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High content analysis of estrogen receptor activity: a mechanism-driven approach to compound testing

ABSTRACT: Analysis of the genome-wide response of the ER:PRL-HeLa cell line to treatment with estrogen receptor ligands estradiol, 4H-tamoxifen and bisphenol-A.

ORGANISM(S): Homo sapiens

PROVIDER: GSE22941 | GEO | 2011/07/14

SECONDARY ACCESSION(S): PRJNA127781

REPOSITORIES: GEO

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High content analysis of estrogen receptor activity: a mechanism-driven approach to compound testing

Project description:Analysis of the genome-wide response of the ER:PRL-HeLa cell line to treatment with estrogen receptor ligands estradiol, 4H-tamoxifen and bisphenol-A. Total RNA obtained from ER:PRL-HeLa cells treated for 4 hours with estradiol, 4H-tamoxifen or bisphenol -A is compared to vehicle treated controls

2011-07-13 | E-GEOD-22941 | biostudies-arrayexpress

Effects of Estrogen and Tamoxifen on Ishikawa cells after 24h and 48h

2006-02-01 | GSE3762 | GEO

Effects of Estrogen and Tamoxifen on Ishikawa cells after 24h and 48h

Project description:Treatment with the breast cancer drug tamoxifen confers a risk of developing uterine tumors or other endometrial pathologies. Tamoxifen is a selective estrogen receptor modulator, which demonstrates tissue-specific activity although the mechanisms remain poorly understood. Both estradiol and tamoxifen act as estrogen agonists on the human uterus, and therefore have the potential to promote carcinogenicity. Estradiol and tamoxifen elicit cellular responses via the estrogen receptors (ER), which are involved in multiple signalling pathways. The effects at the molecular level are further influenced by the differential recruitment of co-factors and the presence of specific promoter motifs in target genes. In this study, ER positive (+) Ishikawa cells are used as a model to investigate the overall effect of treatment with either 17b-estradiol or 4-hydroxytamoxifen on the gene expression profiles. Ishikawa cells were serum-starved for 72 hours prior to treatment with 10-8M 17b-estradiol (E2) or 10-6M 4-hydroxytamoxifen (tam) for 24 or 48 hours. Cells were collected for total RNA extraction, and the quality and quantity of the RNA was determined spectrophotometrically. cDNA was prepared from treated (tam or E2) and control (vehicle only) Ishikawa cells, and was both forward and reverse labelled using Cy-3 dUTP/ Cy-5 dUTP and hybridised to oligo microarray slides representing >19,000 human genes (MRC HGMP-RFC). The data were analysed using GenePix Pro 3.0 software (Axon instruments) and statistical analyses applied to select significant gene changes (p<0.05).

2010-07-01 | E-GEOD-3762 | biostudies-arrayexpress

Genome wide analysis of the transcription induced by estrogen and tamoxifen in MCF-7 cells

Project description:The aim of this study is to understand the role of tamoxifen in the transcription regulation of estrogen receptor positive breast cancer cells using GRO-seq experiment. ER positive MCF-7 cells was depleted with lipid hormone in stripped culture media for 4 days, and stimulated with 17-β-estradiol (100nM), 4-OH-tamoxifen (1μM), and the combination of both for 40min. Each treatment was generated in duplicates. Then nuclei was isolated and used as the starting material for GRO-seq experiments. Sequencing data was analyzed and differential gene expression analysis was performed. A rapid induction of gene expression by 17-β-estradiol was observed as previous studies reported. While also a number of genes were also up-regulated by 4-OH-tamoxifen treatment which is considered as a ER antagnist. The data strongly indicate that as a recpressor of estrogen receptor induced transcription, tamoxifen could also perform as a partial agnist at the same time.

2017-06-30 | GSE99508 | GEO

Inflammatory cytokines activate unliganded estrogen receptor and alter the sensitivity of breast cancer cells to tamoxifen

Project description:Genome-wide analyses of the transcriptomes and transcription factor recruitment in estrogen receptor breast cancer cells in response to estradiol, IL1b, or TNFa treatments. Also, the role of inflammatory cytokines on affecting tamoxifen sensitivity is analyzed on a genome-wide scale.

2017-02-20 | GSE67295 | GEO

P21-activated kinase group II small compound inhibitor GNE-2861 perturbs estrogen receptor alpha signaling and restores tamoxifen-sensitivity in breast cancer cells

Project description:Estrogen receptor alpha (ERα) is highly expressed in most breast cancers. Consequently, ERα modulators, such as tamoxifen, are successful in breast cancer treatment, although tamoxifen resistance is commonly observed. While tamoxifen resistance may be caused by altered ERα signaling, the molecular mechanisms regulating ERα signaling and tamoxifen resistance are not entirely clear. Here, we found that PAK4 expression was consistently correlated to poor patient outcome in endocrine treated and tamoxifen-only treated breast cancer patients. Importantly, while PAK4 overexpression promoted tamoxifen resistance in MCF-7 human breast cancer cells, pharmacological treatment with a group II PAK (PAK4, 5, 6) inhibitor, GNE-2861, sensitized tamoxifen resistant MCF-7/LCC2 breast cancer cells to tamoxifen. Mechanistically, we identified a regulatory positive feedback loop, where ERα bound to the PAK4 gene, thereby promoting PAK4 expression, while PAK4 in turn stabilized the ERα protein, activated ERα transcriptional activity and ERα target gene expression. Further, PAK4 phosphorylated ERα-Ser305, a phosphorylation event needed for the PAK4 activation of ERα-dependent transcription. In conclusion, PAK4 may be a suitable target for perturbing ERα signaling and tamoxifen resistance in breast cancer patients.

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Estrogen-driven Prolactin-mediated Gene Expression Networks Hormone Induced Prostatic Dysplasia

Project description:Emerging evidence suggests that estrogen and prolactin (PRL) play a key role in prostate cancer development, yet their relationship and molecular actions in prostate is not well understood. To address this issue, we made the first direct comparison of estrogen and PRL actions in the Noble rat (NBL) prostate dysplasia model. Prostatic dysplasia in lateral prostate (DLP) has been induced by elevated circulating levels of estrogen and PRL in NBL with estrogen (E2)-filled implants, while physiological level of testosterone (T) was maintained with T-filled implants. The effect of estrogen and PRL was studied by using ICI and bromocriptine (Br) as their respective blockers, both can effectively inhibited dysplasia development under T+E2 induction. Transcript expression profile of the four treatment groups (Control, T+E2, T+E2+Br, and T+E2+ICI) has been characterized in this array.

2010-05-09 | E-GEOD-17819 | biostudies-arrayexpress

Estrogen-driven Prolactin-mediated Gene Expression Networks Hormone Induced Prostatic Dysplasia

2010-05-09 | GSE17819 | 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

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

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