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Homo sapiens

ABSTRACT: Cis-Regulatory Circuits Regulating NEK6 Kinase Overexpression in Transformed B Cells Are Super-Enhancer-Independent (4C-seq)

PROVIDER: PRJNA344335 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4293200.fastq.gz	Fastqsanger.gz
	SRR4293191.fastq.gz	Fastqsanger.gz
	SRR4293201.fastq.gz	Fastqsanger.gz
	SRR4293192.fastq.gz	Fastqsanger.gz
	SRR4293202.fastq.gz	Fastqsanger.gz

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Similar Datasets

Cis-Regulatory Circuits Regulating NEK6 Kinase Overexpression in Transformed B Cells Are Super-Enhancer-Independent

Project description:Cis-Regulatory Circuits Regulating NEK6 Kinase Overexpression in Transformed B Cells Are Super-Enhancer-Independent

| PRJNA344333 | ENA

Homo sapiens

Project description:Cis-Regulatory Circuits Regulating NEK6 Kinase Overexpression in Transformed B Cells Are Super-Enhancer-Independent (RNA-seq)

| PRJNA344336 | ENA

Cis-Regulatory Circuits Regulating NEK6 Kinase Overexpression in Transformed B Cells Are Super-Enhancer-Independent (4C-seq)

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

Cis-Regulatory Circuits Regulating NEK6 Kinase Overexpression in Transformed B Cells Are Super-Enhancer-Independent (RNA-seq)

2017-02-23 | GSE87320 | GEO

ena-DATASET-ErasmusMC-hema-18-12-2020-23:56:29:352-90 - samples

Project description:The viewpoints used in the 4C-seq data were either the EVI1 promoter or the MYC super-enhancer

| EGAD00001006818 | EGA

SREBF1 coordinates with master transcription factors in regulating lipid metabolism and cancer-promoting pathways in squamous cell carcinoma [4C]

Project description:To determine whether a TP63/KLF5-regulated super-enhancer region can impact SREBF1 transcription, circularized chromosome conformation capture (4C) assays were performed. 4C assays identified complex, extensive interactions between the SREBF1 promoter and the super-enhancer region Moreover, these DNA-DNA contacts were strictly confined within the super-enhancer region, highlighting the specificity of chromatin interactions

2021-06-26 | GSE178923 | GEO

Defining super-enhancer landscape in triple-negative breast cancer by multiomic profiling

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 |

Chromatin interactions involving super-enhancers associate with specific expression patterns of target genes

Project description:Super-enhancers may regulate target genes through chromatin looping. We connected super-enhancers in the K562 chronic myelogenous leukemia cell line with chromatin interactions identified from Chromatin Interaction Analysis with Paired-End Tag (ChIA-PET) data. Gene expression at proximal elements that are connected with distal super-enhancers showed significantly higher cell-type specificity than at proximal elements connected with other elements or not involved in interaction. 4C and Episwitch analysis of chromatin interactions showed that certain chromatin interactions are cell-specific, but others are more general. While super-enhancers upstream of c-MYC at the MYC-335 element can be found in other cancers, only super-enhancers downstream of c-MYC can be found in K562. 4C analysis of the c-MYC promoter revealed no chromatin interactions that are directed upstream of c-MYC, but only downstream of c-MYC, in the PVT1 long non-coding RNA gene. Cell-specific usage of super-enhancers could explain why the MYC-335 element that is associated with many solid cancers such as colorectal cancer and breast cancer, but not with leukemia. Surprisingly, we found that a chromatin interaction between c-MYC and a c-MYC super-enhancer is lost in chronic myelogenous leukemia patient blood as compared with blood from individuals without the disease through Oxford Biodynamicsâ?? Episwitch analysis. These results provide evidence for fine-tuning of expression patterns, such as cell-specific regulation of target genes by distal super-enhancers through chromatin interactions and an association between chromatin interactions and disease, and highlight that super-enhancers are more complex than previously described. Examination of several chromatin interactions involving super-enhancers using 4C-Seq and Episwitch (TM)

2017-05-01 | E-GEOD-77125 | biostudies-arrayexpress

Epstein-Barr Virus oncoprotein super-enhancers control B cell growth

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

ChIP-seq for the identification of enhancer and super enhancers in Acute Myeloid Leukemia cells with a 3q-aberration

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

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