Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA154099 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
2012-06-19 | E-GEOD-31146 | biostudies-arrayexpress
Project description:MicroRNA expression profiling of Ewing sarcoma cell lines
| PRJNA140303 | ENA
Project description:We have recently demonstrated that human paediatric mesenchymal stem cells can be reprogrammed toward a Ewing’s sarcoma family tumor (ESFT) cancer stem cell (CSC) phenotype by mechanisms that implicate microRNAs (miRNAs). Here, we show that the miRNA profile of ESFT CSC is shared by embryonic stem cells and CSC from divergent tumor types. We also provide evidence that the miRNA profile of ESFT CSC is the result of reversible disruption of TARBP2-dependent miRNA maturation. Restoration of TARBP2 activity and systemic delivery of synthetic forms of either of two of its targets, miRNA-143 or miRNA-145, inhibited ESFT CSC clonogenicity and tumor growth in vivo. Our observations suggest that CSC self-renewal and tumor initiation may depend on deregulation of TARBP2-dependent miRNA expression. 3 Ewing sarcoma cell lines: comparison between TARBP2 silencing by shRNA and control.
2012-06-19 | E-GEOD-31144 | biostudies-arrayexpress
Project description:STAG2 is a member of cohesin complex and its gene is one of the most recurrently mutated in human cancer including in Ewing sarcoma. Here, we investigated STAG2 function in the context of Ewing sarcoma and performed transcriptome profiling of a panel of 15 WT and 15 mutated STAG2 established Ewing sarcoma cell lines.
2021-04-29 | GSE171948 | GEO
Project description:We have recently demonstrated that human paediatric mesenchymal stem cells can be reprogrammed toward a Ewing’s sarcoma family tumor (ESFT) cancer stem cell (CSC) phenotype by mechanisms that implicate microRNAs (miRNAs). Here, we show that the miRNA profile of ESFT CSC is shared by embryonic stem cells and CSC from divergent tumor types. We also provide evidence that the miRNA profile of ESFT CSC is the result of reversible disruption of TARBP2-dependent miRNA maturation. Restoration of TARBP2 activity and systemic delivery of synthetic forms of either of two of its targets, miRNA-143 or miRNA-145, inhibited ESFT CSC clonogenicity and tumor growth in vivo. Our observations suggest that CSC self-renewal and tumor initiation may depend on deregulation of TARBP2-dependent miRNA expression. 2 Ewing sarcoma primary samples: comparison between spheres and derived adherent cells.
2012-06-19 | E-GEOD-31145 | biostudies-arrayexpress
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:Tumor: tumor microenvironment (TME) interactions are critical for tumor progression and the composition and structure of the local extracellular matrix (ECM) are key determinants of tumor metastasis. We recently reported that activation of Wnt/beta- catenin signaling in Ewing sarcoma cells induces widespread transcriptional changes that are associated with acquisition of a metastatic tumor phenotype. Significantly, ECM protein-encoding genes were found to be enriched among Wnt/beta-catenin induced transcripts, leading us to hypothesize that activation of canonical Wnt signaling might induce changes in the Ewing sarcoma secretome. To address this hypothesis, conditioned media from Ewing sarcoma cell lines cultured in the presence or absence of Wnt3a was collected for proteomic analysis. Label-free mass spectrometry was used to identify and quantify differentially secreted proteins. We then used in silico databases to identify only proteins annotated as secreted. Comparison of the secretomes of two Ewing sarcoma cell lines revealed numerous shared proteins, as well as a degree of heterogeneity, in both basal and Wnt-stimulated conditions. Gene set enrichment analysis of secreted proteins revealed that Wnt stimulation reproducibly resulted in increased secretion of proteins involved in ECM organization, ECM receptor interactions, and collagen formation. In particular, Wnt-stimulated Ewing sarcoma cells upregulated secretion of structural collagens, as well as matricellular proteins, such as the metastasis-associated protein, tenascin C (TNC). Interrogation of published databases confirmed reproducible correlations between Wnt/beta-catenin activation and TNC and COL1A1 expression in patient tumors. In summary, this first study of the Ewing sarcoma secretome reveals that Wnt/beta-catenin activated tumor cells upregulate secretion of ECM proteins. Such Wnt/beta-catenin mediated changes are likely to impact on tumor: TME interactions that contribute to metastatic progression.
2018-02-07 | PXD007909 | Pride
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
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.
2021-11-22 | GSE184679 | GEO