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ChIP-chip of 6 chromatin marks (FAIRE, H3K4me1, H3K4me3, H3K27me3, H3R17me2, H3AZAce) in breast cancer cell line MCF7

ABSTRACT: Altered gene expression patterns in human diseases reflect perturbations in the transcriptional networks that regulate cellular state. In breast cancer, Nuclear Receptors (NRs) play a prominent role in governing gene expression. NRs have prognostic utility and are therapeutically important targets. Here we describe a complete regulatory map for twenty-four NR proteins that are expressed in the breast cancer cell line MCF-7, as well as fourteen additional breast cancer associated transcription factors (TFs) and six key chromatin state markers.

ORGANISM(S): Homo sapiens

PROVIDER: GSE42617 | GEO | 2013/01/01

SECONDARY ACCESSION(S): PRJNA182368

REPOSITORIES: GEO

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ChIP-chip of 6 chromatin marks (FAIRE, H3K4me1, H3K4me3, H3K27me3, H3R17me2, H3AZAce) in breast cancer cell line MCF7

2013-01-01 | E-GEOD-42617 | biostudies-arrayexpress

ChIP-chip of 38 nuclear receptors and NR co-factors in breast cancer cell line MCF7

Project description:Altered gene expression patterns in human diseases reflect perturbations in the transcriptional networks that regulate cellular state. In breast cancer, Nuclear Receptors (NRs) play a prominent role in governing gene expression. NRs have prognostic utility and are therapeutically important targets. Here we describe a complete regulatory map for twenty-four NR proteins that are expressed in the breast cancer cell line MCF-7, as well as fourteen additional breast cancer associated transcription factors (TFs) and six key chromatin state markers. The CEL files for the 38 NRs ChIP-chip presented in the paper are included, together with the results bar files, except 5 previsouly published ones: ER [GSE10800], RARA, RARG, FOXA1, GATA3 [GSE15244]. The supplementary bed file contains all 200,140 binding sites of all 38 TFs reported in the paper.

2013-01-01 | GSE41995 | GEO

Effect of DC-SCRIPT expression in MCF7 breast cancer cell line

Project description:Breast cancer is one of the most common causes of cancer-related deaths in women. Nuclear receptors (NR) and their regulators are well known for their role in breast cancer. Especially ligands for the type I NRs, Estrogen Receptor (ER) and Progesterone Receptor have growth promoting effects in breast cancer cells. The NR coregulator DC-SCRIPT (ZNF366) has been found to be a strong and independent prognostic marker in ER positive (ESR1) breast cancer patients. DC-SCRIPT modulates the function of multiple NRs and has opposing effects on type I versus type II NRs. It represses the function of the growth promoting type I NRs, whereas it enhances the mainly anti-proliferative type II NRs. In this study we aimed to gain further insight into the functional role of DC-SCRIPT in breast cancer cells. Therefore, the effect of DC-SCRIPT expression on breast cancer cell gene expression was investigated using a novel DC-SCRIPT-inducible MCF7 breast cancer cell line model. In the presence of DC-SCRIPT, multiple cell cycle related genes were differentially expressed, including the tumor suppressor gene CDKN2B.

2015-08-01 | GSE59995 | GEO

Effect of DC-SCRIPT expression in MCF7 breast cancer cell line

2015-08-01 | E-GEOD-59995 | biostudies-arrayexpress

Gene expression profiles of MCF7 with with the following NR ligands: estradiol/E2 (ERÎ± agonist), AM580 (RARA agonist), CD437 (RARG agonist), ATRA (RARA/RARG agonist), GW0742 (PPARD agonist), R5020 (PGR agonist), and dexamethasone (GR/NR3C1 agonist).

Project description:Altered gene expression patterns in human diseases reflect perturbations in the transcriptional networks that regulate cellular state. In breast cancer, Nuclear Receptors (NRs) play a prominent role in governing gene expression. NRs have prognostic utility and are therapeutically important targets. In order to understand the function of nuclear receptors in breast cancer, we treated MCF7 cells with 6 nuclear receptor agonist, and performed expression arrrays with three biological replicates each. MCF-7 cells were cultured for 48 hours in medium with 10% charcoal-stripped FBS, and then were treated with 6 diffferent NR ligand (E2, AM580, CD437, ATRA, R5020, DEX) separately for 24h before collection and processing for microarrays. Three biological replicates were collected and processed for both control and treatment. with the 100nM GW0742 (PPARD specific ligand) and 100nM ATRA (RARs ligand), then collected after 24h for microarray processing. Controls were non-treated MCF7 cells. Both treatments and controls have three biological replicates.

