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Subversion of mRNA degradation pathways by EWSR1::FLI1 represents a therapeutic vulnerability in Ewing sarcoma

Nature Communications. 2025-07; 
Bartimée Galvan, Loïc Ongena, Jonathan Bruyr, Gregory Fettweis, Eva Lucarelli, Arnaud Lavergne, Emeline Mariavelle, Tina M O'Grady, Zahrat El Oula Hassoun, Margaux Claes, Laurence Dubois, Kevin A W Lee, Véronique Kruys, Cyril Gueydan, Jules Durand, Eric Hervouet, Florian H Geyer, Ana Banito, Roland Imle, Lianghao Mao, Ashok K Jayavelu, Thomas G P Grünewald, Florencia Cidre-Aranaz, Jean-Claude Twizere, Franck Dequiedt Laboratory of Gene Expression and Cancer, GIGA Institute, University of Liège (ULiège), Liège, Belgium.
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摘要

Many cancers are defined by gene fusions that frequently encode oncogenic transcription factors (TFs), such as EWSR1::FLI1 in Ewing sarcoma (EwS). Here, we report that independently to its canonical roles in transcription, EWSR1::FLI1 also functions as an mRNA decay factor, reshaping mRNA stability in EwS. This function participates in EWSR1::FLI1 tumorigenicity and involves interactions of EWSR1::FLI1 with the CCR4-NOT deadenylation complex via its EWSR1-derived low-complexity domain and with the RNA-binding protein HuR/ELAVL1 via its FLI1-derived region. Strikingly, we find that EWSR1::FLI1-mediated mRNA decay antagonizes the normal mRNA protective function of HuR and renders EwS cells highly sensitive to HuR... More

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