ArticlePloS one2017
Identification of two types of GGAA-microsatellites and their roles in EWS/FLI binding and gene regulation in Ewing sarcoma.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 66 citations in OpenAlex.
- A Drosophila Study Model for EWS::FLI1-Induced Molecular Pathways.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Ancient and animal-specific regulatory modes of EWS::FLI1 revealed by a minimal yeast model.PNAS nexus · 2026Article
- Fusion Oncoprotein EWSR1::FLI1 Invades Nucleosomes at Consensus ETS Motifs and GGAA Microsatellites.bioRxiv : the preprint server for biology · 2026Article
- Article
- Long-read analysis of tetrameric microsatellites with vmwhere supports GGAA repeat length-dependent chromatin state association in Ewing sarcoma.bioRxiv : the preprint server for biology · 2026Article
- Mithramycin alters EWS::FLI1 DNA binding and RNA polymerase II processivity to inhibit nascent transcription.Nature communications · 2026Article
- Modelling EWS::FLI1 protein fluctuations reveal determinants of tumor plasticity in Ewing sarcoma.EMBO molecular medicine · 2026Article
- Rewiring the Fusion Oncoprotein EWSR1::FLI1 in Ewing Sarcoma with Bivalent Small Molecules.Journal of the American Chemical Society · 2025Article
- Large-scale discovery of chromatin dysregulation induced by oncofusions and other protein-coding variants.Nature biotechnology · 2025Article
- Human EWS-FLI protein levels and neomorphic functions show a complex, function-specific dose-response relationship inOpen biology · 2024Article
- ETV6 dependency in Ewing sarcoma by antagonism of EWS-FLI1-mediated enhancer activation.Nature cell biology · 2023Article
- Global chromatin landscapes identify candidate noncoding modifiers of cardiac rhythm.The Journal of clinical investigation · 2023Article
- Fli1 and Tissue Fibrosis in Various Diseases.International journal of molecular sciences · 2023Review
- Systematic multi-omics cell line profiling uncovers principles of Ewing sarcoma fusion oncogene-mediated gene regulation.Cell reports · 2022Article
- EWS::FLI1 and HOXD13 Control Tumor Cell Plasticity in Ewing Sarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Neomorphic DNA-binding enables tumor-specific therapeutic gene expression in fusion-addicted childhood sarcoma.Molecular cancer · 2022Article
- Regulation of Metastasis in Ewing Sarcoma.Cancers · 2022Review
- EWS/FLI mediated reprogramming of 3D chromatin promotes an altered transcriptional state in Ewing sarcoma.Nucleic acids research · 2022Article
- Epigenetic and Transcriptional Signaling in Ewing Sarcoma-Disease Etiology and Therapeutic Opportunities.Biomedicines · 2022Review
- Dysregulated heparan sulfate proteoglycan metabolism promotes Ewing sarcoma tumor growth.eLife · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Ewing sarcoma is a bone malignancy of children and young adults, frequently harboring the EWS/FLI chromosomal translocation. The resulting fusion protein is an aberrant transcription factor that uses highly repetitive GGAA-containing elements (microsatellites) to activate and repress thousands of target genes mediating oncogenesis. However, the mechanisms of EWS/FLI interaction with microsatellites and regulation of target gene expression is not clearly understood. Here, we profile genome-wide protein binding and gene expression. Using a combination of unbiased genome-wide computational and experimental analysis, we define GGAA-microsatellites in a Ewing sarcoma context. We identify two distinct classes of GGAA-microsatellites and demonstrate that EWS/FLI responsiveness is dependent on microsatellite length. At close range "promoter-like" microsatellites, EWS/FLI binding and subsequent target gene activation is highly dependent on number of GGAA-motifs. "Enhancer-like" microsatellites demonstrate length-dependent EWS/FLI binding, but minimal correlation for activated and none for repressed targets. Our data suggest EWS/FLI binds to "promoter-like" and "enhancer-like" microsatellites to mediate activation and repression of target genes through different regulatory mechanisms. Such characterization contributes valuable insight to EWS/FLI transcription factor biology and clarifies the role of GGAA-microsatellites on a global genomic scale. This may provide unique perspective on the role of non-coding DNA in cancer susceptibility and therapeutic development.
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