Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA344336 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4293190.fastq.gz | Fastqsanger.gz | |||
| SRR4293185.fastq.gz | Fastqsanger.gz | |||
| SRR4293186.fastq.gz | Fastqsanger.gz | |||
| SRR4293187.fastq.gz | Fastqsanger.gz | |||
| SRR4293188.fastq.gz | Fastqsanger.gz |
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Project description:Cis-Regulatory Circuits Regulating NEK6 Kinase Overexpression in Transformed B Cells Are Super-Enhancer-Independent
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Project description:Cis-Regulatory Circuits Regulating NEK6 Kinase Overexpression in Transformed B Cells Are Super-Enhancer-Independent (4C-seq)
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Project description:Alterations in distal regulatory elements that control gene expression underlie many diseases, including cancer. Epigenomic analyses of normal and diseased cells have produced correlative predictions for connections between dysregulated enhancers and target genes involved in pathogenesis. However, with few exceptions, these predicted cis-regulatory circuits remain untested. Here, we dissect cis-regulatory circuits that lead to overexpression of NEK6, a mitosis-associated kinase, in human B cell lymphoma. We find that only a minor subset of predicted enhancers is required for NEK6 expression. Indeed, an annotated super-enhancer is dispensable for NEK6 overexpression and for maintaining the architecture of a B cell-specific regulatory hub. A CTCF cluster serves as a chromatin and architectural boundary to block communication of the NEK6 regulatory hub with neighboring genes. Our findings emphasize that validation of predicted cis-regulatory circuits and super-enhancers is needed to prioritize transcriptional control elements as therapeutic targets.
2017-02-23 | GSE87322 | GEO
Project description:Alterations in distal regulatory elements that control gene expression underlie many diseases, including cancer. Epigenomic analyses of normal and diseased cells have produced correlative predictions for connections between dysregulated enhancers and target genes involved in pathogenesis. However, with few exceptions, these predicted cis-regulatory circuits remain untested. Here, we dissect cis-regulatory circuits that lead to overexpression of NEK6, a mitosis-associated kinase, in human B cell lymphoma. We find that only a minor subset of predicted enhancers is required for NEK6 expression. Indeed, an annotated super-enhancer is dispensable for NEK6 overexpression and for maintaining the architecture of a B cell-specific regulatory hub. A CTCF cluster serves as a chromatin and architectural boundary to block communication of the NEK6 regulatory hub with neighboring genes. Our findings emphasize that validation of predicted cis-regulatory circuits and super-enhancers is needed to prioritize transcriptional control elements as therapeutic targets.
2017-02-23 | GSE87320 | GEO
Project description:Esophageal squamous cell carcinoma (SCC) is frequently diagnosed at advanced stage and associated with poor prognosis. This study aimed to identify differentially expressed genes for further evaluated as biomarkers for predicting survival of the patients. Five paired of cancerous and normal tissues from esophageal SCC patients were subjected to cDNA microarray analysis and one of these differentially expressed genes, NEK6, was further verified in esophageal SCC tissues. The data showed 444 up-regulated genes and 918 down-regulated genes in tumor tissues (2 folds as a cut-off value). qRT-PCR data showed that 20 of 30 (66.7%) increased levels of NEK6 mRNA in cancerous tissues compared to that of distant normal tissues, while immunohistochemical data showed that 49/94 (52.13%) of the archived esophageal SCC tissues expressed higher levels of NEK6 than that of normal tissues. NEK6 expression was associated with depth of tumor invasion (P=0.005), lymph node metastasis (P=0.018), and advanced clinical tumor stages (P=0.004) of these 94 patients. Kaplan Meier curve showed that the overall survival of NEK6-positive patients was much lower than those of NEK6-negative patients (P<0.001). The median survival of NEK6-positive patients was 23 months, whereas the median survival of NEK6-negative patients was 64 months. The cumulative 5-year survival rate of NEK6-positive patients was 14.3% (7/49), whereas the rate of NEK6-negative patients was 64.4% (29/45). Multivariate analysis showed that N classification (P=0.002) and NEK6 expression (P<0.001) were independent predictors for esophageal SCC patients. These data demonstrated that NEK6 expression may serve as an independent prognostic indicator for patients with esophageal SCC.
