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Chip-seq analysis of meiotic Cohesin complexes (mei-Cohesins) subunits, CTCF, and BORIS/CTCFL in Macaca fascicularis testis

ABSTRACT: Chip-seq analysis of meiotic Cohesin complexes (mei-Cohesins) subunits, CTCF, and BORIS/CTCFL in Macaca fascicularis testis

PROVIDER: PRJNA483999 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14019000_1.fastq.gz	Fastqsanger.gz
	SRR14019000_2.fastq.gz	Fastqsanger.gz
	SRR14019001_1.fastq.gz	Fastqsanger.gz
	SRR14019001_2.fastq.gz	Fastqsanger.gz
	SRR14019002_1.fastq.gz	Fastqsanger.gz

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Chip-seq analysis of meiotic Cohesin complexes (mei-Cohesins) subunits, CTCF, and BORIS/CTCFL in Macaca fascicularis testis

Project description:The study involved chromatin IP analyzed by high-throughput sequencing analysis using purifird germ cells from M. fascucularis testis M. fascicularis is a monkey with non-seasonal male germ cells production, and the most popular primate for preclinical animal studies. The goal of the study was to investigate the epigenome of M. fscicularis testis with respect to mei-Cohesin complexes, CTCF and BORIS

2022-09-30 | GSE118006 | GEO

RNA-seq analysis of BORIS/CTCFL knockdown in K562 cell line

Project description:The study involved transcriptome analysis using RNA-seq knockdown of BORIS/CTCFL gene expression in K652 cancer cell line using inducible shRNA. The K562 cell line is the only cancer cell line that is known to be dependent on BORIS for proliferation and self-renewal of stemness. The goal of the study was to investigate the early/immediate transcriptional response to BORIS downregulation (over 10-fold reduction in protein level) using an inducible shRNA.

2017-09-25 | GSE99825 | GEO

Small RNA (sRNA) RNA-seq analysis of BORIS/CTCFL knockdown in K562 cell line

Project description:The study involved transcriptome analysis using RNA-seq knockdown of BORIS/CTCFL gene expression in K652 cancer cell line using inducible shRNA. The K562 cell line is the only cancer cell line that is known to be dependent on BORIS for proliferation and self-renewal of stemness. The goal of the study was to investigate the early/immediate small RNA transcriptional response to BORIS downregulation (over 10-fold reduction in protein level) using an inducible shRNA.

2017-09-25 | GSE99899 | GEO

Human tandem repeat custom custom microarray ChIP-chip with anti-CTCF and anti-CTCFL/BORIS antibodies in K562 cell line

Project description:A common aberration in cancer is the activation of germline-specific proteins. The DNA-binding proteins among them generate novel chromatin states, not found in normal cells. The chromatin architecture protein CTCF has a germline-specific paralog BORIS/CTCFL, which is often erroneously activated in cancers. Another common feature of malignancies is the changed expression and epigenetic states of genomic repeats. The investigation of BORIS and CTCF binding to DNA repeats in cancer cell lines by ChIP-chip revealed three classes: elements cohabited by BORIS and CTCF, CTCF-bound only, or BORIS-only.

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Expression data from ovarian cancer cell line OVCAR3 following Knockdown or Knockout of BORIS (CTCFL)

Project description:The identification of prognostic biomarkers is a priority for patients suffering from high-grade serous ovarian cancer (SOC), which accounts for >70% of ovarian cancer (OC) deaths. Meanwhile borderline ovarian cancer (BOC) is a low malignancy tumor and usually patients undergo surgery with low probabilities of recurrence. However, SOC remains the most lethal neoplasm due to the lack of biomarkers for early diagnosis and prognosis. In this regard BORIS (CTCFL), a CTCF paralog, is a promising cancer biomarker that is overexpressed and controls transcription in several cancer types, mainly in OC. Studies suggest that BORIS has an important function in OC by altering gene expression, but the effect and extent to which BORIS influences transcription in OC from a genome-wide perspective is unclear. Here we sought to identify BORIS target genes in an OC cell line (OVCAR3) with potential biomarker use in OC tumor samples. To achieve this, we performed in vitro knockout (KO) and knockdown (KD) experiments of BORIS in OVCAR3 cell line followed by expression microarrays and bioinformatics network enrichment analysis to identify relevant BORIS target genes.

