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ETS Family Transcriptional Regulators Drive Chromatin Dynamics and Malignancy in Squamous Cell Carcinomas (ChIP-Seq II)

ABSTRACT: After characterizing super-enhancer-associated chromatin dynamics accompanied by malignant progression of skin stem cells, we show that ETS family members auto-regulate themselves and a cohort of cancer-associated super-enhancer transcription factors which together are essential for tumor maintenance. Control and ETS2(T72D) super-activated epidermal basal stem cells were FACS-purified for ChIP-sequencing.

ORGANISM(S): Mus musculus

SUBMITTER: Hanseul Yang

PROVIDER: E-GEOD-74867 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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ETS family transcriptional regulators drive chromatin dynamics and malignancy in squamous cell carcinomas.

Yang Hanseul H Schramek Daniel D Adam Rene C RC Keyes Brice E BE Wang Ping P Zheng Deyou D Fuchs Elaine E

eLife 20151121

Tumor-initiating stem cells (SCs) exhibit distinct patterns of transcription factors and gene expression compared to healthy counterparts. Here, we show that dramatic shifts in large open-chromatin domain (super-enhancer) landscapes underlie these differences and reflect tumor microenvironment. By in vivo super-enhancer and transcriptional profiling, we uncover a dynamic cancer-specific epigenetic network selectively enriched for binding motifs of a transcription factor cohort expressed in squam ...[more]

PMID: 26590320

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ETS Family Transcriptional Regulators Drive Chromatin Dynamics and Malignancy in Squamous Cell Carcinomas (ChIP-Seq I)

Project description:After characterizing super-enhancer-associated chromatin dynamics accompanied by malignant progression of skin stem cells, we show that ETS family members auto-regulate themselves and a cohort of cancer-associated super-enhancer transcription factors which together are essential for tumor maintenance. Mouse skin squamouse cell carcinoma (SCC) tumor-initiating stem cells (SCs) were FACS-purified for ChIP-sequencing.

2015-11-22 | E-GEOD-72145 | biostudies-arrayexpress

ETS Family Transcriptional Regulators Drive Chromatin Dynamics and Malignancy in Squamous Cell Carcinomas

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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2015-11-22 | E-GEOD-74868 | biostudies-arrayexpress

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Project description:Proinflammatory stimuli rapidly and globally remodel chromatin landscape, thereby enabling transcriptional responses. Yet, the mechanisms coupling chromatin regulators to the master regulatory inflammatory transcription factor NF-kB remain poorly understood. We report in human endothelial cells (ECs) that activated NF-kB binds to enhancers, provoking a rapid, global redistribution of BRD4 preferentially at super-enhancers, large enhancer domains highly bound by chromatin regulators. Newly established NF-kB super-enhancers drive nearby canonical inflammatory response genes. In both ECs and macrophages BET bromodomain inhibition prevents super-enhancer formation downstream of NF-kB activation, abrogating proinflammatory transcription. In TNFa-activated endothelium this culminates in functional suppression of leukocyte rolling, adhesion and transmigration. Sustained BET bromodomain inhibitor treatment of LDLr -/- animals suppresses atherogenesis, a disease process rooted in pathological vascular inflammation involving endothelium and macrophages. These data establish BET-bromodomains as key effectors of inflammatory response through their role in the dynamic, global reorganization of super-enhancers during NF-kB activation. ChIP-Seq for various transcription factors, RNA Polymerase II, and histone modifications in human endothelial cells

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2013-02-13 | E-GEOD-44286 | biostudies-arrayexpress

Transcriptional super-enhancers connected to cell identity and disease

Project description:Super-enhancers are large clusters of transcriptional enhancers that drive expression of genes that control and define cell identity. Improved understanding of the roles super-enhancers play in biology would be afforded by knowing the constellation of factors that constitute these domains and by identifying super-enhancers across the spectrum of human cell types. We describe here the population of transcription factors, cofactors, chromatin regulators and core transcription apparatus that occupy super-enhancers in embryonic stem cells (ESCs) and evidence that super-enhancers are highly transcribed. We then use epigenomic data to produce a catalogue of super-enhancers in a broad range of human cell types. These super-enhancer domains are associated with genes encoding master transcription factors and other components that play important roles in the biology of these cells. Interestingly, sequence variation associated with a broad spectrum of diseases is especially enriched in the super-enhancers of disease-relevant cell types. Furthermore, we find that cancer cells generate super-enhancers at oncogenes and other genes that play important roles in tumor pathogenesis. We discuss these insights and their implications for future study of human health and disease. ChIP-Seq for transcription factors in mouse embryonic stem cells and H3K27ac in Jurkat T-ALL cell line RNA-Seq for mouse embryonic stem cells

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Selective Inhibition of Tumor Oncogenes by Disruption of Super-Enhancers

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