Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA134579 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The study aims to define gene expression changes associated with mithramycin treatment of Ewing Sarcoma cell lines. The data consist of 12 arrays. Two cell lines, TC71 and TC32, were treated with solvent control or with mithramycin, and RNA was extracted at 6 hours. Three biological replicates per cell line/treatment.
2011-04-18 | E-GEOD-25127 | biostudies-arrayexpress
Project description:The study aims to define gene expression changes associated with mithramycin treatment of Ewing Sarcoma cell lines.
2011-04-18 | GSE25127 | GEO
Project description:Genome-wide profiling of siRNA targeting PRKDC in Ewing sarcoma and non-Ewing sarcoma cell lines
| PRJNA360025 | ENA
Project description:Purpose: Our experimental results demonstrate an essential role for the lncRNA HOTAIR in Ewing sarcoma. We have repressed HOTAIR expression in three Ewing sarcoma cell lines and overexpressed HOTAIR, alone and with EWS-FLI1, in htert-immortalized human mesenchymal stem cells to evaluate its effects on gene expression in this cancer. Methods: RNA-Seq of Ewing sarcoma cell lines with HOTAIR represssed by GapmeR or treated with nonsilencing control, and hTERT-immortalized hMSCs with expression of control GFP, HOTAIR, or HOTAIR and EWS-FLI1, was used for gene expression analysis. Results: Defined gene expression signatures were defined as driven by HOTAIR in each cell line model, with a consensus set of gene identified in the Ewing sarcoma cell lines. Additionally, a set of genes regulated by HOTAIR independently of EWS-FLI1 was identified in the hTERT-hMSC models. Conclusions: HOTAIR expression regulates a set of genes critical to viability, cell adhesion, cell motility, and other markers of EMT and metastasis in Ewing sarcoma, independently of EWS-FLI1.
2018-01-24 | GSE109483 | GEO
Project description:We show that EWS-FLI1, an aberrant transcription factor responsible for the pathogenesis of Ewing sarcoma, reprograms gene regulatory circuits by directly inducing or directly repressing enhancers. At GGAA repeats, which lack regulatory potential in other cell types and are not evolutionarily conserved, EWS- FLI1 multimers potently induce chromatin opening, recruit p300 and WDR5, and create de novo enhancers. GGAA repeat enhancers can loop to physically interact with target promoters, as demonstrated by chromosome conformation capture assays. Conversely, EWS-FLI1 inactivates conserved enhancers containing canonical ETS motifs by displacing wild-type ETS transcription factors and abrogating p300 recruitment. ChIP-seq for of 4 histone modifications (H3K27ac, H3K4me1, H3K4me3 and H3K27me3), FLI1, p300, WDR5, ELF1 and GABPA in primary Ewing sarcomas, Ewing sarcoma cell lines (A673 and SKMNC cells), and mesenchymal stem cells (MSC). EWS-FLI1 was knocked down in Ewing sarcoma cell lines with lentiviral shRNAs (shFLI1 and shGFP control). EWS-FLI1 was expressed in MSCs with lentiviral expression vectors (pLIV EWSFLI1 or pLIV empty vector control). * Raw data not provided for the MSC and Primary Ewing sarcoma samples. *
2014-10-30 | E-GEOD-61944 | biostudies-arrayexpress
Project description:Genome-wide profiling of Ewing sarcoma cell lines with nu7441 treatment
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Project description:MicroRNA expression profiling of Ewing sarcoma cell lines upon TARBP2 depletion
| PRJNA154099 | ENA
Project description:Study of promoter methylation of ewing sarcoma cell lines and mesenchymal stem cell from ewing sarcoma patients and healthy donors
2018-10-24 | GSE118872 | GEO
Project description:The Ewing Sarcoma cell lines A673, SK-ES-1, and SK-N-MC were treated with without 5-AZA to identify upregulated genes
2012-09-01 | GSE36858 | GEO