ArticleCell cycle (Georgetown, Tex.)2014
Ewing sarcoma EWS protein regulates midzone formation by recruiting Aurora B kinase to the midzone.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- EWSR1::FLI1 promotes neocentromere formation in ewing sarcoma cells.Cell reports · 2026Article
- The Puzzle of Genetic Stability and Chromosomal Copy Number Alterations for the Therapy of Ewing Sarcoma.Cancers · 2025Review
- Regulation of EWSR1-FLI1 Function by Post-Transcriptional and Post-Translational Modifications.Cancers · 2023Review
- EWSR1 prevents the induction of aneuploidy through direct regulation of Aurora B.Frontiers in cell and developmental biology · 2023Article
- The Landscape of Regulatory Noncoding RNAs in Ewing's Sarcoma.Biomedicines · 2021Review
- EWSR1 overexpression is a pro-oncogenic event in multiple myeloma.International journal of hematology · 2021Article
- Precision Oncology in Sarcomas: Divide and Conquer.JCO precision oncology · 2019Review
- O-GlcNAc: A Sweetheart of the Cell Cycle and DNA Damage Response.Frontiers in endocrinology · 2018Review
- Loss of Ewing sarcoma EWS allele promotes tumorigenesis by inducing chromosomal instability in zebrafish.Scientific reports · 2016Article
- EWSR1 regulates mitosis by dynamically influencing microtubule acetylation.Cell cycle (Georgetown, Tex.) · 2016Article
- O-GlcNAcylation: A sweet thorn in the spindle!Cell cycle (Georgetown, Tex.) · 2016Article
- Reduced O-GlcNAcase expression promotes mitotic errors and spindle defects.Cell cycle (Georgetown, Tex.) · 2016Article
- PRAS40 deregulates apoptosis in Ewing sarcoma family tumors by enhancing the insulin receptor/Akt and mTOR signaling pathways.American journal of cancer research · 2016Article
- Ewing sarcoma ewsa protein regulates chondrogenesis of Meckel's cartilage through modulation of Sox9 in zebrafish.PloS one · 2015Article
- Article
- Chromosomal localization of Ewing sarcoma EWSR1/FLI1 protein promotes the induction of aneuploidy.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Ewing sarcoma is a malignant bone cancer that primarily occurs in children and adolescents. Eighty-five percent of Ewing sarcoma is characterized by the presence of the aberrant chimeric EWS/FLI1 fusion gene. Previously, we demonstrated that an interaction between EWS/FLI1 and wild-type EWS led to the inhibition of EWS activity and mitotic dysfunction. Although defective mitosis is considered to be a critical step in cancer initiation, it is unknown how interference with EWS contributes to Ewing sarcoma formation. Here, we demonstrate that EWS/FLI1- and EWS-knockdown cells display a high incidence of defects in the midzone, a midline structure located between segregating chromatids during anaphase. Defects in the midzone can lead to the failure of cytokinesis and can result in the induction of aneuploidy. The similarity among the phenotypes of EWS/FLI1- and EWS siRNA-transfected HeLa cells points to the inhibition of EWS as the key mechanism for the induction of midzone defects. Supporting this observation, the ectopic expression of EWS rescues the high incidence of midzone defects observed in Ewing sarcoma A673 cells. We discovered that EWS interacts with Aurora B kinase, and that EWS is also required for recruiting Aurora B to the midzone. A domain analysis revealed that the R565 in the RGG3 domain of EWS is essential for both Aurora B interaction and the recruitment of Aurora B to the midzone. Here, we propose that the impairment of EWS-dependent midzone formation via the recruitment of Aurora B is a potential mechanism of Ewing sarcoma development.
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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.