2013-09-30 | GSE45168 | GEO
Project description:Esophageal squamous cell carcinoma (SCC) is frequently diagnosed at advanced stage and associated with poor prognosis. This study aimed to identify differentially expressed genes for further evaluated as biomarkers for predicting survival of the patients. Five paired of cancerous and normal tissues from esophageal SCC patients were subjected to cDNA microarray analysis and one of these differentially expressed genes, NEK6, was further verified in esophageal SCC tissues. The data showed 444 up-regulated genes and 918 down-regulated genes in tumor tissues (2 folds as a cut-off value). qRT-PCR data showed that 20 of 30 (66.7%) increased levels of NEK6 mRNA in cancerous tissues compared to that of distant normal tissues, while immunohistochemical data showed that 49/94 (52.13%) of the archived esophageal SCC tissues expressed higher levels of NEK6 than that of normal tissues. NEK6 expression was associated with depth of tumor invasion (P=0.005), lymph node metastasis (P=0.018), and advanced clinical tumor stages (P=0.004) of these 94 patients. Kaplan Meier curve showed that the overall survival of NEK6-positive patients was much lower than those of NEK6-negative patients (P<0.001). The median survival of NEK6-positive patients was 23 months, whereas the median survival of NEK6-negative patients was 64 months. The cumulative 5-year survival rate of NEK6-positive patients was 14.3% (7/49), whereas the rate of NEK6-negative patients was 64.4% (29/45). Multivariate analysis showed that N classification (P=0.002) and NEK6 expression (P<0.001) were independent predictors for esophageal SCC patients. These data demonstrated that NEK6 expression may serve as an independent prognostic indicator for patients with esophageal SCC. Gene expression in five paired of cancerous and normal tissues from esophageal SCC patients were measured using Human Genome 4x44K v2 Microarray.
2013-09-30 | E-GEOD-45168 | biostudies-arrayexpress
Project description:Here we apply integrated epigenomic and transcriptomic profiling to uncover super-enhancer heterogeneity between breast cancer subtypes, and provide clinically relevant biological insights towards TNBC. Using CRISPR/Cas9-mediated gene editing, we identify genes that are specifically regulated by TNBC-specific super-enhancers, including FOXC1 and MET, thereby unveiling a mechanism for specific overexpression of the key oncogenes in TNBC. We also identify ANLN as a novel TNBC-specific gene regulated by super-enhancer. Our studies reveal a TNBC-specific epigenomic landscape, contributing to the dysregulated oncogene expression in breast tumorigenesis.
2021-03-04 | PXD024505 |
Project description:Super-enhancers are principal determinants of cell transcription, development, phenotype, and oncogenesis, not yet implicated in host-pathogen interactions. We found four Epstein-Barr virus (EBV) oncoproteins and five EBV-activated NF-M-oM-^AM-+B subunits co-occupying thousand of enhancer sites in EBV-transformed lymphoblastoid cells (LCLs). Of these, 187 had markedly higher and broader histone H3K27ac signals characteristic of super-enhancer formation, and were designated M-bM-^@M-^\EBV super-enhancersM-bM-^@M-^]. EBV super-enhancer associated genes included MYC and BCL2, which enable LCL proliferation and survival. EBV super-enhancers were enriched for specific B cell transcription factor motifs and had high STAT5 and NFAT co-occupancy. EBV super-enhancer associated genes were more highly expressed than other LCL genes. Disruption of EBV super-enhancers by the bromo-domain inhibitor, JQ1, by conditional inactivation of an EBV oncoprotein or NF-M-oM-^AM-+B, decreased MYC or BCL2 gene expression and arrested LCL growth. These findings provide novel insights into the mechanisms by which EBV causes lymphoproliferation and identify opportunities for therapeutic intervention. ChIP-seq was used to define the BRD4 genome-wide landscape in GM12878 lymphoblastoid cells.
2014-11-01 | E-GEOD-62912 | biostudies-arrayexpress
Project description:To infer enhancers and super enhancers in Acute Myeloid Leukemia (AML) Cell lines with a 3q-aberration we determined regions enriched for H3K27AC, H3K4ME3, H3K4ME1, P300, and BRD4 in MOLM1. Additionally we determined regions enriched for P300 and BRD4 in the cell line Mutz3 which also harbors a 3q-aberration. As an control we performed Chip-Seq to determine enrichment for BRD4 in K562, which overexpresses the proto-oncogene EVI1, but has no apparent 3q-aberration. Ultimately, the ChipSeq experiments were utilized to infer which enhancer or super enhancer drives the overexpression of EVI1 in AMLs with a 3q-aberration. Finally, the effect of the compound JQ1 on the inferred super enhancers and the overexpression of EVI1 is tested by treating the cell line MOLM1 for 6 hours and determining the residual binding of BRD4.
2014-04-03 | E-MTAB-2224 | biostudies-arrayexpress
Project description:Many genes determining cell identity are regulated by a set of enhancer elements collectively referred to as super-enhancers. It has been suggested that super-enhancers represent a new class of cis-element, in which the assembly of enhancers confers an emergent property from the extended regulatory domain. To investigate this, we used published criteria to define one of the strongest super-enhancers in mouse erythroid cells – a 24kb region regulating α-globin expression, which comprises five enhancer-like components. Using homologous recombination, we deleted each component of this super-enhancer, singly and in informative combinations, and examined hematologic phenotype, gene expression, chromatin structure and chromosome conformation. Each component behaves independently, in an additive rather than synergistic manner. We conclude that the sub-classification of enhancers is unjustified beyond a description of their strength, which is defined by the number of lineage-specific transcription factors they bind. These findings ask afresh why enhancer-like elements cluster at key genes.
2016-06-02 | GSE78804 | GEO