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BRD8 maintains glioblastoma by epigenetic reprogramming of the P53 network [RNA-seq]

ABSTRACT: Transcriptome analysis by high throughput sequencing

ORGANISM(S): Homo sapiens

PROVIDER: GSE158550 | GEO | 2022/09/16

REPOSITORIES: GEO

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BRD8 maintains glioblastoma by epigenetic reprogramming of the p53 network.

Project description:Inhibition of the tumour suppressive function of p53 (encoded by TP53) is paramount for cancer development in humans. However, p53 remains unmutated in the majority of cases of glioblastoma (GBM)-the most common and deadly adult brain malignancy1,2. Thus, how p53-mediated tumour suppression is countered in TP53 wild-type (TP53WT) GBM is unknown. Here we describe a GBM-specific epigenetic mechanism in which the chromatin regulator bromodomain-containing protein 8 (BRD8) maintains H2AZ occupancy at p53 target loci through the EP400 histone acetyltransferase complex. This mechanism causes a repressive chromatin state that prevents transactivation by p53 and sustains proliferation. Notably, targeting the bromodomain of BRD8 displaces H2AZ, enhances chromatin accessibility and engages p53 transactivation. This in turn enforces cell cycle arrest and tumour suppression in TP53WT GBM. In line with these findings, BRD8 is highly expressed with H2AZ in proliferating single cells of patient-derived GBM, and is inversely correlated with CDKN1A, a canonical p53 target that encodes p21 (refs. 3,4). This work identifies BRD8 as a selective epigenetic vulnerability for a malignancy for which treatment has not improved for decades. Moreover, targeting the bromodomain of BRD8 may be a promising therapeutic strategy for patients with TP53WT GBM.

| S-EPMC10189659 | biostudies-literature

BRD8 maintains glioblastoma by epigenetic reprogramming of the P53 network [ATAC-seq]

Project description:Chromatin accessibility profiling by high throughput sequencing

2022-09-16 | GSE199364 | GEO

BRD8 maintains glioblastoma by epigenetic reprogramming of the P53 network [ChIP-seq]

Project description:Genome-wide binding/occupancy profiling by high throughput sequencing

2022-09-16 | GSE158549 | GEO

BRD8 maintains glioblastoma by epigenetic reprogramming of the P53 network

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

2022-09-15 | GSE158551 | GEO

BRD8 maintains glioblastoma by epigenetic reprogramming of the P53 network

Project description:BRD8 maintains glioblastoma by epigenetic reprogramming of the P53 network

| PRJNA665550 | ENA

BRD8 maintains glioblastoma by epigenetic reprogramming of the P53 network [ChIP-seq]

Project description:BRD8 maintains glioblastoma by epigenetic reprogramming of the P53 network [ChIP-seq]

| PRJNA665554 | ENA

BRD8 maintains glioblastoma by epigenetic reprogramming of the P53 network [RNA-seq]

Project description:BRD8 maintains glioblastoma by epigenetic reprogramming of the P53 network [RNA-seq]

| PRJNA665555 | ENA

BRD8 maintains glioblastoma by epigenetic reprogramming of the P53 network [ATAC-seq]

Project description:BRD8 maintains glioblastoma by epigenetic reprogramming of the P53 network [ATAC-seq]

| PRJNA819459 | ENA

Reconstructed Metabolic Network Models Predict Flux-Level Metabolic Reprogramming in Glioblastoma.

Project description:Developments in genome scale metabolic modeling techniques and omics technologies have enabled the reconstruction of context-specific metabolic models. In this study, glioblastoma multiforme (GBM), one of the most common and aggressive malignant brain tumors, is investigated by mapping GBM gene expression data on the growth-implemented brain specific genome-scale metabolic network, and GBM-specific models are generated. The models are used to calculate metabolic flux distributions in the tumor cells. Metabolic phenotypes predicted by the GBM-specific metabolic models reconstructed in this work reflect the general metabolic reprogramming of GBM, reported both in in-vitro and in-vivo experiments. The computed flux profiles quantitatively predict that major sources of the acetyl-CoA and oxaloacetic acid pool used in TCA cycle are pyruvate dehydrogenase from glycolysis and anaplerotic flux from glutaminolysis, respectively. Also, our results, in accordance with recent studies, predict a contribution of oxidative phosphorylation to ATP pool via a slightly active TCA cycle in addition to the major contributor aerobic glycolysis. We verified our results by using different computational methods that incorporate transcriptome data with genome-scale models and by using different transcriptome datasets. Correct predictions of flux distributions in glycolysis, glutaminolysis, TCA cycle and lipid precursor metabolism validate the reconstructed models for further use in future to simulate more specific metabolic patterns for GBM.

| S-EPMC4834348 | biostudies-literature

Persistent Epigenetic Reprogramming of Sweet Taste by Diet

Project description:We report the application of ribosomal profiling based RNA sequencing technology for high-throughput profiling of the Gr5a cells of male Drosophila melanogaster adults. By expressing the UAS-Rpl3-3XFLAG transgene using the Gr5a-GAL4 driver.

2020-11-11 | GSE146214 | GEO

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