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BORIS knockdown in colorectal cancer cells HCT116 and Caco-2

ABSTRACT: BORIS expresses abnormally in colorectal cancer cells. Both the expression and the copy number of BORIS are remarkably higher in colorectal cancer cells than in normal colon or rectal cells. BORIS is potential diagnosis, prognosis or therapeutic target for colorectal cancer. To expand our view of the signaling pathway related with BORIS, altered gene expression by BORIS knockdown was assessed by microarray assay. To study the gene regulation by BORIS knockdown, microarray assay was applied to screen the gene expression regulated by BORIS siRNA in colorectal cancer cells HCT116 and Caco-2

ORGANISM(S): Homo sapiens

PROVIDER: GSE86172 | GEO | 2018/07/01

REPOSITORIES: GEO

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Homo sapiens

Project description:BORIS knockdown in colorectal cancer cells HCT116 and Caco-2

| PRJNA340459 | ENA

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

Gene expression profile of colorectal cancer cell Caco-2 after OCC-1 knockdown

Project description:OCC-1 is one of the earliest annotated long noncoding RNAs (lncRNAs) in colorectal cancer (CRC). In our study, we found that knockdown of OCC-1 by shRNAs promotes CRC cell growth both in vitro and in vivo. To gain insight into the molecular function of OCC-1, we profiled the gene expression of Caco-2 cells after OCC-1 knockdown by microarray.

2018-03-11 | GSE108816 | GEO

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.

2019-07-31 | GSE130163 | GEO

Comparative analyses of CTCF and BORIS occupancies uncover two distinct classes of CTCF binding genomic regions

Project description:CTCF and BORIS (CTCFL), two paralogous mammalian proteins sharing nearly identical DNA binding domains, are thought to function in mutually exclusive manners in DNA binding and transcriptional regulation. Here we show that these two proteins co-occupy a specific subset of regulatory elements consisting of clustered CTCF binding motifs (termed 2xCTSes). BORIS occupancy at 2xCTSes is largely invariant in BORIS-positive cancer cells, with the genomic pattern recapitulating the germline-specific BORIS binding to chromatin. In contrast to the single-motif CTCF target sites (1xCTSes), the 2xCTS elements are preferentially found at active promoters and enhancers, both in cancer and germ cells. 2xCTSes are also enriched in genomic regions that escape histone to protamine replacement in human and mouse sperm. Depletion of BORIS gene leads to altered transcription of a large number of genes and the differentiation of K562 cells, while the ectopic expression of this CTCF paralog leads to specific changes in transcription in MCF7 cells. In summary, we discover two functionally and structurally different classes of CTCF binding regions, 2xCTSes and 1xCTSes, revealed by their predisposition to bind BORIS. We propose that 2xCTSes play key roles in the transcriptional program of cancer and germ cells Genome-wide mapping of CTCF and BORIS occupancies in both germ and cancer cells. ChIP-seq and expression profiling by high throughput sequencing

2015-07-23 | E-GEOD-70764 | biostudies-arrayexpress

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

Effect of BORIS depletion on transcriptome of breast cancer cell line MCF7

Project description:Transcriptome analysis of BORIS depleted MCF7 cells To delineate the alternative pre-mRNA splicing program mediated by BORIS in breast cancer cells, BORIS was depleted in MCF7 using shRNA, and the resultant changes in alternative pre-mRNA splicing and mRNA expression pattern was profiled using Affymetrix Human Transcriptome 2.0 Array

2017-09-25 | GSE81001 | GEO

A Gene Expression Signature for Chemoradiosensitivity of Colorectal Cancer Cells

Project description:In this study, we use cancer cell lines to investigate the molecular differences between resistant and responsive colorectal cancer cells. Since the treatment of patients with locally advanced rectal cancers involves chemoradiotherapy (CT/RT), we specifically implemented an in vitro protocol that mimics this clinical setting. We anticipate that this analysis will unveil relevant pathways underlying the resistance of rectal cancers to CT/RT, and enable the identification of novel therapeutic target genes. 12 colorectal cancer (CRC) cell lines were obtained from the ATCC, and cultured in the respective tissue culture medium as recommended by the ATCC: Caco-2, HT-29, LS411N, LS513, LS1034, SW403, SW480, SW620, SW837, SW1116, SW1463, and WiDr. For each cell line, RNA was independently isolated at three different passages, and hybridized to a gene expression array. Accordingly, there are three biological triplicates per cell line. Additionally, SW480 (triplicate), SW837 (triplicate), and Caco-2 (duplicate) were cultured in RPMI.

2011-02-10 | E-GEOD-20298 | biostudies-arrayexpress

The combined action of CTCF and its testis-specific paralog BORIS is essential for spermatogenesis

Project description:CTCF is a key organizer of the 3D genome. Its specialized paralog, BORIS, heterodimerizes with CTCF but is expressed only in male germ cells and in cancer states. Unexpectedly, BORIS-null mice have only minimal germ cell defects. To understand the CTCF-BORIS relationship, mouse models with varied CTCF and BORIS levels were generated. Whereas Ctcf+/+Boris+/+, Ctcf+/-Boris+/+, and Ctcf+/+Boris-/- males are fertile, Ctcf+/-Boris-/- (Compound Mutant; CM) males are sterile. Testes with combined depletion of both CTCF and BORIS show reduced size, defective meiotic recombination, increased apoptosis, and malformed spermatozoa. Although CM germ cells exhibit only 25% of CTCF WT expression, chromatin binding of CTCF is preferentially lost from CTCF-BORIS heterodimeric sites. Furthermore, CM testes lose the expression of a large number of spermatogenesis genes and gain the expression of developmentally inappropriate genes that are “toxic” to fertility. Thus, a combined action of CTCF and BORIS is required to both repress pre-meiotic genes and activate post-meiotic genes for a complete spermatogenesis program.

2021-04-22 | GSE154249 | GEO

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