Project description:We performed ChIPseq on histone modification marks, transcriptional factors and chromatin architectural proteins in TC-32 and TC-71 Ewing sarcoma cell lines.
Project description:This dataset comprises trnscriptome data of two Ewing sarcoma cell lines (SK-N-MC and TC-71) after re-expression of the gene TCF7L1
Project description:In this dataset, we include the gene expression and exon splicing variants of two Ewing sarcoma cell lines (RDES and TC-32) after knockdown of the transcription factor SOX6 in order to obtain differentially expressed genes and different exon splicing variants.
Project description:Ewing's Sarcoma cell lines were made resistant to different IGF-1R drugs to investigate mechanisms and pathways modulated by the resistance. EWS TC-71 cell line was exposed to increasing concentration to three different anti-IGF-1R drugs (HAb AVE1642, TKI NVP-AEW541, HAb CP-751,871, cell lines named respectively as TC/AVE, TC/AEW or TC/CP) for at least six months. Expression profile of resistant cell variants was compared either singularly for each resistance or commonly vs. parental cell line. Two technical replicates for resistant variants and three biological replicated for parental cell were present.
Project description:Genome wide epigenomic analysis of Ewing Sarcoma human cell lines treated with 5AzadC and MC3343. Samples included 9 x TC-71, 9 x A673 samples, and 8 x PDX samples. For each cell line and condition ( 5AzadC, MC3343, Contol), we created 3 replicates, except PDX with 5AzadC treatment for which only 2 samples were created.
Project description:Affymetrix exon array data were generated from total RNA that was isolated from localized Ewing sarcoma biopsy specimens. Expression of transcript summarized data was compared to data generated from normal stem cells and normal adult tissues. Total RNA was extracted from 32 archived tumor biopsy specimens obtained from patients with localized Ewing sarcoma. Samples were analyzed by Affymetrix exon arrays using standard procedures. Data were compared to human neural crest and mesenchymal stem cells (in triplicate: GSE21511) as well as to 33 normal adult tissues (Affymetrix tissue controls; 11 tissues in triplicate: cel files obtained from: http://www.affymetrix.com/support/technical/sample_data/exon_array_data.affx). Normalization was achieved by RMA using Parkek Genomics Suite
Project description:This SuperSeries is composed of the following subset Series: GSE36857: Goldengate Methylation analysis: Ewing Sarcoma GSE36858: 5- AZA treatment of EWS cell lines Refer to individual Series
Project description:Ewing sarcoma is an aggressive pediatric small round cell tumor that predominantly occurs in bone. Approximately 85% of Ewing sarcomas harbor the EWS/FLI fusion protein, which arises from a chromosomal translocation, t(11:22)(q24:q12). EWS/FLI interacts with numerous lineage-essential transcription factors to maintain mesenchymal progenitors in an undifferentiated state. We previously showed that EWS/FLI binds the osteogenic transcription factor RUNX2 and prevents osteoblast differentiation. In this study, we investigated the role of another Runt-domain protein, RUNX3, in Ewing sarcoma. RUNX3 participates in mesenchymal-derived bone formation and is a context dependent tumor suppressor and oncogene. RUNX3 was detected in all Ewing sarcoma cells examined, whereas RUNX2 was detected in only 73% of specimens. Like RUNX2, RUNX3 binds to EWS/FLI via its Runt domain. EWS/FLI prevented RUNX3 from activating the transcription of a RUNX-responsive reporter, p6OSE2. Stable suppression of RUNX3 expression in the Ewing sarcoma cell line A673 delayed colony growth in anchorage independent soft agar assays and reversed expression of EWS/FLI-responsive genes. These results demonstrate an important role for RUNX3 in Ewing sarcoma. RNA-seq to compare transcriptiome of control A673 ewing sarcoma cells stably expression a non-target or RUNX3 shRNA
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.