ArticleGenes & cancer2012
The EWS/FLI Oncogene Drives Changes in Cellular Morphology, Adhesion, and Migration in Ewing Sarcoma.
Article in Genes & cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 111 citations in OpenAlex.
- Targeting Neuropeptide Y/DPP4 Signalling Suppresses Ewing Sarcoma Survival and Improves Monocyte Viability.International journal of molecular sciences · 2026Article
- Article
- Modelling EWS::FLI1 protein fluctuations reveal determinants of tumor plasticity in Ewing sarcoma.EMBO molecular medicine · 2026Article
- Suppressing the Aberrant Transcriptional Functionality of EWS::FLI1 Oncoprotein by Designer polyQ Fusions with Its Homologous Peptides.Biomedicines · 2026Article
- High Tau expression correlates with reduced invasion and prolonged survival in Ewing sarcoma.Cell death discovery · 2025Article
- Caveolin-1 regulates context-dependent signaling and survival in Ewing sarcoma.bioRxiv : the preprint server for biology · 2025Article
- Establishment and characterization of a patient-derived metastatic extraskeletal Ewing sarcoma cell line ES-ZSS-1.Human cell · 2024Article
- Endogenous EWSR1-FLI1 degron alleles enable control of fusion oncoprotein expression in tumor cell lines and xenografts.bioRxiv : the preprint server for biology · 2024Article
- CD99 contributes to the EWS::FLI1 transcriptome by specifically affecting FOXM1-targets involved in the G2/M cell cycle phase, thus influencing the Ewing sarcoma genetic landscape.Journal of cell communication and signaling · 2024Article
- ETS1, a Target Gene of the EWSR1::FLI1 Fusion Oncoprotein, Regulates the Expression of the Focal Adhesion Protein TENSIN3.Molecular cancer research : MCR · 2024Article
- Human EWS-FLI protein levels and neomorphic functions show a complex, function-specific dose-response relationship inOpen biology · 2024Article
- CD99 Modulates the Proteomic Landscape of Ewing Sarcoma Cells and Related Extracellular Vesicles.International journal of molecular sciences · 2024Article
- ETS1, a target gene of the EWSR1::FLI1 fusion oncoprotein, regulates the expression of the focal adhesion protein TENSIN3.bioRxiv : the preprint server for biology · 2023Article
- The PMA phorbol ester tumor promoter increases canonical Wnt signaling via macropinocytosis.eLife · 2023Article
- EWS/FLI1 Characterization, Activation, Repression, Target Genes and Therapeutic Opportunities in Ewing Sarcoma.International journal of molecular sciences · 2023Review
- Extracellular vesicle-associated IGF2BP3 tunes Ewing sarcoma cell migration and affects PI3K/Akt pathway in neighboring cells.Cancer gene therapy · 2023Article
- SIX1 and EWS/FLI1 co-regulate an anti-metastatic gene network in Ewing Sarcoma.Nature communications · 2023Article
- ETV6 dependency in Ewing sarcoma by antagonism of EWS-FLI1-mediated enhancer activation.Nature cell biology · 2023Article
- Ewing sarcoma from molecular biology to the clinic.Frontiers in cell and developmental biology · 2023Review
- A Druggable Rheostat for Ewing Sarcoma?Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Ewing sarcoma is a tumor of the bone and soft tissue caused by the expression of a translocation-derived oncogenic transcription factor, EWS/FLI. Overt metastases are associated with a poor prognosis in Ewing sarcoma, but patients without overt metastases frequently harbor micrometastatic disease at presentation. This suggests that the metastatic potential of Ewing sarcoma exists at an early stage during tumor development. We have therefore explored whether the inciting oncogenic event in Ewing sarcoma, EWS/FLI, directly modulates tumor cell features that support metastasis, such as cell adhesion, cell migration, and cytoarchitecture. We used an RNAi-based approach in patient-derived Ewing sarcoma cell lines. Although we hypothesized that EWS/FLI might induce classic metastatic features, such as increased cell adhesion, migration, and invasion (similar to the phenotypes observed when epithelial malignancies undergo an epithelial-to-mesenchymal transition during the process of metastasis), surprisingly, we found the opposite. Thus, EWS/FLI expression inhibited the adhesion of isolated cells in culture and prevented adhesion in an in vivo mouse lung assay. Cell migration was similarly inhibited by EWS/FLI expression. Furthermore, EWS/FLI expression caused a striking loss of organized actin stress fibers and focal adhesions and a concomitant loss of cell spreading, suggesting that EWS/FLI disrupts the mesenchymal phenotype of a putative tumor cell-of-origin. These data suggest a new paradigm for the dissemination and metastasis of mesenchymally derived tumors: these tumors may disseminate via a "passive/stochastic" model rather than via an "active" epithelial-to-mesenchymal type transition. In the case of Ewing sarcoma, it appears that the loss of cell adhesion needed to promote tumor cell dissemination might be induced by the EWS/FLI oncogene itself rather than via an accumulation of stepwise mutations.
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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.