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Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma (ChIP-Seq)

ABSTRACT: Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma (ChIP-Seq)

PROVIDER: PRJNA436354 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6792590.fastq.gz	Fastqsanger.gz
	SRR6792600.fastq.gz	Fastqsanger.gz
	SRR6792591.fastq.gz	Fastqsanger.gz
	SRR6792601.fastq.gz	Fastqsanger.gz
	SRR6792592.fastq.gz	Fastqsanger.gz

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Similar Datasets

Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma

Project description:Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma

| PRJNA436353 | ENA

Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma (ChIP-Seq)

Project description:Purpose: Identification of core transcriptional regulatory programs and bromodomain and extraterminal (BET) protein dependency in liposarcoma (LPS) Methods: ChIP-seq and RNA-seq were performed on LPS cells. Antibodies against H3K27ac, H3K4me1, H3K4me3, RNA-Pol2, BRD2, BRD3, BRD4, FOSL2, pan-RUNX, and DDIT3 (FUS-DDIT3) were used for ChIP-seq assays. The transcriptome responses of LPS141 and MLS402 cells to OTX015 and ARV-825 were compared. Result: We generated genome-wide chromatin-state maps of LPS cells. By charting the super-enhancer structures, we identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS. This study also provides a framework for discovering and targeting of core oncogenic transcriptional programs.

2019-04-01 | GSE111253 | GEO

Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma (RNA-Seq)

2019-04-01 | GSE111252 | GEO

Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma (RNA-Seq)

Project description:Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma (RNA-Seq)

| PRJNA436355 | ENA

Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma.

Project description:Liposarcomas (LPSs) are a group of malignant mesenchymal tumors showing adipocytic differentiation. Here, to gain insight into the enhancer dysregulation and transcriptional addiction in this disease, we chart super-enhancer structures in both LPS tissues and cell lines. We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS. Additionally, SNAI2 is identified as a crucial downstream target that enforces both proliferative and metastatic potentials to de-differentiated LPS cells. Genetic depletion of BET genes, core transcriptional factors, or SNAI2 mitigates consistently LPS malignancy. We also reveal a compelling susceptibility of LPS cells to BET protein degrader ARV-825. BET protein depletion confers additional advantages to circumvent acquired resistance to Trabectedin, a chemotherapy drug for LPS. Moreover, this study provides a framework for discovering and targeting of core oncogenic transcriptional programs in human cancers.

| S-EPMC6430783 | biostudies-literature

Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-04-01 | GSE111254 | GEO

Bromodomain and Extraterminal Inhibition Blocks Inflammation-Induced Cardiac Dysfunction and SARS-CoV2 Infection

Project description:Bromodomain and Extraterminal Inhibition Blocks Inflammation-Induced Cardiac Dysfunction and SARS-CoV2 Infection

| PRJEB43658 | ENA

The Bromodomain and extraterminal (BET) inhibitor attenuates inflammatory response and cell migration in human microglia

Project description:The Bromodomain and extraterminal (BET) inhibitor attenuates inflammatory response and cell migration in human microglia

| PRJNA649597 | ENA

Targeting bromodomain and extraterminal proteins in breast cancer.

Project description:Breast cancer is a collection of distinct tumor subtypes that are driven by unique gene expression profiles. These transcriptomes are controlled by various epigenetic marks that dictate which genes are expressed and suppressed. During carcinogenesis, extensive restructuring of the epigenome occurs, including aberrant acetylation, alteration of methylation patterns, and accumulation of epigenetic readers at oncogenes. As epigenetic alterations are reversible, epigenome-modulating drugs could provide a mechanism to silence numerous oncogenes simultaneously. Here, we review the impact of inhibitors of the Bromodomain and Extraterminal (BET) family of epigenetic readers in breast cancer. These agents, including the prototypical BET inhibitor JQ1, have been shown to suppress a variety of oncogenic pathways while inducing minimal, if any, toxicity in models of several subtypes of breast cancer. BET inhibitors also synergize with multiple approved anti-cancer drugs, providing a greater response in breast cancer cell lines and mouse models than either single agent. The combined findings of the studies discussed here provide an excellent rationale for the continued investigation of the utility of BET inhibitors in breast cancer.

| S-EPMC5828951 | biostudies-literature

BET bromodomain inhibition rescues PD-1-mediated T cell exhaustion in acute myeloid leukemia

Project description:We report that the bromodomain and extraterminal domain (BET) inhibitor JQ1 inhibits PD-1 expression in Jurkat T cells, primary T cells, and a T cell exhaustion model. Furthermore, JQ1 dramatically impaired the expression of PD-1 and T cell immunoglobulin mucin-domain-containing-3 (Tim-3), and promoted the secretion of cytokines in T cells from patients with acute myeloid leukemia (AML).

2022-08-16 | GSE205605 | GEO

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