ArticleOncogene2005
EWS-FLI1 target genes recovered from Ewing's sarcoma chromatin.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 88 citations in OpenAlex.
- Leveraging Single-Cell RNA Sequencing to Characterize Murine Ewing Sarcoma Xenografts.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Chromatin Immunoprecipitation Followed by Next-Generation Sequencing in Ewing Sarcoma.Methods in molecular biology (Clifton, N.J.) · 2027Article
- FET fusion oncoproteins enrich SWI/SNF complex subtypes and interaction partners.Cellular & molecular biology letters · 2025Article
- Caveolin-1 regulates context-dependent signaling and survival in Ewing sarcoma.bioRxiv : the preprint server for biology · 2025Article
- Understanding Pseudophosphatase Function Through Biochemical Interactions.Methods in molecular biology (Clifton, N.J.) · 2024Article
- The pseudoenzyme ADPRHL1 affects cardiac function by regulating the ROCK pathway.Stem cell research & therapy · 2023Article
- EHD1-dependent traffic of IGF-1 receptor to the cell surface is essential for Ewing sarcoma tumorigenesis and metastasis.Communications biology · 2023Article
- Regulation of EWSR1-FLI1 Function by Post-Transcriptional and Post-Translational Modifications.Cancers · 2023Review
- FET fusion oncoproteins interact with BRD4 and SWI/SNF chromatin remodelling complex subtypes in sarcoma.Molecular oncology · 2022Article
- Pseudophosphatases as Regulators of MAPK Signaling.International journal of molecular sciences · 2021Review
- The Roles of Pseudophosphatases in Disease.International journal of molecular sciences · 2021Review
- Cancer biology functional genomics: From small RNAs to big dreams.Molecular carcinogenesis · 2020Article
- A polypeptide from the junction region sequence of EWS-FLI1 inhibits Ewing's sarcoma cells, interacts with the EWS-FLI1 and partner proteins.Scientific reports · 2017Article
- MK-STYX Alters the Morphology of Primary Neurons, and Outgrowths in MK-STYX Overexpressing PC-12 Cells Develop a Neuronal Phenotype.Frontiers in molecular biosciences · 2017Article
- Targeted therapies for advanced Ewing sarcoma family of tumors.Cancer treatment reviews · 2015Review
- Suppression of FOXO1 is responsible for a growth regulatory repressive transcriptional sub-signature of EWS-FLI1 in Ewing sarcoma.Oncogene · 2014Article
- The regulatory roles of phosphatases in cancer.Oncogene · 2014Review
- Article
- The pseudophosphatase MK-STYX inhibits stress granule assembly independently of Ser149 phosphorylation of G3BP-1.The FEBS journal · 2013Article
- The biology of ewing sarcoma.ISRN oncology · 2013Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In all, 85% of Ewing's sarcoma family tumors (ESFT), a neoplasm of unknown histogenesis, express EWS-FLI1 transcription factor gene fusions. To characterize direct target genes avoiding artificial model systems, we cloned genomic DNA from ESFT chromatin precipitating with EWS-FLI1. We now present a comprehensive list of 99 putative transcription factor targets identified, for the first time, by a hypothesis-free approach based on physical interaction. Gene-derived chromatin fragments co-precipitating with EWS-FLI1 were nonrandomly distributed over the human genome and localized predominantly to the upstream region and the first two introns of the genes. At least 20% of putative direct EWS-FLI1 targets were neural genes. One-third of genes recovered showed a significant ESFT-specific expression pattern and were found to be altered upon RNAi-mediated knockdown of EWS-FLI1. Among them, MK-STYX, encoding a MAP kinase phosphatase-like protein, was consistently expressed in ESFT. EWS-FLI1 was found to drive MK-STYX expression by binding to a single ETS binding motif within the first gene intron. MK-STYX serves as precedence for successful recovery of direct EWS-FLI1 targets from the authentic ESFT cellular context, the most relevant system to study oncogenic mechanisms for the discovery of new therapeutic targets in this disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.