Affiliation:
1. Children's Cancer Institute Porto Alegre Brazil
2. National Science and Technology Institute for Children's Cancer Biology and Pediatric Oncology – INCT BioOncoPed Porto Alegre Brazil
3. Universidade de São Paulo Brazil
4. Department of Physics Universidade Federal de Santa Maria Brazil
Abstract
Ewing sarcoma (ES) is a highly aggressive pediatric tumor driven by the RNA‐binding protein EWS (EWS)/friend leukemia integration 1 transcription factor (FLI1) chimeric transcription factor, which is involved in epithelial–mesenchymal transition (EMT). EMT stabilizes a hybrid cell state, boosting metastatic potential and drug resistance. Nevertheless, the mechanisms underlying the maintenance of this hybrid phenotype in ES remain elusive. Our study proposes a logical EMT model for ES, highlighting zinc finger E‐box‐binding homeobox 2 (ZEB2), miR‐145, and miR‐200 circuits that maintain hybrid states. The model aligns with experimental findings and reveals a previously unknown circuit supporting the mesenchymal phenotype. These insights emphasize the role of ZEB2 in the maintenance of the hybrid state in ES.
Funder
Conselho Nacional de Desenvolvimento Científico e Tecnológico
Fundação de Amparo à Pesquisa do Estado de São Paulo
Ministério da Saúde
Subject
Cell Biology,Genetics,Molecular Biology,Biochemistry,Structural Biology,Biophysics
Cited by
2 articles.
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