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BRD4 connects enhancer remodeling to senescence immune surveillance

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE74328 | GEO | 2016/04/15

SECONDARY ACCESSION(S): PRJNA299780

REPOSITORIES: GEO

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BRD4 Connects Enhancer Remodeling to Senescence Immune Surveillance.

Project description:UnlabelledOncogene-induced senescence is a potent barrier to tumorigenesis that limits cellular expansion following certain oncogenic events. Senescent cells display a repressive chromatin configuration thought to stably silence proliferation-promoting genes while simultaneously activating an unusual form of immune surveillance involving a secretory program referred to as the senescence-associated secretory phenotype (SASP). Here, we demonstrate that senescence also involves a global remodeling of the enhancer landscape with recruitment of the chromatin reader BRD4 to newly activated super-enhancers adjacent to key SASP genes. Transcriptional profiling and functional studies indicate that BRD4 is required for the SASP and downstream paracrine signaling. Consequently, BRD4 inhibition disrupts immune cell-mediated targeting and elimination of premalignant senescent cells in vitro and in vivo Our results identify a critical role for BRD4-bound super-enhancers in senescence immune surveillance and in the proper execution of a tumor-suppressive program.SignificanceThis study reveals how cells undergoing oncogene-induced senescence acquire a distinctive enhancer landscape that includes formation of super-enhancers adjacent to immune-modulatory genes required for paracrine immune activation. This process links BRD4 and super-enhancers to a tumor-suppressive immune surveillance program that can be disrupted by small molecule inhibitors of the bromo and extra terminal domain family of proteins. Cancer Discov; 6(6); 612-29. ©2016 AACR.See related commentary by Vizioli and Adams, p. 576This article is highlighted in the In This Issue feature, p. 561.

| S-EPMC4893996 | biostudies-literature

BRD4 connects enhancer remodeling to senescence immune surveillance (RNA-seq)

Project description:Cellular senescence is a homeostatic program associated with tumor suppression, wound healing, and certain age related pathologies. Senescent cells display a repressive chromatin configuration thought to stably silence proliferation-promoting genes, while at the same time activate an unusual form of immune surveillance involving a secretory program referred to as the senescence-associated secretory phenotype (SASP). Here we demonstrate that senescence also involves a global remodeling of the enhancer landscape with recruitment of the chromatin reader BRD4 to newly activated super-enhancers adjacent to key SASP genes. Transcriptional profiling and functional studies indicate that BRD4 is required for the SASP and downstream paracrine signaling. Consequently, BRD4 inhibition disrupts immune cell-mediated targeting and elimination of premalignant senescent cells in vitro and in vivo. Our results identify a critical role for BRD4-bound super-enhancers in senescence immune surveillance and in the proper execution of a tumor-suppressive program.

2016-04-15 | GSE74324 | GEO

BRD4 connects enhancer remodeling to senescence immune surveillance (ChIP-Seq)

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BRD4 connects enhancer remodeling to senescence immune surveillance

Project description:BRD4 connects enhancer remodeling to senescence immune surveillance

| PRJNA299780 | ENA

Senescence-induced endothelial phenotypes underpin immune-mediated senescence surveillance

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2022-05-24 | GSE195616 | GEO

NF-kB coordinates rapid, BRD4-dependent remodeling of proinflammatory super-enhancers

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

2014-09-29 | E-GEOD-54000 | biostudies-arrayexpress

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TEAD4 delays cellular senescence by remodeling chromatin accessibility at H3K27ac-occupied enhancer regions

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Senescence-Induced Immune Remodeling Facilitates Metastatic Adrenal Cancer in a Sex-Dimorphic Manner

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2023-04-03 | GSE201127 | GEO

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