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Homo sapiens strain:A673 cell line

ABSTRACT: GLI1 function in Ewing sarcoma

PROVIDER: PRJNA186635 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR651370.fastq.gz	Fastqsanger.gz
	SRR651371.fastq.gz	Fastqsanger.gz
	SRR651372.fastq.gz	Fastqsanger.gz
	SRR651373.fastq.gz	Fastqsanger.gz
	SRR651374.fastq.gz	Fastqsanger.gz

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Homo sapiens strain:A673 cell line

Project description:EWS function in Ewing sarcoma

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Homo sapiens strain:A673 cell line

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Homo sapiens strain:A673 cell line

Project description:Functional studies of NKX2-2 in Ewing sarcoma

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Homo sapiens strain:TTC-466 cell line

Project description:EWS/ERG function in Ewing sarcoma

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Expression data from A673 cell line treated with compounds at several doses and time points

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). Keywords: time course and dose response

2007-03-01 | GSE6930 | 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

Homo sapiens

Project description:BCL11B function in Ewing sarcoma

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Homo sapiens

Project description:ZEB2 function in Ewing sarcoma

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ChIP-seq data in A673 Ewing cell line (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. We transfected A673 cell line with siCT or 2 differents siSTAG2 (siSA2#6 or siSA2#8) during 72h. The cells were profiled by ChIP-seq for EWS-FLI1, CTCF, cohesin members and H3K27ac marks and highlighted a global conservation of binding for these marks upon STAG2 knock-down

2021-04-29 | GSE156649 | GEO

Microarray analysis of A673 cell line stably transfected with empty vector pc3.1 versus A673 cell lines stably transfected with pcDNA3.1-LMO3-BORCS5

Project description:In order to understand what genes were regulated by the presence of a new fusion transcript (LMO3-BORCS5), we stably transfected either an empty vector (pc3.1) or vector containing LMO3-BORCS5 sequence into A673 human Ewing sarcoma cell line. 2 different clones were obtained for each condition (4 conditions total), and 4 different RNA extractions were performed for each clone (4 x 4 = 16 conditions total).

2019-06-30 | E-MTAB-7021 | biostudies-arrayexpress

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