Ontology highlight
ABSTRACT:
PROVIDER: PRJNA126941 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR043438.fastq.gz | Fastqsanger.gz | |||
| SRR043439.fastq.gz | Fastqsanger.gz | |||
| SRR043440.fastq.gz | Fastqsanger.gz | |||
| SRR043441.fastq.gz | Fastqsanger.gz |
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Project description:This SuperSeries is composed of the following subset Series: GSE21769: Genome wide expression analysis of ER alpha and beta with or without E2 treatment in U2OS cell line. GSE21770: Genome-wide maps of ER beta binding sites in U2OS cells Refer to individual Series
2010-05-11 | E-GEOD-21790 | biostudies-arrayexpress
Project description:Estrogen receptor beta (ERbeta) has potent anti-proliferative and anti-inflammatory properties, suggesting that ER beta-selective agonists might be a new class of therapeutic and chemopreventative agents. To understand how ER beta regulates genes, we identified genes regulated by the unliganded and liganded forms of ER alpha and ER beta in U2OS cells. Microarray data demonstrated that virtually no gene regulation occurred with unliganded ER alpha, whereas many genes were regulated by estradiol (E2). These results demonstrate ER alpha requires a ligand to regulate a single class of genes. In contrast, ER beta regulated three classes of genes. Class I genes were regulated primarily by unliganded ER beta. Class II genes were regulated only with E2, whereas Class III genes were regulated by both unliganded ER beta and E2. There were 453 Class I genes, 258 Class II genes and 83 Class III genes. To explore the mechanism whereby ER beta regulates different classes of genes ChIP-seq was performed to identify ER beta binding sites and adjacent transcription factor motifs in regulated genes. AP1 binding sites were more enriched in Class I genes, whereas ERE, NFKB1 and SP1 sites were more enriched in class II genes. ER beta bound to all three classes of genes demonstrating that ER beta binding is not responsible for differential regulation of genes by unliganded and liganded ER beta. The coactivator, NCOA2 was differentially recruited to several target genes. Our findings indicate that the unliganded and liganded forms of ER beta regulate three classes of genes by interacting with different transcription factors and coactivators. Examination of ER beta binding sites in U2OS cells with or without E2 treatment
2010-05-12 | E-GEOD-21770 | biostudies-arrayexpress
Project description:Estrogen receptorï? beta (ER beta) has potent anti-proliferative and anti-inflammatory properties, suggesting that ER beta-selective agonists might be a new class of therapeutic and chemopreventative agents. To understand how ER beta regulates genes, we identified genes regulated by the unliganded and liganded forms of ER alpha and ER beta in U2OS cells. Microarray data demonstrated that virtually no gene regulation occurred with unliganded ER alpha, whereas many genes were regulated by estradiol (E2). These results demonstrate ER alpha requires a ligand to regulate a single class of genes. In contrast, ER beta regulated three classes of genes. Class I genes were regulated primarily by unliganded ER beta. Class II genes were regulated only with E2, whereas Class III genes were regulated by both unliganded ER beta and E2. There were 453 Class I genes, 258 Class II genes and 83 Class III genes. To explore the mechanism whereby ER beta regulates different classes of genes ChIP-seq was performed to identify ER beta binding sites and adjacent transcription factor motifs in regulated genes. AP1 binding sites were more enriched in Class I genes, whereas ERE, NFKB1 and SP1 sites were more enriched in class II genes. ER beta bound to all three classes of genes demonstrating that ER beta binding is not responsible for differential regulation of genes by unliganded and liganded ER beta. The coactivator, NCOA2 was differentially recruited to several target genes. Our findings indicate that the unliganded and liganded forms of ER beta regulate three classes of genes by interacting with different transcription factors and coactivators. U2OS cell lines are stably transfected with a doxycycline-inducible ER alpha or beta. 18 samples are analyzed with triplicate for each of the 6 conditions. The 6 conditions include ER alpha transfected without doxycycline added, ER alpha transfected with doxycycline added, ER alpha transfected with doxycycline added and E2 treatment, ER beta transfected without doxycycline added, ER beta transfected with doxycycline added, and ER beta transfected with doxycycline added and E2 treatment.
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Project description:Genome wide expression analysis of ER alpha and beta with or without E2 treatment in U2OS cell line.
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Project description:We have utilized ChIPseq to identify the ER-beta cistrome in ER-beta expressing MDA-MB-231 triple negative breast cancer cells. ER-beta has been identified as a tumor suppressor in breast cancer and recent reports have demonstrated that ER-beta protein is detectable at moderate to high levels in approximately 30% of triple negative breast tumors. Increased expression of ER-beta in triple negative breast cancer has also been reported to be associated with improved recurrence-free survival. Treatment of ER-beta expressing triple negative breast cancer cells with estrogen, or the ER-beta selective agonist, LY500307, results in decreased cell proliferation, invasion and migration. To begin to identify the molecular mechanisms by which ER-beta elicits tumor suppressive effects in triple negative breast cancer, we performed ChIPseq studies and identified the genome-wide binding sites for ER-beta following exposure to 1nM estrogen or 10nM LY500307 for 3 hours. Over 28,000 and 10,000 unique ER-beta binding sites were identifed in response to these two ligands respectively. The top transcription factor motifs identified under both treatment conditions were estrogen response elements and AP1 response elements. The majority of ER-beta binding sites were found at enhancer regions located within introns or intergenic chromatin regions followed by gene promoters.
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Project description:Estrogen receptor beta (ERbeta) has potent anti-proliferative and anti-inflammatory properties, suggesting that ER beta-selective agonists might be a new class of therapeutic and chemopreventative agents. To understand how ER beta regulates genes, we identified genes regulated by the unliganded and liganded forms of ER alpha and ER beta in U2OS cells. Microarray data demonstrated that virtually no gene regulation occurred with unliganded ER alpha, whereas many genes were regulated by estradiol (E2). These results demonstrate ER alpha requires a ligand to regulate a single class of genes. In contrast, ER beta regulated three classes of genes. Class I genes were regulated primarily by unliganded ER beta. Class II genes were regulated only with E2, whereas Class III genes were regulated by both unliganded ER beta and E2. There were 453 Class I genes, 258 Class II genes and 83 Class III genes. To explore the mechanism whereby ER beta regulates different classes of genes ChIP-seq was performed to identify ER beta binding sites and adjacent transcription factor motifs in regulated genes. AP1 binding sites were more enriched in Class I genes, whereas ERE, NFKB1 and SP1 sites were more enriched in class II genes. ER beta bound to all three classes of genes demonstrating that ER beta binding is not responsible for differential regulation of genes by unliganded and liganded ER beta. The coactivator, NCOA2 was differentially recruited to several target genes. Our findings indicate that the unliganded and liganded forms of ER beta regulate three classes of genes by interacting with different transcription factors and coactivators.
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