ArticleGenes & cancer2019
Transcriptomic analysis functionally maps the intrinsically disordered domain of EWS/FLI and reveals novel transcriptional dependencies for oncogenesis.
Article in Genes & cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Seclidemstat (SP-2577) Induces Transcriptomic Reprogramming and Cytotoxicity in Multiple Fusion-Positive Sarcomas.Cancer research communications · 2025Article
- Endogenous EWSR1-FLI1 degron alleles enable control of fusion oncoprotein expression in tumor cell lines and xenografts.bioRxiv : the preprint server for biology · 2024Article
- Seclidemstat blocks the transcriptional function of multiple FET-fusion oncoproteins.bioRxiv : the preprint server for biology · 2024Article
- Ewing Sarcoma Related protein 1 recognizes R-loops by binding DNA forks.Biopolymers · 2024Article
- Ewing Sarcoma Related protein 1 recognizes R-loops by binding DNA forks.bioRxiv : the preprint server for biology · 2024Article
- Article
- EWS/FLI mediated reprogramming of 3D chromatin promotes an altered transcriptional state in Ewing sarcoma.Nucleic acids research · 2022Article
- Mitochondrial Dysfunction Is a Driver of SP-2509 Drug Resistance in Ewing Sarcoma.Molecular cancer research : MCR · 2022Article
- Lysine specific demethylase 1 is a molecular driver and therapeutic target in sarcoma.Frontiers in oncology · 2022Review
- Identification of a NovelMolecular cancer research : MCR · 2021Article
- EWS-FLI1 and Menin Converge to Regulate ATF4 Activity in Ewing Sarcoma.Molecular cancer research : MCR · 2021Article
- Article
- Chromatin profiling reveals relocalization of lysine-specific demethylase 1 by an oncogenic fusion protein.Epigenetics · 2021Article
- Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis.Journal of visualized experiments : JoVE · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
EWS/FLI is the pathognomic fusion oncoprotein that drives Ewing sarcoma. The amino-terminal EWS portion coordinates transcriptional regulation and the carboxy-terminal FLI portion contains an ETS DNA-binding domain. EWS/FLI acts as an aberrant transcription factor, orchestrating a complex mix of gene activation and repression, from both high affinity ETS motifs and repetitive GGAA-microsatellites. Our overarching hypothesis is that executing multi-faceted transcriptional regulation requires EWS/FLI to use distinct molecular mechanisms at different loci. Many attempts have been made to map distinct functions to specific features of the EWS domain, but described deletion mutants are either fully active or completely "dead" and other approaches have been limited by the repetitive and disordered nature of the EWS domain. Here, we use transcriptomic approaches to show an EWS/FLI mutant, called DAF, previously thought to be nonfunctional, displays context-dependent and partial transcriptional activity but lacks transforming capacity. Using transcriptomic and phenotypic anchorage-independent growth profiles of other EWS/FLI mutants coupled with reported EWS/FLI localization data, we have mapped the critical structure-function requirements of the EWS domain for EWS/FLI-mediated oncogenesis. This approach defined unique classes of EWS/FLI response elements and revealed novel structure-function relationships required for EWS/FLI activation at these response elements.
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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.