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RNAPol2 accounts for tumor cells liability to JQ1 [ChIP-Seq]

ABSTRACT: We here use B-cell tumors as a model to address the mechanism of action of JQ1, a widely used BET inhibitor.

ORGANISM(S): Homo sapiens

PROVIDER: GSE76191 | GEO | 2016/08/25

SECONDARY ACCESSION(S): PRJNA306758

REPOSITORIES: GEO

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RNAPol2 accounts for tumor cells liability to JQ1 [Affymetrix]

Project description:We here use B-cell tumors as a model to address the mechanism of action of JQ1, a widely used BET inhibitor.

2016-08-25 | GSE76188 | GEO

RNAPol2 accounts for tumor cells liability to JQ1

Project description:RNAPol2 accounts for tumor cells liability to JQ1

| PRJNA306755 | ENA

RNAPol2 accounts for tumor cells liability to JQ1

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

2016-08-25 | GSE76192 | GEO

ChIP-Seq for transcriptional regulators and RNA Polymerase II in tumor cells treated with JQ1

Project description:ChIP-Seq of RNA Polymerase II, and transcriptional regulators in multiple myeloma (MM.1S), glioblastoma (U87-MG), and small cell lung carcinoma (H2171) treated with the BET bromodomain inhibitor JQ1. Cell lines (MM.1S, U87-MG, and H2171) representing multiple myeloma, glioblastoma, and small cell lung carcinoma, were treated with varying concentrations (5nM to 5µM) of the BET bromodomain inhibitor JQ1 followed by ChIP-Seq for RNA Polymerase II and transcriptional regulators. Other datasets from this series of experiments have been release as a part of GSE42355.

2013-07-26 | E-GEOD-49224 | biostudies-arrayexpress

Differential gene expression in neuroblastoma cells after treatment with JQ1, nanaomycin, or combination of JQ1 and nanaomycin

Project description:BET bromodomain inhibitors are emerging as very promising novel anticancer agents. Combination of BET bromodomain inhibitor JQ1 and quinone-containing compound nanaomycin exerts synergistic anticancer effect in neuroblastoma We analysed whether a treatment with BET bromodomain inhibitor JQ1, and quinone-containing compound Nanaomycin synergistically modulate gene expression

2016-12-31 | GSE76066 | GEO

ChIP-Seq for transcriptional regulators and RNA Polymerase II in tumor cells treated with JQ1

2013-07-26 | GSE49224 | GEO

Testis Gene Expression Changes after JQ1 treatment

Project description:JQ1 is a small-molecule (BET family) bromodomain inhibitor that causes a contraceptive effect in mice by blocking spermatogenesis and reducing sperm motility.

2012-08-16 | GSE37894 | GEO

Gene expression change after JQ1 treatment in breast cancer cell

Project description:BET bromodomain inhibitors effectively kill several types of cancer cells. However, the underlying mechanism of BET inhibition resistance remains obscure. We sought to identify the gene expression change upon treatment of JQ1, a well-known BET inhibitor, in basal-like breast cancer cells. In this dataset, we used RNA-sequencing to characterize the mRNA expression profiles from DMSO and JQ1-treated MDA-MB-231 breast tumor cells.

2019-11-07 | GSE140003 | GEO

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.

2016-03-31 | E-GEOD-75960 | biostudies-arrayexpress

Syngergistic Effect of JQ1 and Rapamycin for Treatment of Human Osteosarcoma

Project description:Bromodomain and extra terminal domain (BET) proteins are important epigenetic regulators facilitating the transcription of genes in chromatin areas linked to acetylated histones. JQ1, a BET protein inhibitor, has antiproliferative activity against many cancers, mainly through inhibition of c-MYC and upregulation of p21. In this research, we investigated the use of JQ1 for human osteosarcoma (OS) treatment. JQ1 significantly inhibited the proliferation and survival of OS cells inducing G1 cell cycle arrest, premature senescence, but little effect on apoptosis. Interestingly, c-MYC protein levels in JQ1-treated cells remained unchanged, whereas the upregulation of p21 protein was still observable. Although effective in vitro, JQ1 alone failed to reduce the size of the MNNG/HOS xenografts in immunocompromised mice. To overcome the resistance of OS cells to JQ1 treatment, we combined JQ1 with rapamycin, an mTOR inhibitor. JQ1 and rapamycin synergistically inhibited the growth and survival of OS cells in vitro and in vivo. We also identified that RUNX2 is a direct target of BRD4 inhibition by JQ1 in OS cells. Chromatin immunoprecipitation (ChIP) showed that enrichment of BRD4 protein around RUNX2 transcription start sites diminished with JQ1 treatment in MNNG/HOS cells. Overexpression of RUNX2 protected JQ1-sensitive OS cells from the effect of JQ1, and siRNA-mediated inhibition of RUNX2 sensitized the same cells to JQ1. In conclusion, our findings suggest that JQ1, in combination with rapamycin, is an effective chemotherapeutic option for OS treatment. We also show that inhibition of RUNX2 expression by JQ1 partly explains antiproliferative activity of JQ1 in OS cells. MNNG/HOS cells treated with 7.5mM JQ1, 12.5nM Rapamycin or both were used for RNA extraction and hybridization on Affymetrix microarrays. We compared these microarray samples with the corresponding control (treated with DMSO).

2015-05-01 | E-GEOD-57203 | biostudies-arrayexpress

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