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MZ1, a BRD4 inhibitor, exerted its anti-cancer effects by targeting the super-enhancer-regulated gene SDC1 in Glioblastoma

ABSTRACT: MZ1, a BRD4 inhibitor, exerted its anti-cancer effects by targeting the super-enhancer-regulated gene SDC1 in Glioblastoma

PROVIDER: PRJNA1025846 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26319940.fastq.gz	Fastqsanger.gz
	SRR26319941.fastq.gz	Fastqsanger.gz
	SRR26319942.fastq.gz	Fastqsanger.gz
	SRR26318081_1.fastq.gz	Fastqsanger.gz
	SRR26318081_2.fastq.gz	Fastqsanger.gz

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MZ1, a BRD4 inhibitor, exerted its anti-cancer effects by targeting the super-enhancer-regulated gene SDC1 in Glioblastoma [ChIP-Seq]

Project description:MZ1, a BRD4 inhibitor, exerted its anti-cancer effects by targeting the super-enhancer-regulated gene SDC1 in Glioblastoma [ChIP-Seq]

| PRJNA1025848 | ENA

MZ1, a BRD4 inhibitor, exerted its anti-cancer effects by targeting the super-enhancer-regulated gene SDC1 in Glioblastoma [RNA-Seq]

Project description:MZ1, a BRD4 inhibitor, exerted its anti-cancer effects by targeting the super-enhancer-regulated gene SDC1 in Glioblastoma [RNA-Seq]

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MZ1, a BRD4 inhibitor, exerted its anti-cancer effects by targeting the super-enhancer-regulated gene SDC1 in Glioblastoma [ChIP-Seq]

Project description:Glioblastoma (GBM) is a relatively more common primary central nervous system tumor with a high degree of malignancy, high mortality, and complex surgical complete resection. MZ1 is a von Hippel-Lindau tumor suppressor (VHL)-based pan-BET-targeting PROTAC, which can bind to the target proteins (BET proteins, including BRD2, BRD3, and BRD4) and recruit them to the ubiquitin/ proteasome system for degradation. However, the function of MZ1 has not been assessed in GBM cells so far. In the present study, ChIP-Seq analysis was performed to explore the effect of MZ1 on GBM cells.

2023-10-16 | GSE244893 | GEO

MZ1, a BRD4 inhibitor, exerted its anti-cancer effects by targeting the super-enhancer-regulated gene SDC1 in Glioblastoma [RNA-Seq]

Project description:To investigate the function of MZ1 in the regulation of gene expression, we treated U87 cells with control (DMSO) or MZ1, respectively. We then performed gene expression profiling analysis using data obtained from RNA-seq of control and MZ1 treatment.

2023-10-16 | GSE244878 | GEO

BRD4 inhibitor MZ1 exerts anti-cancer effects in Neuroblastoma

Project description:MZ1 is a newly designed pan-BET-targeting PROTAC that binds to target proteins (BET proteins such as BRD2, BRD3, and BRD4) and recruits them to the ubiquitin/protease pathway for selective destruction. However, the role of MZ1 in NB models has yet to be determined. The effect of MZ1 on NB cells was investigated using RNA-seq analysis in this work. MZ1 is a newly designed pan-BET-targeting PROTAC that binds to target proteins (BET proteins such as BRD2, BRD3, and BRD4) and recruits them to the ubiquitin/protease pathway for selective destruction. However, the role of MZ1 in NB models has yet to be determined. The effect of MZ1 on NB cells was investigated using RNA-seq analysis in this work.

2022-08-29 | GSE193767 | GEO

MZ1, a BRD4 inhibitor, exerted its anti-cancer effects by suppressing SDC1 in glioblastoma

Project description: Not available

| S-EPMC10870565 | biostudies-literature

BRD4 inhibitor MZ1 exerts anti-cancer effects in Neuroblastoma

Project description:BRD4 inhibitor MZ1 exerts anti-cancer effects in Neuroblastoma

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Targeting super-enhancer induced gene expression using novel BRD4 inhibitor OTX015 in preclinical models of MYCN-amplified neuroblastoma

Project description:Bromodomain-containing protein 4 (BRD4) functions as an epigenetic reader and binds to so-called super-enhancer regions of driving oncogenes such as MYC in cancer. We investigated the possibility to target super-enhancer regulated genes in neuroblastoma and in MYCN amplified disease in particular. We used OTX015, the first small-molecule BRD4 inhibitor to enter clinical phase I/II trials in adults, to test the feasibility to specifically target super-enhancer regulated gene-expression in neuroblastoma. BRD4 inhibition lead to significant transcriptional down-regulation of genes that were associated with super-enhancers, supporting the notion that BRD4 preferentially acts at these chromatin sites. BRD4 inhibition not only attenuated MYCN transcription but most significantly affected MYCN-regulated transcriptional programs.

2016-07-03 | E-MTAB-3672 | biostudies-arrayexpress

MZ1, a BRD4 inhibitor, exerted its anti-cancer effects by targeting the super-enhancer-regulated gene SDC1 in Glioblastoma

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

2023-10-16 | GSE244894 | GEO

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

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. Gene expression analysis of human endothelial cells in resting state, treatment with TNFalpha or TNFalpha with the BET bromodomain inhibitor JQ1

2014-09-29 | E-GEOD-53999 | biostudies-arrayexpress

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