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Tumor Microenvironment-induced BRD4 Activation Results in Chromatin Remodeling and Therapy Resistance in Colorectal Cancer

ABSTRACT: Tumor Microenvironment-induced BRD4 Activation Results in Chromatin Remodeling and Therapy Resistance in Colorectal Cancer

PROVIDER: PRJNA671678 | ENA |

REPOSITORIES: ENA

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Tumor Microenvironment-induced BRD4 Activation Results in Chromatin Remodeling and Therapy Resistance in Colorectal Cancer [ChIP-seq]

Project description:Tumor microenvironment promotes tumorigenesis, but its role in modulating tumor chromatin activity is poorly understood. Here, we show that inflammatory cytokines interleukin-6 and -8 in the tumor microenvironment induces JAK2-mediated phosphorylation of bromodomain-containing protein 4 (BRD4), which results in interaction with UCHL3 deubiquitinase, leading to increased BRD4 protein stabilization in colorectal cancer. JAK2-phosphorylated BRD4 shows enhanced activity binding to chromatin but reduced binding to BRD4 inhibitors, leading to treatment resistance. Moreover, BRD4 phosphorylation promotes interaction with STAT3 to induce chromatin remodeling through concurrent binding to enhancers and super-enhancers, supporting a tumor-promoting transcriptional program. Thus, the inflammatory tumor microenvironment provides a powerful mechanism for tumor chromatin remodeling and oncogenic transcription, which suggests a unrecognized new strategy to enhance BRD4 inhibitor response.

2021-06-07 | GSE160352 | GEO

Tumor Microenvironment-induced BRD4 Activation Results in Chromatin Remodeling and Therapy Resistance in Colorectal Cancer [ChIP-seq]

Project description:Tumor Microenvironment-induced BRD4 Activation Results in Chromatin Remodeling and Therapy Resistance in Colorectal Cancer [ChIP-seq]

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Tumor Microenvironment-induced BRD4 Activation Results in Chromatin Remodeling and Therapy Resistance in Colorectal Cancer

Project description:Analysis of gene expression profiles of patient-derived colorectal cancer cell which is mono-cultured or co-cultured with CAFs in the presence of vehicle, JQ1, pacritinib or combo.

2021-06-08 | GSE160035 | GEO

BRD4 connects enhancer remodeling to senescence immune surveillance

Project description:BRD4 connects enhancer remodeling to senescence immune surveillance

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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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QPCTL deletion results in a rewiring of the tumor microenvironment

Project description:QPCTL deletion results in a rewiring of the tumor microenvironment

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Regulation of the KEAP1/NRF2 oxidative stress response pathway by BRD4 in prostate and colorectal cancer

Project description:To identify genes regulated by BRD4 and to provide insight into new mechanisms de-regulated by BRD4, such as the response to oxidative stress, we integrated BRD4-binding regions with BRD4 gene expression data. For this analysis we performed BRD4 chromatin immunoprecipitation experiments and BRD4 knock down experiments followed by RNA-Seq analyses. By integration of both gene lists we identified top candidate genes regulated by BRD4. HEK cells have been investigated for genomewide BRD4 binding sites and expression changes after knock down of BRD4. Illumina sequencing was used to gather data of the type ChIP Seq and mRNA Seq.

2014-02-28 | E-GEOD-50491 | biostudies-arrayexpress

Stromal induction of BRD4 phosphorylation Results in Chromatin Remodeling and BET inhibitor Resistance in Colorectal Cancer.

Project description: Not available

| S-EPMC8295257 | biostudies-literature

Loss of sarcolipin results in atrial remodeling

Project description:Sarcolipin (SLN) is a key regulator of SERCA pump in atria. To determine the role of SLN in atrial Ca2+ homeostasis, we have generated a SLN null (sln-/-) mouse model. Ablation of SLN results in increased SR Ca2+ load and Ca2+ transients in atria. Further, loss of SLN results in electrophysiological and strcutural remodeling of atria. The SLN knockout and C57/BL6 wildtype mice (each n=3) were selected for RNA extraction. The cRNA probes were hybridized to Affymetrix gene array.

2010-11-01 | E-GEOD-23403 | biostudies-arrayexpress

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