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Therapeutic Targeting of EZH2 and BET BRD4 in Pediatric Rhabdoid Tumor [ChIP-Seq]

ABSTRACT: We proved that histone H3K27me3 and H3K27ac were elevated in AT/RT cells and distributed in distinct chromatin regions to regulate specific gene expression and to promote AT/RT growth. Targeting EZH2 and BRD4 activity is therefore a potential combination therapy for AT/RT.

ORGANISM(S): Homo sapiens

PROVIDER: GSE196056 | GEO | 2022/02/06

REPOSITORIES: GEO

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Therapeutic Targeting of EZH2 and BET BRD4 in Pediatric Rhabdoid Tumor

Project description:We proved that histone H3K27me3 and H3K27ac were elevated in AT/RT cells and distributed in distinct chromatin regions to regulate specific gene expression and to promote AT/RT growth. Targeting EZH2 and BRD4 activity is therefore a potential combination therapy for AT/RT.

2022-02-10 | GSE196440 | GEO

Therapeutic Targeting of EZH2 and BET BRD4 in Pediatric Rhabdoid Tumor [RNA-Seq]

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Therapeutic Targeting of EZH2 and BET BRD4 in Pediatric Rhabdoid Tumor

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Therapeutic Targeting of EZH2 and BET BRD4 in Pediatric Rhabdoid Tumor

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Therapeutic Targeting of EZH2 and BET BRD4 in Pediatric Rhabdoid Tumor [RNA-Seq]

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Therapeutic Targeting of EZH2 and BET BRD4 in Pediatric Rhabdoid Tumor

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

2022-02-06 | GSE196058 | GEO

CUT&RUN profiling of histone H3K27ac and H3K27me3 localization after pharmacological inhibition of EZH2 and BET proteins

Project description:NUT carcinoma (NC), an aggressive carcinoma, is driven by the BRD4-NUT fusion oncoprotein. BRD4, a BET protein, binds to chromatin through its two bromodomains, and when fused to NUT forms very large super-enhancers, termed megadomains. Targeting BRD4-NUT with BET bromodomain inhibitors (BETi) are a promising treatment, but limited as monotherapy. To identify additional dependencies in NC, we performed a genetic rescue screen in NC cells depleted of BRD4-NUT and identified EZH2 as a top correlated hit. Indeed, inhibition of EZH2 using the clinical compound, tazemetostat (taz), potently blocked growth of NC cells, and when combined with BETi was highly synergistic. Epigenetic and transcriptomic analysis revealed that taz reversed the EZH2-specific H3K27me3 silencing mark, and restored expression of multiple tumor suppressor genes while having no effect on megadomain-associated genes. CDKN2A was identified as the only amongst all taz-derepressed genes to confer resistance to taz in a CRISPR-CAS9 screen. In pre-clinical models, combined taz and BETi synergistically blocked growth and prolonged survival of NC-xenografted mice, with all mice cured in one cohort.

2023-09-14 | GSE228533 | GEO

Effect of EZH2 and BET bromodomain inhibition, alone and combined, on NUT carcinoma gene expression

Project description:To determine mechanisms of synergy between EZH2 and BRD4-NUT, we treated NUT carcinoma cell lines with EZH2 inhibitor, tazemetostat, and/or BET bromodomain inhibitors (ABBV075 pan-BET inhibitor or ABBV744 BD2-selective inhibitor). We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different NUT carcinoma cell lines at two time points, 6h and 96h.

2023-10-05 | GSE208774 | GEO

Transcriptome analysis of dominant-negative Brd4 mutants identifies Brd4-specific target genes of BET inhibitor JQ1

Project description:We analyzed anti-proliferative dominant-negative Brd4 mutants that compete with the function of distinct Brd4 domains. We used these Brd4 mutants to compare the Brd4-specific transcriptome with the transcriptome of JQ1 treated cells.

2017-06-09 | GSE92456 | GEO

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