Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIP-seq profiling of estrogen receptor binding in MCF-7 cells exposed to 5α-DTT, Flutamide, Estradiol, and Bisphenol B

ABSTRACT: ChIP-seq profiling of estrogen receptor binding in MCF-7 cells exposed to 5α-DTT, Flutamide, Estradiol, and Bisphenol B

PROVIDER: PRJNA1233327 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR32613147_1.fastq.gz	Fastqsanger.gz
	SRR32613147_2.fastq.gz	Fastqsanger.gz
	SRR32613148_1.fastq.gz	Fastqsanger.gz
	SRR32613148_2.fastq.gz	Fastqsanger.gz
	SRR32613149_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

ChIP-seq profiling of estrogen receptor binding in MCF-7 cells exposed to 5α-DTT, Flutamide, Estradiol, and Bisphenol B

Project description:Endocrine-disrupting chemicals (EDCs) can modulate estrogen receptor (ER) signaling by altering its transcriptional activity. To investigate these effects, we performed chromatin immunoprecipitation sequencing (ChIP-seq) on cells treated with 5α-Dihydrotestosterone (5α-DTT), Flutamide, Estradiol, and Bisphenol B. This dataset includes raw sequencing reads, processed peak files, and metadata, enabling the identification of ER binding sites influenced by each EDC. Gene ontology (GO) analysis of ChIP-enriched regions revealed that these compounds affect key pathways, including antibody-dependent cytotoxicity, BMP signaling in cardiac induction, and hepatocyte growth factor receptor signaling. This dataset provides insights into EDC-induced transcriptional regulation and contributes to the understanding of their role in endocrine disruption.

2025-03-12 | GSE291416 | GEO

Bisphenol A alternatives can effectively substitute for estradiol in promoting cell growth through estrogen receptor alpha in human breast cancer cells

Project description:Plasticizers with estrogenic activity, such as bisphenol A (BPA), have been reported to have potential adverse health effects in humans, especially in fetal and infant stages. Due to mounting evidence and public pressure BPA is being phased out by the plastics manufacturing industry and is being replaced by other bisphenol variants in “BPA-free” products. We have compared estrogenic activity of 7 bisphenol analogues (BPA; bisphenol S, BPS; bisphenol F, BPF; bisphenol AP, BPAP; bisphenol AF, BPAF; bisphenol Z, BPZ; bisphenol B, BPB) in human breast cancer cell lines. We used microarrays to detail the alterations in gene expression profiles associated with MCF-7 cell line exposure to bisphenol A analogues

2017-03-03 | GSE85350 | GEO

Expression Analysis of Bisphenol A (0.1 uM), 17beta-estradiol (0.1 uM), and GSK4716 (0.1 uM) Exposure in Embryonic Zebrafish

Project description:Investigation of whole genome expression pattern of 24 hours post fertilization Danio rerio embryos exposed to bisphenol A, 17beta-estradiol, GSK4716, or 0.1% DMSO vehicle control

2013-03-25 | GSE38960 | GEO

Single-cell RNA sequencing of MCF-7 cells treated with 17-β estradiol or fulvestrant, and fulvestrant resistant derivatives of MCF-7 cells

Project description:Single-cell RNA sequencing (scRNA-seq) on MCF-7 breast cancer cells treated with fulvestrant or 17-β estradiol, and MCF-7 cell line derivatives made resistant to fulvestrant.

2025-11-24 | GSE306192 | GEO

Estrogen-responsive Estrogen Receptor alpha binding sites in MCF-7 by ChIP-seq

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

17beta-estradiol (E2)-regulated gene expression across time in estrogen-dependent and estrogen deprivation-resistant MCF-7-derived breast cancer cell lines.

Project description:A series of MCF-7 variants were previously developed that are either estrogen-dependent for growth (MCF-7:WS8 cells), or resistant to estrogen deprivation and refractory (MCF-7:2A) or sensitive (MCF-7:5C) to E2-induced apoptosis. To identify genes associated with E2-induced apoptosis, estrogen deprivation-resistant/apoptotic-sensitive 5C cells were compared to both estrogen-dependent MCF-7:WS8 and estrogen deprivation/apoptotic-refractory MCF-7:2A cells

2011-11-21 | GSE29917 | GEO

Expression Analysis of Bisphenol A and 17Î²-estradiol Exposure in Embryonic Zebrafish

Project description:Investigation of whole genome expression pattern of 24 hours post fertilization Danio rerio embryos exposed to bisphenol A, 17Î²-estradiol, or 0.1% DMSO vehicle control This data represents 2 experiments using 2 separate microarrays. Microarray 1 [Low]: Embryos were exposed to 0.1 ÂµM BPA, 0.1 ÂµM E2, or control from 8 hpf to 24 hpf. Three biological replicates were collected for each treatment. 40 embryos were pooled to comprise a replicate. Microarray 2 [High]: Embryos were exposed to 80 ÂµM BPA, 15 ÂµM E2, or control from 8 hpf to 24 hpf. Two biological replicates were collected for each treatment. 40 embryos were pooled to comprise a replicate. These 2 microarray experiments are cross-comparable, as described in the associated publication.

2013-03-25 | E-GEOD-38960 | biostudies-arrayexpress

Estrogen-responsive Estrogen Receptor alpha binding sites in MCF-7 by ChIP-seq

2012-12-17 | GSE34759 | GEO

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

Expression data from MCF-7 cells stimulated by Estrogen or IGF-I

Project description:Although estrogen receptor (ER) and insulin-like growth factor (IGF) signaling are important for normal mammary development and breast cancer, cross-talk between these pathways, particularly at the level of gene transcription, remains poorly understood. We performed microarray analysis on MCF-7 breast cancer cells treated with estradiol (E2) or IGF-I for 3hr or 24hr. IGF-I regulated mRNA of 5-10-fold more genes than estradiol, and many genes were co-regulated by both ligands. Importantly, expression of these co-regulated genes correlated with poor prognosis of human breast cancer. Closer examination revealed enrichment of repressed transcripts. Interestingly, a number of potential tumor suppressors were down-regulated by IGF-I and estradiol. In fact, BLNK, one of the top repressed genes, is a potential growth suppressor in breast cancer cells. Analysis of three down-regulated genes showed that E2-mediated repression occurred independently of IGF-IR, and IGF-I-mediated repression occurred independently of ER. However, repression by IGF-I or estradiol required common downstream kinases. In conclusion, E2 and IGF-I co-regulate a set of genes that affect breast cancer outcome. There is enrichment of repressed transcripts, and the down-regulation is independent at the receptor level. This may be important clinically, as tumors with active ER and IGF-IR signaling may require co-targeting of both pathways. KEYWORDS: multiple group comparison Microarray analysis on MCF-7 breast cancer cells treated with estradiol (E2) or IGF-I for 3hr or 24hr.

2011-05-09 | E-GEOD-26834 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data