ArticleThe Journal of biological chemistry2011
Oncogenic fusion protein EWS/FLI1 down-regulates gene expression by both transcriptional and posttranscriptional mechanisms.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Subversion of mRNA degradation pathways by EWSR1::FLI1 represents a therapeutic vulnerability in Ewing sarcoma.Nature communications · 2025Article
- Shifting from a Biological-Agnostic Approach to a Molecular-Driven Strategy in Rare Cancers: Ewing Sarcoma Archetype.Biomedicines · 2023Review
- Regulation of EWSR1-FLI1 Function by Post-Transcriptional and Post-Translational Modifications.Cancers · 2023Review
- Transcriptome profiling of Ewing sarcomas - treatment resistance pathways and IGF-dependency.Molecular oncology · 2020Article
- Establishment of a novel human CIC-DUXScientific reports · 2019Article
- Antitumor effects of β-elemene via targeting the phosphorylation of insulin receptor.Endocrine-related cancer · 2019Article
- Transcriptomic analysis functionally maps the intrinsically disordered domain of EWS/FLI and reveals novel transcriptional dependencies for oncogenesis.Genes & cancer · 2019Article
- A k-mer based transcriptomics approach for antisense drug discovery targeting the Ewing's family of tumors.Oncotarget · 2018Article
- 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
- Potential approaches to the treatment of Ewing's sarcoma.Oncotarget · 2017Review
- Oncogenic fusion protein EWS-FLI1 is a network hub that regulates alternative splicing.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Structure-function based molecular relationships in Ewing's sarcoma.BioMed research international · 2015Review
- Androgen Receptor-Mediated Growth Suppression of HPr-1AR and PC3-Lenti-AR Prostate Epithelial Cells.PloS one · 2015Article
- Suppression of FOXO1 is responsible for a growth regulatory repressive transcriptional sub-signature of EWS-FLI1 in Ewing sarcoma.Oncogene · 2014Article
- SnapShot-Seq: a method for extracting genome-wide, in vivo mRNA dynamics from a single total RNA sample.PloS one · 2014Article
- The adolescent and young adult with cancer: state of the art -- bone tumors.Current oncology reports · 2013Review
- Pediatric sarcomas: translating molecular pathogenesis of disease to novel therapeutic possibilities.Pediatric research · 2012Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Ewing family tumors are characterized by a translocation between the RNA binding protein EWS and one of five ETS transcription factors, most commonly FLI1. The fusion protein produced by the translocation has been thought to act as an aberrant transcription factor, leading to changes in gene expression and cellular transformation. In this study, we investigated the specific processes EWS/FLI1 utilizes to alter gene expression. Using both heterologous NIH 3T3 and human Ewing Family Tumor cell lines, we have demonstrated by quantitative pre-mRNA analysis that EWS/FLI1 repressed the expression of previously validated direct target genes at the level of transcript synthesis. ChIP experiments showed that EWS/FLI1 decreases the amount of Pol II at the promoter of down-regulated genes in both murine and human model systems. However, in down-regulated target genes, there was a significant disparity between the modulation of cognate mRNA and pre-mRNAs, suggesting that these genes could also be regulated at a posttranscriptional level. Confirming this, we found that EWS/FLI1 decreased the transcript half-life of insulin-like growth factor binding protein 3, a down-regulated direct target gene in human tumor-derived Ewing's sarcoma cell lines. Additionally, we have shown through reexpression experiments that full EWS/FLI1-mediated transcriptional repression requires intact EWS and ETS domains. Together these data demonstrate that EWS/FLI1 can dictate steady-state target gene expression by modulating both transcript synthesis and degradation.
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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.