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RNA-Seq in two Ewing sarcoma cell lines: A673 and SKNMC

ABSTRACT: RNA-Seq in two Ewing sarcoma cell lines: A673 and SKNMC

PROVIDER: PRJNA482316 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7550770_1.fastq.gz	Fastqsanger.gz
	SRR7550770_2.fastq.gz	Fastqsanger.gz
	SRR7550771_1.fastq.gz	Fastqsanger.gz
	SRR7550771_2.fastq.gz	Fastqsanger.gz
	SRR7550772_1.fastq.gz	Fastqsanger.gz

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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

CTCF HiChIP data in A673 Ewing sarcoma cell lines (siCT & siSA2)

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. A673 Ewing sarcoma cell line was trasfected with siCT or 2 different siRNA targetting STAG2 during 72h and CTCF HiChIP experiments were preformed for each conditions. Analyses of HiChIP data show that STAG2 knowck-down alters CTCF-anchored loop extrusion.

2021-04-29 | GSE156650 | GEO

CTCF HiChIP data in A673 Ewing sarcoma cell lines (siCT & siSA2)

Project description:CTCF HiChIP data in A673 Ewing sarcoma cell lines (siCT & siSA2)

| PRJNA658584 | ENA

RNA-Seq in two Ewing sarcoma cell lines: A673 and SKNMC

Project description:As the second most common malignant bone tumor in children and adolescents, Ewing sarcoma is initiated and exacerbated by a chimeric oncoprotein, most commonly, EWS-FLI1. In this study, we apply epigenomic analysis to characterize the transcription dysregulation in this cancer, focusing on the investigation of super-enhancer and its associated transcriptional regulatory mechanisms. We demonstrate that super-enhancer-associated transcripts are significantly enriched in EWS-FLI1 target genes, contribute to the aberrant transcriptional network of the disease, and mediate the exceptional sensitivity of Ewing sarcoma to transcriptional inhibition. Through integrative analysis, we identify MEIS1 as a super-enhancer-driven oncogene, which co-operates with EWS-FLI1 in transcriptional regulation, and plays a key pro-survival role in Ewing sarcoma. Moreover, APCDD1, another super-enhancer-associated gene, acting as a downstream target of both MEIS1 and EWS-FLI1, is also characterized as a novel tumor-promoting factor in this malignancy. These data delineate super-enhancer-mediated transcriptional deregulation in Ewing sarcoma, and uncover numerous candidate oncogenes which can be exploited for further understanding of the molecular pathogenesis for this disease.

2018-12-04 | GSE117485 | GEO

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

Ewing sarcoma cell lines

Project description:Ewing sarcoma cell lines

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RNA-seq and MYC ChIP-seq in A673 Ewing sarcoma cells with RUVBL1 knockout

Project description:This dataset examined the effect of RUVBL1 knockout in A673 Ewing sarcoma cells. The gene expression profiling (RNA-seq) and the chromatin targeting of MYC (ChIP-seq) are reported.

2023-03-27 | GSE182378 | GEO

Effect of LOX-PP on the gene expression profile of the A673 cell line (Ewing sarcoma)

Project description:In this study we show that lysyl oxidase (LOX), an enzyme involved in maintaining structural integrity of the extracellular matrix, is expressed at low levels in Ewing sarcoma cells and primary tumors and is downregulated by the EWS/FLI1 oncoprotein characteristic of these tumors. Using a doxycycline inducible system to restore LOX expression in an Ewing sarcoma derived cell line, we show that LOX displays tumor suppressor activities. Interestingly, we show that the tumor suppressor activity resides in the propeptide domain of LOX (LOX-PP), an N-terminal domain produced by proteolytic cleavage during the physiological processing of LOX. Finally, we show that LOX-PP inhibits ERK/MAPK signalling pathway, and that many pathways involved in cell cycle progression were significant deregulated by LOX-PP, providing a mechanistic explanation to the cell proliferation inhibition observed upon LOX-PP expression. In summary, our observations indicate that deregulation of the LOX gene participates in Ewing sarcoma development and identify LOX-PP as a new therapeutic target for one of the most aggressive paediatric malignancies. These findings suggest that therapeutic strategies based in the administration of LOX propeptide or functional analogues could be useful in the treatment of this devastating paediatric cancer. A673 cells derived from Ewing sarcoma were genetically enginereed to express LOX-PP upon doxycycline stimulation (72 hours). Three independent experiments from control cells and three independent experiments from A673 cells expressing LOX-PP were done. Gene expression profile in A673 cells expressing LOX-PP vs control cells were compared.

2013-12-31 | E-GEOD-46407 | biostudies-arrayexpress

KSDM1b Role in Ewing Sarcoma

Project description:This study looks at the transcriptional profile of LSD2 knockdown in A673 Ewing sarcoma cells.

2019-08-29 | GSE126275 | GEO

Transcription profiling of human Ewing sarcoma (A673) cells treated with cytarabine, doxorubicin and puromycin oral tongue squamous cell carcinomas to identify novel potential prognosticators

Project description:An increasing number of cancer-associated mutations have been identified. Unfortunately, little therapy today exploits these tumor-specific genetic lesions. Often, the resulting oncoproteins have been intractable to easy manipulation with current small molecule screening approaches. To overcome this impasse, we developed an expression-based approach to small molecule library screening. We applied this platform to the discovery of modulators of the activity of EWS/FLI, the Ewing sarcoma associated oncoprotein. Cytarabine (ARA-C) was identified as the top hit in a small molecule library screen. ARA-C modulates EWS/FLI by decreasing EWS/FLI protein level and has striking effects on cellular viability and transformation in in vitro and in vivo models of Ewing sarcoma. With poor outcomes for patients with relapsed Ewing sarcoma and the well established safety profile of ARA-C, clinical trials testing ARA-C in Ewing sarcoma are warranted. Expression data was created for A673 cells treated with ARA-C and two other compounds used to treat Ewing sarcoma (Puromycin and Doxorubicin) at two doses (EC50 and 2xEC50) and three time points (24 hours, 3 days, and 5 days). Experiment Overall Design: A673 cells were treated with ARA-C (at doses of EC50 and 2xEC50) or vehicle in triplicate and expression profiled at 24 hours, 3 days, and 5 days. To exclude the possibility that ARA-C's modulation of the EWS/FLI signature was simply a non-specific response to treatment with all cytotoxic agents, we asked whether other compounds known to kill Ewing sarcoma cells (Doxorubicin and Puromycin) would induce the EWS/FLI off genome-wide expression pattern. A673 cells were treated with Doxorubicin and Puromycin (at doses of EC50 and 2xEC50) and expression profiled at 24 hours, 3 days, and 5 days.

2008-11-22 | E-GEOD-6930 | biostudies-arrayexpress

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