER+/PR+ models (eight ER+/PR+ patient tumors, various T47Ds, ZR75) and multiple ER+/PR-negative models (four ER+/PR- patient tuumors, PR-deficient T47D and MCF7 cells) treated with various hormone combinations. Results: In isolation, estrogen and progestin act as genomic agonists by regulating the expression of common target genes in similar directions, but at different levels. Similarly, in isolation, progestin is also a weak phenotypic agonist of estrogen action. However, in the presence of both hormones, progestin behaves as a phenotypic estrogen antagonist. PR remodels nucleosomes to noncompetitively redirect ER genomic binding to distal enhancers enriched for BRCA1 binding motifs and sites that link PR and ER/PR complexes. Importantly, when both hormones are present, progestin modulates estrogen action such that responsive transcriptomes, cellular processes and ER/PR recruitment to genomic sites correlate with those observed with PR alone, but not ER alone. Conclusions: Genomic Agonism and Phenotypic Antagonism between Estrogen and Progesterone Receptors in Breast Cancer. Individual and concerted actions of ER and PR highlight the prognostic and therapeutic value of PR in ER+/PR+ breast cancers. ER+/PR+ and ER+/PR-deficient model systems were deprived of steroids by culturing them in phenol red free RPMI 1640 media that is supplemented with 10% charcoal-stripped fetal bovine serum and 1% penicillin/streptomycin. Subsequently, these steroid-deprived models were treated with either vehicle, 10 nM estradiol, 10 nM progestin R5020 or 10 nM of both the hormones and genomics (ChIP-seq and RNA-seq) was performed. ChIP-seq was done after 45 minutes of hormone treatments. For cell models, RNA-seq was done after 12 hours of hormone treatments. Tumor explants were treated with either 24 or 48 hours.

2016-06-01 | E-GEOD-80366 | biostudies-arrayexpress

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