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5- AZA treatment of EWS cell lines

ABSTRACT: The Ewing Sarcoma cell lines A673, SK-ES-1, and SK-N-MC were treated with without 5-AZA to identify upregulated genes

ORGANISM(S): Homo sapiens

PROVIDER: GSE36858 | GEO | 2012/09/01

SECONDARY ACCESSION(S): PRJNA156961

REPOSITORIES: GEO

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5- AZA treatment of EWS cell lines

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 A673, SK-ES-1, and SK-N-MC were treated with 5-AZA

2012-09-01 | E-GEOD-36858 | biostudies-arrayexpress

Ewing sarcoma compared to a normal body map

Project description:Primary pediatric Ewing sarcoma (ES), one uncharacterized sarcoma as well as primary and well established ES cell lines were compared to probes of different normal tissues 8 Ewing sarcoma patient samples (MuET-x), 3 primary ES cell lines (SB-KMS-y), 3 well established ES cell lines (A673, SK-N-MC, RD-ES) and 22 normal tissues (PBMC, spleen, thymus, stomach, ...., uterus, fetal brain, fetal liver) were analyzed.

2013-05-01 | E-GEOD-45544 | biostudies-arrayexpress

Transcriptomic profiling of Ewing's sarcoma cell lines after knockdown of TRIP6

Project description:This study aimed to explore the role of the Zyxin-related protein TRIP6 (thyroid receptor interacting protein 6) in Ewing's sarcoma (ES). By interrogation of published miccroarray data, we observed that of all seven Zyxin-proteins only TRIP6 is highly overexpressed in ES compared to normal tissues. RNA interference experiments and subsequent microarray and gene-set enrichment analyses indicated that TRIP6 expression is associated wth a pro-proliferative and pro-invasive transcriptional signature. Consistently, functional assays demonstrated that TRIP6 promotes migration, invasion, long-term proliferation and clonogencity of ES cells. A673 and SK-N-MC Ewing sarcoma cells were transfected with specific siRNA against TRIP6 (siTRIP6_4 or siTRIP6_5) or negative control siRNA (siControl) or Mock-transfected.

2014-01-01 | E-GEOD-48010 | biostudies-arrayexpress

Human A673 Ewing sarcoma secretome - effect of EWS-FLI-1 silencing

Project description:EWS-FLI-1 was silenced by an shRNA in A673 Ewing sarcoma cells and the resulting alterations in the secretome was analyzed by GeLC-MS/MS approach (six gel slices for each sample, luciferase shRNA-expressing cell secretome as control)

2021-07-06 | PXD016052 | Pride

Gene expression profiling of human Ewing sarcoma cells after knockdown of EGR2 or EWSR1-FLI1.

Project description:To get insight in the functional role of EGR2 for Ewing sarcoma, we performed a transcriptional profiling of Ewing sarcoma cells after knockdown of EGR2 and compared the resulting transcriptional signature with that of EWSR1-FLI1-silenced Ewing sarcoma cells. In accordance with the strong EGR2-induction by EWSR1-FLI1, both genes highly significantly overlap in their transcriptional signatures. Gene-set enrichment analyses (GSEA) and DAVID (Database for Annotation, Visualisation and Integrated Discovery) gene ontology analyses indicated a strong impact of EGR2 on cholesterol and lipid biosynthesis resembling its function in orchestrating lipid metabolism of myelinating Schwann cells. A673 and SK-N-MC Ewing sarcoma cells were transfected with specific siRNAs directed against EGR2 or EWSR1-FLI1 or non-targeting control siRNA. 48 h thereafter RNA was harvested and processed for microarray analysis.

2015-07-26 | E-GEOD-62090 | biostudies-arrayexpress

Gene expression of two Ewing sarcoma cell lines (SK-N-MC, RDES), transfected with inducible shControl or two different shRNA against PRC1

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Gene expression of two Ewing sarcoma cell lines (SK-N-MC, TC-71), transfected with inducible re-expression of TCF7L1 or Empty control

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EWS::FLI cooperatively binds at GGAA microsatellites via DBD-a4 helix

Project description:Multi-omics study of DBD-a4 helix of EWS::FLI to understand the underlying mechanism of transcriptional regulation in Ewing sarcoma cell line: A673

2024-02-01 | GSE249578 | GEO

RNA-seq data in A673 & TC71 Ewing cell lines (STAG1 and STAG2 knock-out and proficient models and silenced for EWS-FLI1)

Project description:STAG2, a member of cohesin, is one of the most recurrently mutated genes in human cancer. Here, we investigated STAG2 function in the context of Ewing sarcoma, an aggressive bone tumor driven by EWS-FLI1 oncogene chimeric transcription factor. Using a CRISPR/Cas9 approach, we generated three STAG2 knock-out isogenic clones (A673SA2m#1, TC71SA2m#1 and TC71SA2m#2) derived from A673 and TC71 STAG2 wild type (WT) Ewing sarcoma cell line. A STAG2 rescue model (A673_SA2r) generated by correcting the CRISPR mutation in the A673SA2m#1 model was also profiled using RNA-seq. Comparison of RNA-seq data allowed highlighting a broad transcriptional modulation upon STAG2 knock-out. In addition, we compared these analyses with STAG1 knock-out A673 derived model (A673SA1m#1) and with A673 (WT) and TC71 (WT) parental cells lines transfected with siCT or siEWS-FLI1.

2021-04-29 | GSE132966 | GEO

Expression data for analysis of genes regulated by EWS/FLI1 protein levels in Ewing sarcoma cell line A673

Project description:Comparison of gene expression profile of Ewing sarcoma cells which have an exchange of the endogenous EWS/FLI1 to either wild-type or a turnover-deficient mutant EWS/FLI1. Most target genes are saturated as only a few target genes are soly driven by increasing protein amount. The effect of a stable EWS/FLI1 mutant on global gene expression was evaluated in A673 Ewing sarcoma cells.

2016-11-16 | GSE81018 | GEO

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