ArticleNature communications2020
Oncogenic hijacking of a developmental transcription factor evokes vulnerability toward oxidative stress in Ewing sarcoma.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 58 citations in OpenAlex.
- Analysis of Colony Formation Capacity in Ewing Sarcoma.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Application of Resazurin and ATP Detection Cell Viability Assays for Drug Sensitivity Screening in Ewing Sarcoma.Methods in molecular biology (Clifton, N.J.) · 2027Article
- What's new in pediatric bone sarcomas and benign bone tumors.Journal of children's orthopaedics · 2026Article
- UBA1 drives cell cycle to promote malignancy and serves as a therapeutic target in Ewing Sarcoma.BMC cancer · 2026Article
- Targeting GPX4 and FSP1 to exploit ferroptotic vulnerability in Ewing sarcoma.Frontiers in oncology · 2026Article
- A Vascularized Microphysiological System Reproducing Endochondral Ossification in Vitro to Study Ewing Sarcoma Proliferation and Migration.Advanced functional materials · 2026Article
- EWS-RNA Binding Protein 1: Structural Insights into Ewing Sarcoma by Conformational Dynamics Investigations.Current cancer drug targets · 2026Article
- The hegemonic EWSR1::ETS oncoprotein overrules core regulatory circuitry principles in Ewing sarcoma.NPJ precision oncology · 2025Article
- FET fusion oncoproteins enrich SWI/SNF complex subtypes and interaction partners.Cellular & molecular biology letters · 2025Article
- Subversion of mRNA degradation pathways by EWSR1::FLI1 represents a therapeutic vulnerability in Ewing sarcoma.Nature communications · 2025Article
- The interplay between driver mutation and oxidative stress in colorectal cancer: from pathogenesis to therapeutics.Journal of translational medicine · 2025Review
- Robust statistical assessment of Oncogenotype to Organotropism translation in xenografted zebrafish.bioRxiv : the preprint server for biology · 2025Article
- Refined culture conditions with increased physiological relevance uncover oncogene-dependent metabolic signatures in Ewing sarcoma spheroids.Cell reports methods · 2025Article
- Genomic and phenotypic stability of fusion-driven pediatric sarcoma cell lines.Nature communications · 2025Article
- Mammalian copper homeostasis: physiological roles and molecular mechanisms.Physiological reviews · 2025Review
- The outcast of medicine: metals in medicine--from traditional mineral medicine to metallodrugs.Frontiers in pharmacology · 2025Review
- A novel histone acetylation-associated gene signature with prognostic value in Ewing sarcoma.Discover oncology · 2024Article
- Prion-like domain mediated phase separation of ARID1A promotes oncogenic potential of Ewing's sarcoma.Nature communications · 2024Article
- Auranofin and reactive oxygen species inhibit protein synthesis and regulate the level of the PLK1 protein in Ewing sarcoma cells.Frontiers in oncology · 2024Article
- Hypoxia and HIFs in Ewing sarcoma: new perspectives on a multi-facetted relationship.Molecular cancer · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
25 authors at 8 institutions in 4 countries.
Funding
Abstract
Ewing sarcoma (EwS) is an aggressive childhood cancer likely originating from mesenchymal stem cells or osteo-chondrogenic progenitors. It is characterized by fusion oncoproteins involving EWSR1 and variable members of the ETS-family of transcription factors (in 85% FLI1). EWSR1-FLI1 can induce target genes by using GGAA-microsatellites as enhancers.Here, we show that EWSR1-FLI1 hijacks the developmental transcription factor SOX6 - a physiological driver of proliferation of osteo-chondrogenic progenitors - by binding to an intronic GGAA-microsatellite, which promotes EwS growth in vitro and in vivo. Through integration of transcriptome-profiling, published drug-screening data, and functional in vitro and in vivo experiments including 3D and PDX models, we discover that constitutively high SOX6 expression promotes elevated levels of oxidative stress that create a therapeutic vulnerability toward the oxidative stress-inducing drug Elesclomol.Collectively, our results exemplify how aberrant activation of a developmental transcription factor by a dominant oncogene can promote malignancy, but provide opportunities for targeted therapy.
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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.