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Requirement for YAP1 signaling in myxoid liposarcoma.

Journal article
Authors Marcel Trautmann
Ya-Yun Cheng
Patrizia Jensen
Ninel Azoitei
Ines Brunner
Jennifer Hüllein
Mikolaj Slabicki
Ilka Isfort
Magdalene Cyra
Ruth Berthold
Eva Wardelmann
Sebastian Huss
Bianca Altvater
Claudia Rossig
Susanne Hafner
Thomas Simmet
Anders Ståhlberg
Pierre Åman
Thorsten Zenz
Undine Lange
Thomas Kindler
Claudia Scholl
Wolfgang Hartmann
Stefan Fröhling
Published in EMBO molecular medicine
Volume 11
Issue 5
Pages e9889
ISSN 1757-4684
Publication year 2019
Published at Sahlgrenska Cancer Center
Institute of Biomedicine, Department of Pathology
Wallenberg Centre for Molecular and Translational Medicine
Pages e9889
Language en
Links dx.doi.org/10.15252/emmm.201809889
www.ncbi.nlm.nih.gov/entrez/query.f...
Keywords FUS‐DDIT3, Hippo pathway, YAP1; myxoid liposarcoma, verteporfin
Subject categories Cell and Molecular Biology, Cancer and Oncology

Abstract

Myxoid liposarcomas (MLS), malignant tumors of adipocyte origin, are driven by the FUS-DDIT3 fusion gene encoding an aberrant transcription factor. The mechanisms whereby FUS-DDIT3 mediates sarcomagenesis are incompletely understood, and strategies to selectively target MLS cells remain elusive. Here we show, using an unbiased functional genomic approach, that FUS-DDIT3-expressing mesenchymal stem cells and MLS cell lines are dependent on YAP1, a transcriptional co-activator and central effector of the Hippo pathway involved in tissue growth and tumorigenesis, and that increased YAP1 activity is a hallmark of human MLS Mechanistically, FUS-DDIT3 promotes YAP1 expression, nuclear localization, and transcriptional activity and physically associates with YAP1 in the nucleus of MLS cells. Pharmacologic inhibition of YAP1 activity impairs the growth of MLS cells in vitro and in vivo These findings identify overactive YAP1 signaling as unifying feature of MLS development that could represent a novel target for therapeutic intervention.

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