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ChIP-seq analysis of subunits of meiotic cohesin complexes (mei-Cohesins) in transgenic human cancer cell lines

Project description:The study involved chromatin IP analyzed by high-throughput sequencing analysis using stable transgenic human cancer cell lines, which express Tet-inducible combinations of mei-cohesin subunits. The following individual genes and combinations of mei-cohesin subunits were expressed in human cells : STAG3, SMC1beta, STAG3+SMC1beta+REC8, and STAG3+SMC1beta+RAD21L The goal of the study was to investigate the epigenomic properties of somatic cells in response to the induction of mei-cohesin subunits using Tet-on inducible transgenes activated by an rtTA transgene and doxycicline.

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BORIS/CTCFL epigenetically reprograms clustered CTCF binding sites into alternative transcriptional start sites.

Project description:Pervasive usage of alternative promoters leads to deregulation of gene expression in carcinogenesis and may drive the emergence of new genes in spermatogenesis. However, little is known regarding the mechanisms underpinning the activation of alternative promoters. In our present study, we uncovered a novel mechanism by which alternative cancer-testis-specific transcription is activated from the intergenic and intronic clustered CTCF binding sites, which are transcriptionally inert in normal somatic cells. BORIS/CTCFL, a paralog of CTCF with cancer-testis-specific expression forms a heterodimer with CTCF at the clustered binding sites thus triggering epigenetic reprogramming of these sites into units of active transcription. BORIS binding to CTCF sites leads to the recruitment of chromatin-remodeling factor SRCAP, with subsequent replacement of H2A histone with H2A.Z, therefore creating a more relaxed chromatin state in the nucleosomes flanking the clustered binding sites. This facilitates opening of chromatin beyond CTCF/BORIS binding sites and paves the way to the recruitment of multiple additional transcription factors, thereby activating transcription from a given binding site. We demonstrate that the CTCF binding sites, epigenetically reprogrammed by ectopic BORIS expression can drive the expression of cancer-testis genes, long-noncoding RNAs, retro-pseudogenes, and dormant transposable elements harbored by activated long transcripts. Taking together, our results reveal that BORIS functions as a transcription factor that epigenetically reprograms clustered CTCF binding sites into transcriptional start sites, promoting transcription from alternative promoters in both germ cells and cancer cells.

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Ectopic CTCFL/BORIS expression in ovarian cancer precursor cells enhances cellular motility and invasion through GALNT14 and alters CTCF chromatin occupancy

Project description:High-grade serous carcinoma (HGSC) is the most aggressive and predominant form of epithelial ovarian cancer and the leading cause of gynecological cancer death. We have previously shown that CTCFL (also known as BORIS, Brother of the Regulator of Imprinted Sites) is expressed in a large proportion of ovarian cancers, which is associated with global and promoter-specific DNA hypomethylation, advanced tumor stage, and poor prognosis. To explore its functional role in HGSC, we expressed BORIS in human fallopian tube secretory epithelial cells (FTSEC), the presumptive cell of origin for HGSC. BORIS-expressing cells exhibited increased motility and invasion, and BORIS expression was associated with alterations in several cancer-associated gene expression networks, including fatty acid metabolism, TNF signaling, cell migration, and ECM-receptor interactions. Importantly, GALNT14, a glycosyltransferase gene previously implicated in cancer cell migration and invasion, was highly induced by BORIS, and GALNT14 knockdown significantly abrogated BORIS-induced cell motility and invasion. In addition, in silico analyses provided evidence for BORIS and GALNT14 co-expression in several human cancers. Finally, ChIP-seq demonstrated that expression of BORIS in FTSEC cells was associated with de novo and enhanced binding of CTCF at hundreds of loci, many of which correlated with activation of transcription at target genes, including GALNT14. Taken together, our data indicate that BORIS may promote cell motility and invasion in HGSC via upregulation of GALNT14, and suggests BORIS as a potential therapeutic target in this malignancy.

2019-07-01 | GSE131931 | GEO

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Project description:ChIP-seq analysis of subunits of meiotic cohesin complexes (mei-Cohesins) in transgenic human cancer cell lines

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