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Inhibition of histone readers bromodomain extra-terminal proteins alleviates scleroderma fibrosis

ABSTRACT: Inhibition of histone readers bromodomain extra-terminal proteins alleviates scleroderma fibrosis

PROVIDER: PRJNA776895 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16683313_1.fastq.gz	Fastqsanger.gz
	SRR16683313_2.fastq.gz	Fastqsanger.gz
	SRR16683314_1.fastq.gz	Fastqsanger.gz
	SRR16683314_2.fastq.gz	Fastqsanger.gz
	SRR16683315_1.fastq.gz	Fastqsanger.gz

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Inhibition of histone readers bromodomain extra-terminal proteins alleviates scleroderma fibrosis

Project description:We assessed transcriptomic changes in fibroblasts isolated from skin biopsies from diffuse cutaneous scleroderma patients before and after BET inhibitor JQ1 treatment

2022-03-01 | GSE186961 | GEO

Inhibition of bromodomain extraterminal histone readers alleviates skin fibrosis in experimental models of scleroderma.

Project description:Binding of the bromodomain and extraterminal domain proteins (BETs) to acetylated histone residues is critical for gene transcription. We sought to determine the antifibrotic efficacy and potential mechanisms of BET inhibition in systemic sclerosis (SSc). Blockade of BETs was done using a pan-BET inhibitor, JQ1; BRD2 inhibitor, BIC1; or BRD4 inhibitors AZD5153 or ARV825. BET inhibition, specifically BRD4 blockade, showed antifibrotic effects in an animal model of SSc and in patient-derived diffuse cutaneous SSc (dcSSc) fibroblasts. Transcriptome analysis of JQ1-treated dcSSc fibroblasts revealed differentially expressed genes related to extracellular matrix, cell cycle, and calcium (Ca2+) signaling. The antifibrotic effect of BRD4 inhibition was mediated at least in part by downregulation of Ca2+/calmodulin-dependent protein kinase II α and reduction of intracellular Ca2+ concentrations. On the basis of these results, we propose targeting Ca2+ pathways or BRD4 as potentially novel therapeutic approaches for progressive tissue fibrosis.

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ChIPSeq data from melanoma cancer cell line CHL-1 after Bromodomain and extra terminal (Bet) domain inhibitor treatment

Project description:Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites finally leading to genome wide changes in gene transcription. We used ChIPSeq profiling to investigate genome wide changes in promoter and enhancer occupancy induced by BET inhibitors BAY 1238097 and OTX-015, respectively.

2017-09-30 | GSE95585 | GEO

Expression data from melanoma cancer cell line CHL-1 after Bromodomain and extra terminal domain inhibitor BAY 1238097 treatment

Project description:Bromodomain and extra terminal domain (BET) inhibtion reduces occupancy of BET-family at promoter and enhancer sites. This finally leads to genome wide changes in the transcription of specific genes. We used microarray profiling to investigate the changes made by BET inhibitor BAY 1238097, trying to identify the underlying changes of gene regulation that lead to sensitivity.

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Global transcriptome profiling of triple-negative breast cancer cell lines treated with small-molecules targeting Bromodomain and Extra Terminal (BET) proteins

Project description:Triple negative breast cancer (TNBC) represents the most clinically challenging subtypes of breast cancer for which targeted therapeutics are still lacking. Bromodomain and Extra Terminal (BET) proteins, including ubiquitously expressed BRD2, BRD3, BRD4 and testis-specific BRDT, are epigenetic “readers” and play a major role in epigenetic regulation of gene transcription. BET proteins have emerged as new therapeutic targets for human cancer and other diseases. Based upon a new class of BET bromodomain (BRD) inhibitor, BETi-211, we have developed a highly selective and potent BET protein degrader, BETd-246. In comparison, BETd-246 is much more potent and effective than the corresponding BET inhibitor BETi-211 in growth inhibition and apoptosis induction in TNBC cell lines, indicating critical differences between these two different BET targeting approaches in their regulation of gene transcription. To understand the mechanisms of actions of BETi-211 and BETd-246 in TNBC, we performed RNA-seq analysis on MDA-MB-157, MDA-MB-231 and MDA-MB-468. These cell lines were treated for 3 h to capture the early transcriptional responses to BETi-211 or BETd-246. RNA-seq analysis reveals that BETd-246 predominantly down-regulates the expression of a large number of genes whereas BETi-211 up- and down-regulates an approximately equal number of genes in TNBC cells. Critically, transcriptomic analysis uncovers that a set of proliferation and survival-related genes, including MCL1 and BRD2, were oppositely regulated by BETd-246 and BETi-211 in these TNBC cell lines.

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Expression data from non-small cell lung cancer cell line DV90 after Bromodomain and extra terminal domain (BET) inhibitor JQ1 treatment

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Expression data from non-small cell lung cancer cell line DV90 after Bromodomain and extra terminal domain (BET) inhibitor JQ1 treatment

Project description:Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites resulting in changes in the transcription of specific genes. We used microarray profiling to investigate the transcriptional changes induced by BET inhibitor JQ1 treatment in DV90 cells to identify the underlying changes of gene regulation that lead to JQ1 sensitivity. DV90 cells (JQ1 sensitive non-small cell lung cancer cell line) were treated with 135 nM (IC50) or 785 nM (IC90) of JQ1 for 4h and 24h. DMSO treated controls served as reference and at least four replicates per condition were collected. RNA was extracted and hybridized to Affymetrix HuGene-2.1ST microarrays to identify treatment induced transcriptional changes.

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Determining the impact of the Bromodomain and extra-terminal inhibitor JQ1 on the GATA2 cistrome in castrate-resistant prostate cancer

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Crosstalk between combinatorial histone H4 post-translational modifications influence ATAD2B bromodomain activity

Project description:Investigation of bromodomain activity of the ATPase family which contains ATAD2B. Specifically we explore the cross talk between histone H4 post translational modifications and their modulation of chromatin readers of the ATAD2B bromodomain

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Crosstalk between combinatorial histone H4 post-translational modifications influence ATAD2B bromodomain activity

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