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

ABSTRACT:

SUBMITTER: Li G

PROVIDER: S-EPMC10870565 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature

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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

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.

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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.

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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 targeting the super-enhancer-regulated gene SDC1 in Glioblastoma

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

| PRJNA1025846 | ENA

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]

| PRJNA1025266 | ENA

BRD4 inhibitor MZ1 exerts anti-cancer effects in Neuroblastoma

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

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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 GNE987 exerts anti-cancer effects by targeting super-enhancers in neuroblastoma.

Project description:BackgroundNeuroblastoma (NB) is a common extracranial malignancy with high mortality in children. Recently, super-enhancers (SEs) have been reported to play a critical role in the tumorigenesis and development of NB via regulating a wide range of oncogenes Thus, the synthesis and identification of chemical inhibitors specifically targeting SEs are of great urgency for the clinical therapy of NB. This study aimed to characterize the activity of the SEs inhibitor GNE987, which targets BRD4, in NB.ResultsIn this study, we found that nanomolar concentrations of GNE987 markedly diminished NB cell proliferation and survival via degrading BRD4. Meanwhile, GNE987 significantly induced NB cell apoptosis and cell cycle arrest. Consistent with in vitro results, GNE987 administration (0.25 mg/kg) markedly decreased the tumor size in the xenograft model, with less toxicity, and induced similar BRD4 protein degradation to that observed in vitro. Mechanically, GNE987 led to significant downregulation of hallmark genes associated with MYC and the global disruption of the SEs landscape in NB cells. Moreover, a novel candidate oncogenic transcript, FAM163A, was identified through analysis of the RNA-seq and ChIP-seq data. FAM163A is abnormally transcribed by SEs, playing an important role in NB occurrence and development.ConclusionGNE987 destroyed the abnormal transcriptional regulation of oncogenes in NB by downregulating BRD4, which could be a potential therapeutic candidate for NB.

| S-EPMC8932231 | biostudies-literature

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