2013-01-01 | E-GEOD-42619 | biostudies-arrayexpress

Gene expression profile of NR2E3 in MCF7 cells

Project description:While the roles of individual nuclear receptor (NR) in human diseases have been well characterized, interplays among NRs have not been extensively characterized due, in part, to technical difficulties in simultaneously monitoring molecular activities of all 48 NR genes. Using systems-level analysis of publically available gene expression data from NCI-60 cell lines, we uncovered novel interaction between ESR1 and orphan receptor NR2E3. Expression of NR2E3 is significantly associated with expression of ESR1 in NCI-60 cell lines as well as in breast cancer patients. To investigate how NR2E3 gene signatures are globally correlated with ESR1 signaling pathway, we performed microarray after knocking down NR2E3 or ESR1 in MCF-7 cells. Keywords: DNA microarray (Illumina human Ht12 V3) 3 shControl, 3 shNR2E3, 3 siLuc, 3 siESR1

2011-12-22 | E-GEOD-18431 | biostudies-arrayexpress

Gene expression profile of NR2E3 in MCF7 cells

2011-12-22 | GSE18431 | GEO

Gene expression profiles of MCF7 with with the following NR ligands: estradiol/E2 (ERα agonist), AM580 (RARA agonist), CD437 (RARG agonist), ATRA (RARA/RARG agonist), GW0742 (PPARD agonist), R5020 (PGR agonist), and dexamethasone (GR/NR3C1 agonist).

2013-01-01 | GSE42619 | GEO

Comprehensive Study of Nuclear Receptor DNA Binding Provides a Revised Framework for Understanding Receptor Specificity

Project description:The type II nuclear receptors (NRs) function as heterodimeric transcription factors with the retinoid X receptor (RXR) to regulate diverse biological processes in response to endogenous ligands and therapeutic drugs. DNA-binding specificity has been proposed as a primary mechanism for NR gene regulatory specificity. We use protein-binding microarrays (PBMs) to comprehensively analyze the DNA binding of 12 NR:RXRα heterodimers. We find more promiscuous NR-DNA binding than has been reported, challenging the view that NR binding specificity is defined by half-site spacing. We show that NRs bind DNA using two distinct modes, explaining widespread NR binding to half-sites in vivo. Finally, we show that the current models of NR specificity better reflect binding-site activity rather than binding-site affinity. Our rich dataset and revised NR binding models provide a framework for understanding NR regulatory specificity and will facilitate more accurate analyses of genomic datasets.

2019-01-12 | GSE124910 | GEO

Characterization of stem cell-derived liver and intestinal organoids as a model system to study nuclear receptor biology.

Project description:Nuclear receptors (NRs) are ligand-activated transcription factors regulating a large variety of processes involved in reproduction, development, and metabolism. NRs are ideal drug targets. Immortalized cell lines recapitulate NR biology very poorly and primary cultures are laborious and require a constant need for donor material. There is a clear need for development of novel preclinical model systems that better resemble human physiology since technical uncertainty early in drug development is the cause of many preclinical drugs not reaching the clinic. Here, we studied whether organoids, mini-organs derived from the respective tissue’s stem cells, can serve as a novel (preclinical) model system to study NR biology and targeteability. We characterized mRNA expression profiles of the NR superfamily in mouse liver, ileum, and colon organoids. NR mRNA expression patterns were similar to the respective tissues, indicating their suitability for NR research. Metabolic NRs Fxrα, Lxrα, Lxrβ, Pparα, and Pparγ were responsive to ligands in an NR-dependent fashion, as demonstrated by regulation of expression and binding to endogenous target genes. Transcriptome analyses of wildtype colonic organoids stimulated with Rosiglitazone showed that lipid metabolism was the highest significant changed function, greatly mimicking the known function of PPARs and Rosiglitazone in vivo. In conclusion, our results demonstrate that organoids constitutes a versatile and promising in vitro system to study NR biology and targeteability.

2017-05-22 | GSE82111 | GEO

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