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BET inhibitors enhance the expression of fetal and embryonic hemoglobin genes

ABSTRACT: BET inhibitors enhance the expression of fetal and embryonic hemoglobin genes

PROVIDER: PRJNA686882 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13280523.fastq.gz	Fastqsanger.gz
	SRR13280524.fastq.gz	Fastqsanger.gz
	SRR13280525.fastq.gz	Fastqsanger.gz
	SRR13280526.fastq.gz	Fastqsanger.gz
	SRR13280527.fastq.gz	Fastqsanger.gz

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BET inhibitors enhance the expression of fetal and embryonic hemoglobin genes [K562]

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BET inhibitors enhance the expression of fetal and embryonic hemoglobin genes [TF-1]

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BET inhibitors enhance the expression of fetal and embryonic hemoglobin genes [K562]

Project description:We performed RNA-sequencing on erythroid cell lines treated with DMSO or JQ1. We found that JQ1 induces erythropoiesis and specifically upregulated fetal and embryonic globin genes at the beta globin locus.

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BET inhibitors enhance the expression of fetal and embryonic hemoglobin genes [TF-1]

2021-12-01 | GSE163595 | GEO

microRNA expression profiles of reticulocytes for hereditary persistence of fetal hemoglobin and β-thalssemia minor with high fetal hemoglobin.

Project description:We used microarrays to investigate differential microRNA (miRNA) expression in reticulocytes comparing reticulocytes from control individuals with normal fetal hemoglobin (HbF) level to hereditary persistence of fetal hemoglobin (HPFH) and β-thalssemia minor with high HbF, and try to find out some miRNAs associated with the mechanisms of HbF induction.

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Critical Vulnerabilities of the NuRD Complex for Fetal Hemoglobin Control

Project description:High-resolution CRISPR functional genomics reveals critical vulnerabilities of the NuRD complex for fetal hemoglobin control

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The long noncoding RNA expression profiles of reticulocytes for hereditary persistence of fetal hemoglobin and β-thalssemia minor with high fetal hemoglobin.

Project description:To explore long noncoding RNA (lncRNA) expression and the biological functions of lncRNAs in fetal hemoglobin (HbF) induction, we surveyed lncRNA and mRNA expression profiles using circulating reticulocytes isolated from individuals with hereditary persistence of fetal hemoglobin (HPFH) and β-thalassaemia minor with high HbF.

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BET inhibitors enhance the expression of fetal and embryonic hemoglobin genes

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

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Adaptation of the Kinome Promotes Resistance to BET Bromodomain Inhibitors in Ovarian Cancer

Project description:Small molecule BET bromodomain inhibitors (BETi) are actively being pursued in clinical trials for the treatment of a variety of cancers, however, the mechanisms of resistance to targeted BET protein inhibitors remain poorly understood. Using a novel mass spectrometry approach that globally measures kinase signaling at the proteomic level, we evaluated the response of the kinome to targeted BET inhibitor treatment in a panel of BRD4-dependent ovarian carcinoma (OC) cell lines. Despite initial inhibitory effects of BETi, OC cells acquired resistance following sustained treatment with the BETi, JQ1. Through application of Multiplexed Inhibitor Beads (MIBs) and mass spectrometry, we demonstrate that BETi resistance is mediated by adaptive kinome reprogramming, where activation of compensatory pro-survival kinase networks overcomes BET protein inhibition. Furthermore, drug combinations blocking these kinases may prevent or delay the development of drug resistance and enhance the efficacy of BET inhibitor therapy. RNAseq was employed to identify changes in kinase RNA expression following short term (48h) or chronic (JQ1R) JQ1 treatment in three different ovarian cancer cell lines.

2016-07-21 | E-GEOD-82329 | biostudies-arrayexpress

RAPID RESISTANCE TO BET INHIBITORS IS MEDIATED BY FGFR1 IN GLIOBLASTOMA

Project description:Bromodomain and extra-terminal domain (BET) proteins are therapeutic targets in several cancers including the most common malignant adult brain tumor glioblastoma (GBM). Multiple small molecule inhibitors of BET proteins have been utilized in preclinical and clinical studies. Unfortunately, BET inhibitors have not shown efficacy in clinical trials enrolling GBM patients. One possible reason for this may stem from resistance mechanisms that arise after prolonged treatment within a clinical setting. However, the mechanisms and timeframe of resistance to BET inhibitors in GBM is not known. To identify the temporal order of resistance mechanisms in GBM we performed quantitative proteomics using multiplex-inhibitor bead mass spectrometry and demonstrated that resistance to BET inhibitors in GBM treatment occurs rapidly within hours and involves the fibroblast growth factor receptor 1 (FGFR1) protein. Small molecule inhibition of BET proteins and FGFR1 simultaneously induces synergy in reducing GBM tumor growth in vitro and in vivo. Further, FGFR1 knockdown synergizes with BET inhibitor mediated reduction of GBM cell proliferation. Collectively, our studies suggest that co-targeting BET and FGFR1 may dampen resistance mechanisms to yield a clinical response in GBM.

2024-06-16 | PXD043214 | Pride

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