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BRD4 inhibitor GNE987 exerts anti-cancer effects by targeting C-Myc and S100A16 in Glioblastoma [ChIP-seq]

ABSTRACT: Glioblastoma (GBM) in children is a relatively more common primary central nervous system tumor with a high degree of malignancy, high mortality, and complex surgical complete resection.. GNE987 is a newly developed 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 GNE987 has not been assessed in GBM cells so far. In the present study, ChIP-Seq analysis was performed to explore the effect of GNE987 on GBM cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE202484 | GEO | 2022/11/09

REPOSITORIES: GEO

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BRD4 inhibitor GNE987 exerts anti-cancer effects in Neuroblastoma

Project description:Neuroblastoma (NB) is the most common extracranial solid tumor of childhood, which is derived from primordial neural crest cells. GNE987 is a newly developed 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 selective degradation. However, the function of GNE987 has not been assessed in NB models so far. In the present study, RNA-seq analysis was performed to explore the effect of GNE987 on NB cells.

2022-03-23 | GSE190002 | GEO

BRD4 inhibitor GNE987 exerts anti-cancer effects in Neuroblastoma (ChIP-Seq)

Project description:Neuroblastoma (NB) is the most common extracranial solid tumor of childhood, which is derived from primordial neural crest cells. GNE987 is a newly developed 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 selective degradation. However, the function of GNE987 has not been assessed in NB models so far. In the present study, ChIP-Seq analysis was performed to explore the effect of GNE987 on NB cells.

2022-03-23 | GSE194430 | GEO

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

BRD4 inhibitor GNE987 exerts anti-cancer effects by targeting C-Myc and S100A16 in Glioblastoma

Project description:To investigate the function of GNE987 in the regulation of gene expression, we treated U87 cells with control (DMSO) or GNE987, respectively. We then performed gene expression profiling analysis using data obtained from RNA-seq of control and GNE987 treatment.

2022-11-09 | GSE202362 | 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

dBET57 exerts anti-cancer effects in neuroblastoma

Project description:Neuroblastoma (NB) is the most common extracranial solid tumor of childhood, which is derived from primordial neural crest cells. dBET57, a new cereblon (CRBN) based inhibitor developed by PROTAC technology. It binds to the BET protein families BRD2, BRD3, and BRD4, which are recruited to the proteasome system for selective ubiquitination degradation. However, the function of dBET57 has not been assessed in NB models so far. In the present study, RNA-seq analysis was performed to explore the effect of dBET57 on NB cells.

2022-12-09 | GSE208184 | GEO

BRD4 inhibitor GNE987 exerts anti-cancer effects in Neuroblastoma

Project description:BRD4 inhibitor GNE987 exerts anti-cancer effects in Neuroblastoma

| PRJNA785569 | ENA

RUNX1 knockdown and BET protein proteolysis targeting chimera (PROTAC) exerts potent lethal activity against mtRUNX1 AML cells

Project description:Bromodomain extraterminal protein (BETP) inhibitors transcriptionally repress oncoproteins which undermines the growth and survival of AML cells. However, BETi treatment causes accumulation of BETPs, associated with reversible binding and incomplete inhibition of BRD4, which potentially compromises the activity of BETi in AML cells. Unlike BETi, BET-PROTAC (proteolysis-targeting chimera) ARV-825 recruits and utilize an E3-ubiquitin ligase to effectively degrade BETPs in AML cells. BET-PROTACs induce more apoptosis than BETi of mtRUNX1 AML cells. BET-PROTAC treatment induced more perturbations in the mRNA and protein expressions than BETi. It was noted that treatment with BETi or BET-PROTAC caused significant and sustained depletion of RUNX1 in AML cells. We also determined the effects of global depletion of RUNX1 in mtRUNX1 expressing AML OCI-AML5 cells. We observed an overlap in the signature of RUNX1 knockdown by shRNA with that of OTX015 and ARV-825 in OCI-AML5 cells.

2020-08-11 | GSE119261 | GEO

Genome-wide mapping of Hif-1Î± binding sites in zebrafish [ChIP-seq]

Project description:Analysis of the binding sites of Hif-1Î± in both wild-type and von Hippel Lindau mutant zebrafish lines at 4dpf by ChIP linked next generation sequencing. The von Hippel Lindau mutant displays a systemic hypoxic response under normoxic conditions. Results show the extent of Hif-1Î± binding to the genome, and provide a basis for analysis of the transcriptional response to genetically induced hypoxia in zebrafish. Analysis of the DNA binding sites of Hif-1Î± in both wild-type and von Hippel Lindau mutant zebrafish lines at 4dpf. The von Hippel Lindau mutant displays a systemic hypoxic response under normoxic conditions. Results show the extent of Hif-1Î± binding to the genome, and provide a basis for analysis of the dependency of the transcriptional response on Hif-1Î± in conditions of genetically induced hypoxia in zebrafish.

2016-03-22 | E-GEOD-70727 | biostudies-arrayexpress

Genome-wide mapping of Hif-1Î± binding sites in zebrafish [microarray]

Project description:Analysis of gene expression changes in the von Hippel Lindau when mutant compared to wild-type at 4dpf using a whole genome microarray expression profiling. The von Hippel Lindau mutant displays a systemic hypoxic response under normoxic conditions. We performed single-colour microarrays to identify the gene expression changes which underpin the hypoxic phenotype. We used 3 biological replicates from both mutant and control, followed by analysis using Limma to identify significant gene expression changes. This work, together with ChIP-seq data for the Hif-1Î± in von Hippel Lindau mutants, should allow for the Hif-1Î± dependency of these gene expression changes to be assessed. The changes in gene expression between von Hippel Lindau mutants and wild-type controls was measured at 4 days post fertilisation. For both wild-type and mutant, 3 biological replicates, each of 30 embryos were used.

2016-03-22 | E-GEOD-70885 | biostudies-arrayexpress

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