ChIP-seq of ER in MCF-7 cells post ligand treatment
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA483772 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7629150.fastq.gz | Fastqsanger.gz | |||
| SRR7629151.fastq.gz | Fastqsanger.gz | |||
| SRR7629145.fastq.gz | Fastqsanger.gz | |||
| SRR7629146.fastq.gz | Fastqsanger.gz | |||
| SRR7629147.fastq.gz | Fastqsanger.gz |
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Project description:Goal: study the impact of estrogen receptor (ER) ligands on ER binding to chromatin in MCF-7 cells Methods: ER Chromatin Immunoprecipitation and Sequencing (ChIP-seq) Results: All tested ligands increase binding of ER onto DNA in MCF-7 breast cells. These ligands thus promote an association between ER and DNA, irrespective of their mode of action: selective ER modulator (SERM) 4-OH tamoxifen, and selective ER degraders (SERD) fulvestrant and GDC-0927.
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Project description:Goal: study the impact of estrogen receptor ligands on chromatin accessibility in MCF-7 cells Methods: Assay for Transposase-Accessible Chromatin using Sequencing (ATAC-Seq) Results: Ligand 4-OH tamoxifen, a selective ER modulator (SERM), significantly alters chromatin accessibility and partially mimics the effect of natural ligand E2 on chromatin accessibility in MCF-7 breast cells. Selective ER degraders (SERD) fulvestrant and GDC-0927 on the other hand have very little impact on chromatin accessibility.
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Project description:ATAC-seq of MCF-7 cells post ligand treatment
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Project description:Goal: study the impact of estrogen receptor ligands on gene expression in HR+ breast cancer cells Methods: RNA sequencing Results: Ligand 4-OH tamoxifen, a selective ER modulator (SERM), promotes transcriptional activation of ER and mimics the transcriptional effect of natural ligand E2 for a subset of ER target genes, consistently across the seven breast cell lines (MCF-7, HCC1500, MDA-MB-330, EFM-19, T-47D, BT-474, and CAMA-1). Selective ER degraders (SERD) fulvestrant and GDC-0927 on the other hand do not induce, or induce very weakly the expression of ER target genes. The effect of GDC-0810 depends on the cellular context.
2019-07-25 | GSE117942 | GEO
Project description:Goal: study the impact of estrogen receptor ligands on gene expression in HR+ breast cancer cells Methods: RNA sequencing Results: Ligand 4-OH tamoxifen, a selective ER modulator (SERM), promotes transcriptional activation of ER and mimics the transcriptional effect of natural ligand E2 for a subset of ER target genes, consistently across the seven breast cell lines (MDA-MB-134 VI, MDA-MB-330, EFM-19, T-47D, and BT-474). Selective ER degraders (SERD) fulvestrant and GDC-0927 on the other hand do not induce, or induce very weakly the expression of ER target genes. The effect of GDC-0810 depends on the cellular context.
2019-07-25 | GSE128911 | GEO
Project description:We report YAP could repress ER positive breat cancer progression and MST inhibitor treat MCF-7 cells were used as the model.
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Project description:Estrogen receptor M-NM-1 (ER), a member of the nuclear hormone receptor superfamily, regulates transcriptional activity by ligand-dependent recruitment of cofactors which, in turn, locally alter chromatin structure. It is generally believed that co-factor activity at target promoters leads to a more open, transcriptionally permissive chromatin structure, however, these mechanisms remain to be fully established. Peptidylarginine deiminases (PADIs) catalyze the conversion of positively charged arginine and methylarginine residues to neutrally charged citrulline and this activity has been linked to the gene regulation. Here, we found that PADI2 citrullinate H3 Arginine 26 (H3R26) in vitro and, using a specific H3R26 citrulline (H3Cit26) antibody, we demonstrate that H3Cit26 occurs in vivo following 17M-NM-2-estradiol (E2) stimulation and this unique and pronounced global activation of H3Cit26 is ER-dependent. Using a mammalian-based promoter chromosomal array system, we observed that citrullination at H3R26 is robust and co-localizes with ER at decondensed chromatin loci. Additionally, this histone modification is specifically enriched at ER bound regions of target promoters, forming a permissive chromatin environment for gene transactivation. Interestingly, we have shown in a reciprocal way, that either depletion of PADI2 or inhibition of ER not only dramatically abolished E2-induced activation of H3Cit26 on gene promoters but also affect ER recruitment. Collectively, our results demonstrate that citrullination of H3R26 by PADI2 following estrogen stimulation plays a role in ER target gene activation, likely via decondensation of the local chromatin architecture. Two H3Cit26 ChIP-chip biological replicates under vehicle treatment and two H3Cit26 ChIP-chip biological replicates under E2 stimulation from MCF-7 human breast cancer cells are included.
2012-09-04 | E-GEOD-32599 | biostudies-arrayexpress
Project description:RNA-seq of breast cancer cell lines post ligand treatment II
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Project description:RNA-seq of breast cancer cell lines post ligand treatment I
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Project description:Quantitative phosphoproteome and transcriptome analysis of ligand-stimulated MCF-7 human breast cancer cells was performed to understand the mechanisms of tamoxifen resistance at a systems level. Phosphoproteome data revealed that wild type (WT) cells were more enriched with phospho-proteins than tamoxifen-resistant (TamR) cells after stimulation with ligands. Surprisingly, decreased phosphorylation after ligand perturbation was more common than increased phosphorylation. In particular, 17beta-estradiol (E2) induced down-regulation in WT cells at a very high rate. E2 and the ErbB ligand, heregulin (HRG) induced almost equal numbers of up-regulated phospho-proteins in WT cells. Pathway and motif activity analyses using transcriptome data additionally suggested that deregulated activation of GSK3B?(glycogen synthase kinase 3 beta) and MAPK1/3 signaling might be associated with altered activation of CREB and AP-1 transcription factors in TamR cells and this hypothesis was validated by reporter assays. An examination of clinical samples revealed that, inhibitory phosphorylation of GSK3B at serine 9 was significantly lower in tamoxifen-treated breast cancer patients that eventually had relapses, implying that activation of GSK3B may be associated with the tamoxifen resistant phenotype. Thus, the combined phosphoproteome and transcriptome dataset analyses revealed distinct signal-transcription programs in tumor cells and provided a novel molecular target to understand tamoxifen resistance. The MCF-7 human breast cancer cell line and tamoxifen-resistant MCF-7 cells were stimulated by the growth hormone heregulin (HRG) or 17beta-estradiol (E2) in the presence or absence of tamoxifen. Control was set as non-treated cells.
2010-11-03 | E-GEOD-21618 | biostudies-arrayexpress