Expression profiling tumor cells from MYCN-driven neuroblastoma upon BRD4 or AURKA inhibition
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ABSTRACT: Amplification of MYCN is the most prominent genetic marker of high-stage neuroblastoma, a childhood tumor originating from the neural crest. We generated a cell line (mNB-A1) from tumors developed in transgenic mouse and treated these cells with DMSO (n=6), the BRD4-inhibitor JQ1 (n=3) or the AURKA-inhibitor MLN8237 (n=3) for 24 h. The expression profiles of vehicle (DMSO)-treated mNB-A1 cells were compared to JQ1- or MLN8237-treated mNB-A1 cells.
Project description:Amplification of MYCN is the most prominent genetic marker of high-stage neuroblastoma, a childhood tumor originating from the neural crest. We generated a cell line (mNB-A1) from tumors developed in transgenic mouse and treated these cells with DMSO (n=6), the BRD4-inhibitor JQ1 (n=3) or the AURKA-inhibitor MLN8237 (n=3) for 24 h.
Project description:The goal of this experiment was to understand the changes in gene expression in the human basal-like breast cancer cell line HCC1143 following treatment with the MEK inhibitor Trametinib (T), PI3K/mTOR inhibitor BEZ235 (B), the BET inhibition JQ1 (JQ), Trametinib + JQ1 (TJ), or BEZ235 + JQ1(BJ), compared to a DMSO control (D). Samples were treated for 72hr and run in triplicate.
Project description:As part of the preclinical research for a recently published trial of combination therapy with the HDAC inhibitor entinostat and the PD1 inhibitor pembrolizumab, an experiment was performed to determined the influence of entinostat and the BET inhibitor JQ1 on the transcriptome of three uveal melanoma cell lines. The cell lines were cultured and treated with either entinostat, JQ1 or DMSO and subjected to RNA-seq for identification of differentially expressed genes.
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.
Project description:T84 cells were treated with DMSO, 30nM trametinib (MEKi), 1µM JQ1 (BRD4i) or the combination of trametinib and JQ1 (combo) for 24h.
Project description:Identification of the mechanisms through which BET inhibitor (OTX-015) stimulates natural killer (NK) activation. RNA-seq was performed comparing vehicle- (DMSO) to OTX-015-treated NK-92 cell line.
Project description:SKBR-3 or BT474m1 HER2+ breast cancer cells were treated with either DMSO, 300nM lapatinib, 300nM JQ1, or lapatinib and JQ1 in combination for 48h.
Project description:Estrogen signaling pathway is critical for breast cancer development and has remained the major adjuvant therapeutic target for this disease. Tamoxifen has been used in clinic for many years to treat ER-positive breast cancer. However a great many (30%) suffer relapse due to drug resistance. In this study, the bromodomain inhibitor JQ1 was found to down-regulate ERalpha gene expression and have anti-tumor effect in cultured tamoxifen-resisant breast cancer cells. We used microarrays to detail the global programme of gene expression in tamoxifen-resistant MCF7 cells treated with the bromodomain inhibitor JQ1. Tamoxifen-resistant breast cancer MCF7 cells were treated with DMSO (vehicle) or JQ1 (0.2 uM) for 24 hours before total RNA was purified for microarray. Each sample was triplicated.
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.
Project description:Purpose: Study the changes in the transcriptome of metastatic melanoma PDX cells upon combination treatment with AURKA and MEK inhibitors Methods: RNAseq analysis of melanoma PDX cells treated with AURKA inhibitor Alisertib (500nM) and MEK inhibitor trametinib (100nM) for 72 h