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.
Project description:We examined the role of the USP6 oncogene in the patient-derived immortalized ewing sarcoma cell line RD-ES. RNA-sequncing revealed that USP6 induces numerous genes that overlap with genes induced by interferon treatment. When USP6-expressing cells were treated with IFN, many of the overlapping genes were synergistically upregulated, indicating an overlap in signaling pathways.
Project description:Analysis of differentially expressed genes in wild type MHH-ES-1 Ewing Sarcoma cells when compared to MHH-ES-1 Ewing Sarcoma cells that received six 4 Gy fractions (cumulative dose of 24 Gy) of ionizing radiation (radiation-adapted cell line). The hypothesis tested being that repeated ionizing radiation exposure of modifies radiation therapy response in Ewing Sarcoma.
Project description:Identification of genes and pathways altered by PlaB, a bacterial natural product that acts as a spliceosome modulator by targeting the SF3b subunit of the spliceosome SKNMC, TC32, TC71, and RD-ES Ewing sarcoma cell lines were treated with 0.1% (v/v) DMSO vehicle or 5nM PlaB for 24 hours. Three samples in each group were analyzed.
Project description:We identified slow-cycling cells (SCCs) in Ewing sarcoma using a label retention assay with CFSE. We labeled cells of SK-ES-1, an Ewing sarcoma cell line, with CFSE. After 5 days culture, we isolated cells retaining strong fluorescence (upper, ~10%) as SCCs and other cells (lower, ~90%) as non-slow-cycling cells (non-SCCs) using FACS AriaTM Ⅲ cell sorter.
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
Project description:Transcriptomic analysis of the well-characterized Ewing sarcoma cell line A673 indicated that one of the genes more strongly upregulated by EWSR1-FLI1 was FEZF1 (FEZ family zinc finger protein 1), a transcriptional repressor involved in brain development and neural cell identity. FEZF1 was highly expressed in Ewing sarcoma cells but not in other bone tumors such as osteosarcoma or chondrosarcoma. FEZF1 promoter contains a large GGAA-microsatellite and the number of GGAA repeats correlated positively with FEZF1 expression levels in Ewing sarcoma cell lines. To characterize the functional role of FEZF1 in Ewing sarcoma we analyzed the effect of FEZF1 knockdown in three Ewing sarcoma cell lines (A673, SKNMC, SKES1). FEZF1 knockdown inhibited clone formation in clonogenic assays and cell proliferation. Finally, we analyzed the FEZF1-dependent expression profile in A673 cells by RNAseq. Interestingly, several neural genes regulated by FEZF1 were concomitantly regulated by EWSR1-FLI1. In summary, FEZF1 is a transcriptional target of EWSR1-FLI1 in Ewing sarcoma cells involved in the regulation of neural-specific genes which could explain, at least in part, the neural-like phenotype observed in several Ewing sarcoma tumors and derived cell lines.
Project description:This SuperSeries is composed of the following subset Series: GSE30513: MicroRNA expression profiling of Ewing sarcoma cancer stem cells GSE31144: MicroRNA expression profiling of Ewing sarcoma cell lines upon TARBP2 depletion GSE31145: MicroRNA expression profiling of Ewing sarcoma spheres vs. adherent cells Refer to individual Series
