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Gene expression of two Ewing sarcoma cell lines (A-673, ES7), treated with triapine (3-AP) or vehicle (DMSO)

ABSTRACT: This dataset comprises transcriptome data of two Ewing sarcoma cell lines (A-673, ES7) after treatment with triapine (3-AP) or vehicle (DMSO) for 72h.

ORGANISM(S): Homo sapiens

PROVIDER: GSE166419 | GEO | 2021/08/03

REPOSITORIES: GEO

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Gene expression of two Ewing sarcoma cell lines (A-673, ES7), treated with triapine (3-AP) or vehicle (DMSO)

Project description:Gene expression of two Ewing sarcoma cell lines (A-673, ES7), treated with triapine (3-AP) or vehicle (DMSO)

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Gene expression of two Ewing sarcoma cell lines (A-673, ES7), transduced with inducible shControl or two different shRNA against RRM2

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Ewing Sarcoma

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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

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Project description:Ribonucleotide reductase (RNR) is the rate limiting enzyme in the synthesis of deoxyribonucleotides and the target of multiple chemotherapy drugs, including gemcitabine and hydroxyurea. In previous work, we identified that inhibition of RNR in Ewing sarcoma tumors upregulates the expression levels of multiple members of the activator protein-1 (AP-1) transcription factor family, including c-Jun and c-Fos, and downregulates the expression of c-Myc. However, the broader functions and downstream targets of AP-1, which are highly context- and cell-dependent, are unknown in Ewing sarcoma tumors. Consequently, in this work, we used genetically defined models, transcriptome profiling, and gene set enrichment analysis to identify that AP-1 and EWS-FLI1, the driver oncogene in most Ewing sarcoma tumors, reciprocally regulate the expression of multiple extracellular matrix proteins, including fibronectins, integrins, and collagens. AP-1 expression in Ewing sarcoma cells also drives, coincident with these perturbations in gene and protein expression, changes in cell morphology and phenotype. Furthermore, we also identified that the EWS-FLI1 oncoprotein dysregulates the expression of multiple AP-1 proteins, aligning with previous reports demonstrating genetic and physical interactions between EWS-FLI1 and AP-1. Overall, these results provide novel insight into the distinct, EWS-FLI1-dependent features of Ewing sarcoma tumors and identify a novel, reciprocal regulation of extracellular matrix components by EWS-FLI1 and AP-1.

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