The ERβ cistrome in colon cancer
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA630726 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11713423.fastq.gz | Fastqsanger.gz | |||
| SRR11713424.fastq.gz | Fastqsanger.gz | |||
| SRR11713425.fastq.gz | Fastqsanger.gz | |||
| SRR11713426.fastq.gz | Fastqsanger.gz | |||
| SRR11713427.fastq.gz | Fastqsanger.gz |
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Project description:In order to elucidate the mechanism of ERβ in the colon, we validated ERβ antibodies, opti-mized chromatin-immunoprecipitation (ChIP), and performed ChIP-Seq of CRC engineered cell lines re-expressing ERβ.We present for the first time, the cistrome of nuclear receptor ERβ in different CRC cell lines.
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Project description:Inflammation is involved in both initiation and promotion of colorectal cancer (CRC), and patients with inflammatory bowel disease (IBC) have increased risk of developing CRC. Tumor necrosis factor alpha (TNFα) is a cytokine secreted by e.g. macrophages, and this signaling is deregulated in IBD and CRC. TNFα activates the pro-survival transcription factor complex NFκB, which is composed of several subunits including p65 (RELA). We recently characterized the genome-wide transcriptional impact by TNFα in two CRC cell lines, but how p65 binds the chromatin, its cistrome, in colorectal cancer cells has not been explored. We here used p65 chromatin immunoprecipitation followed by sequencing (ChIP-Seq) in HT29 and SW480 cells, and correlated with the transcriptomic impact of TNFα. Further, estrogen receptor beta (ERβ) has anti-inflammatory and anti-tumorigenic effects in colon cells and interacts with NFκB main targets. We have shown that ERβ impacts TNFα signaling in CRC cells and ERβ impacts the P65 cistrome.
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Project description:Estrogen Receptor beta (ERβ) has an essential role in endometriosis progression. However, the role of genomic ERβ in the pathogenesis of endometriosis is not elucidated, yet. To get ERβ cistrome, we employed endometrium specific ERβ overexpression (ERBOE) mouse model by crossing mouse having pCAG promoter-loxPSTOPloxP-ERβ cassette with PRCre knockin mice that Cre recombinase cDNA was inserted into exon 1 of PR gene. Using ERBOE mouse model, we determine ERβ-cistrome in endometriotic lesions and eutopic endometrium of mice with endometriosis.
2019-09-12 | GSE114047 | GEO
Project description:In order to elucidate the mechanism of ERβ in the colon, we validated ERβ antibodies, optimized chromatin-immunoprecipitation (ChIP), and performed ChIP-Seq of CRC engineered cell lines re-expressing ERβ. In addition, we also performed H3K27AC ChIP-Seq to analyse histone marks in presence of ERβ. We present for the first time, the cistrome of nuclear receptor ERβ in different CRC cell lines and corresponding H3K27AC histone marks.
2021-03-05 | GSE166194 | GEO
Project description:ERβ is predominantly expressed in granulosa cells of the ovary, where its important for normal ovarian function and plays a vital role in folliculogenesis. However, the genome wide binding landscape of ERβ in the ovary was not determined and its interaction targets are unknown. To characterize the mechanism of ERβ, we performed ChIP-Seq using endogenous ERβ expression and mapped the cistrome of ERβ in the ovary using a validated antibody.
2023-11-17 | GSE203391 | GEO
Project description:The C4-12/Flag.ERβ cell line which stably expressed Flag.ERβ is used to study ERβ genomic functions without ERα interference. Mapping ERβ binding sites in these cells reveals ERβ unique distribution and motif enrichment patterns. Accompanying our mapping results, nascent RNA profiling is performed on cells at the same treatment time. The combined results allow the identification of ERβ target genes. Gene ontology analysis reveals that ERβ targets are enriched in differentiation, development and apoptosis. Concurrently, E2 treatment suppresses proliferation in these cells. Within ERβ binding sites, while the most prevalent binding motif is the canonical ERE, motifs of known ER interactors are also enriched in ERβ binding sites. Moreover, among enriched binding motifs are those of GFI, REST and EBF1, which are unique to ERβ binding sites in these cells. Further characterization confirms the association between EBF1 and the estrogen receptors, which favors the N-terminal region of the receptor. Furthermore, EBF1 negatively regulates ERs at the protein level. In summary, by studying ERβ genomic functions in our cell model, we confirm the anti-proliferative role of ERβ and discover the novel cross talk of ERβ with EBF1 which has various implications in normal physiology. C4-12/Flag.ERβ cells were treated with 10nM E2 for 1 hour then crosslinked with 1% formaldehyde; EtOH treatment was used as control. Crosslinked samples were processed for ChIP-seq and sequenced with Illumina Genome Analyzer II and aligned to hg18. QuEST was used as the peak-calling software, using default parameters recommended to analyze transcription factor ChIP-seq data. The entire ChIP-seq process was performed once on each sample (Vehicle or E2-treated).
2013-06-21 | E-GEOD-48096 | biostudies-arrayexpress
Project description:The C4-12/Flag.ERβ cell line which stably expressed Flag.ERβ is used to study ERβ genomic functions without ERα interference. Mapping ERβ binding sites in these cells reveals ERβ unique distribution and motif enrichment patterns. Accompanying our mapping results, nascent RNA profiling is performed on cells at the same treatment time. The combined results allow the identification of ERβ target genes. Gene ontology analysis reveals that ERβ targets are enriched in differentiation, development and apoptosis. Concurrently, E2 treatment suppresses proliferation in these cells. Within ERβ binding sites, while the most prevalent binding motif is the canonical ERE, motifs of known ER interactors are also enriched in ERβ binding sites. Moreover, among enriched binding motifs are those of GFI, REST and EBF1, which are unique to ERβ binding sites in these cells. Further characterization confirms the association between EBF1 and the estrogen receptors, which favors the N-terminal region of the receptor. Furthermore, EBF1 negatively regulates ERs at the protein level. In summary, by studying ERβ genomic functions in our cell model, we confirm the anti-proliferative role of ERβ and discover the novel cross talk of ERβ with EBF1 which has various implications in normal physiology.
2013-06-21 | GSE48096 | GEO
Project description:Breast cancer (BC) is the second most common type of cancer in women and one of the leading causes of cancer-related deaths worldwide. BC classification is based on the detection of three main histological markers: estrogen receptor alpha (ERα), progesterone receptor (PR) and the amplification of epidermal growth factor receptor 2 (HER2/neu). A specific BC subtype, named triple-negative BC (TNBC), lacks the aforementioned markers but a fraction of them express the estrogen receptor beta (ERβ). To investigate the functional role of ERβ in these tumors, interaction proteomics coupled to mass spectrometry (MS) was applied to deeply characterize the nuclear interactors partners in MDA-MD-468 and HCC1806 TNBC cells.
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