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FET family fusion oncoproteins target the SWI/SNF chromatin remodeling complex

Journal article
Authors Malin Lindén
Christer Thomsen
Pernilla Grundevik
Emma Jonasson
Daniel Andersson
Rikard Runnberg
Soheila Dolatabadi
Christoffer Vannas
Manuel Luna Santamarίa
Henrik Fagman
Anders Ståhlberg
Pierre Åman
Published in EMBO Reports
Volume 20
ISSN 1469-221X
Publication year 2019
Published at Sahlgrenska Cancer Center
Institute of Biomedicine, Department of Pathology
Wallenberg Centre for Molecular and Translational Medicine
Language en
Links dx.doi.org/10.15252/embr.201845766
Keywords EWSR1-FLI1, FET proteins, FUS-DDIT3, fusion oncogenes, SWI/SNF chromatin remodeling complex
Subject categories Medical Genetics

Abstract

Members of the human FET family of RNA-binding proteins, comprising FUS, EWSR1, and TAF15, are ubiquitously expressed and engage at several levels of gene regulation. Many sarcomas and leukemias are characterized by the expression of fusion oncogenes with FET genes as 5′ partners and alternative transcription factor-coding genes as 3′ partners. Here, we report that the N terminus of normal FET proteins and their oncogenic fusion counterparts interact with the SWI/SNF chromatin remodeling complex. In contrast to normal FET proteins, increased fractions of FET oncoproteins bind SWI/SNF, indicating a deregulated and enhanced interaction in cancer. Forced expression of FET oncogenes caused changes of global H3K27 trimethylation levels, accompanied by altered gene expression patterns suggesting a shift in the antagonistic balance between SWI/SNF and repressive polycomb group complexes. Thus, deregulation of SWI/SNF activity could provide a unifying pathogenic mechanism for the large group of tumors caused by FET fusion oncoproteins. These results may help to develop common strategies for therapy. © 2019 The Authors. Published under the terms of the CC BY 4.0 license

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