Journal
PLOS ONE
Volume 15, Issue 6, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0234243
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Funding
- Asociacion Espanola Contra el Cancer (AECC)
- Ministry of Economy and Competitiveness of Spain-FEDER (CIBERONC) [PI11700464, RD06/0020/0059]
- European Commission (FP7HEALTH-2011-two-stage) [ID278742 EUROSARC]
- CIBERONC [CB16/12/00361]
- Consejeria de Salud, Junta de Andalucia [PI-0197-2016, PI-0013-2018]
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The presence of the chimeric EWSR1-FLI1 oncoprotein is the main and initiating event defining Ewing sarcoma (ES). The dysregulation of epigenomic and proteomic homeostasis induced by the oncoprotein contributes to a wide variety of events involved in oncogenesis and tumor progression. Attempts at studying the effects of EWSR1-FLI1 in non-tumor cells to understand the mechanisms underlying sarcomagenesis have been unsuccessful to date, as ectopic expression of EWSR1-FLI1 blocks cell cycle progression and induces apoptosis in the tested cell lines. Therefore, it is essential to find a permissive cell type for EWSR1-FLI1 expression that allows its endogenous molecular functions to be studied. Here we have demonstrated that HeLa cell lines are permissive to EWSR1-FLI1 ectopic expression, and that our model substantially recapitulates the endogenous activity of the EWSR1-FLI1 fusion protein. This model could contribute to better understanding ES sarcomagenesis by helping to understand the molecular mechanisms induced by the EWSR1-FLI1 oncoprotein.
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