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• W1559920963 abstract "// Henriette Franz 1 , Holger Greschik 1 , Dominica Willmann 1 , Luka Ozretić 2 , Cordula Annette Jilg 1 , Eva Wardelmann 3 , Manfred Jung 4, 6 , Reinhard Buettner 2 , Roland Schüle 1, 5, 6 1 Urologische Klinik und Zentrale Klinische Forschung, Klinikum der Universität Freiburg, Freiburg, Germany 2 Universitätsklinikum Köln, Institut für Pathologie, Köln, Germany 3 Universitätsklinikum Münster, Gerhard-Domagk-Insitut für Pathologie, Münster, Germany 4 Institut für Pharmazeutische Wissenschaften, Albert-Ludwigs-Universität Freiburg, Freiburg, Germany 5 BIOSS Centre of Biological Signaling Studies, Albert-Ludwigs-University, Freiburg, Germany 6 Deutsches Konsortium für Translationale Krebsforschung (DKTK), Standort Freiburg, Germany Correspondence to: Roland Schüle, e-mail: roland.schuele@uniklinik-freiburg.de Keywords: SPIN1, histone code reader, GDNF, RET signaling, MAZ Received: October 30, 2014      Accepted: December 21, 2014      Published: February 25, 2015 ABSTRACT The histone code reader Spindlin1 (SPIN1) has been implicated in tumorigenesis and tumor growth, but the underlying molecular mechanisms remain poorly understood. Here, we show that reducing SPIN1 levels strongly impairs proliferation and increases apoptosis of liposarcoma cells in vitro and in xenograft mouse models. Combining signaling pathway, genome-wide chromatin binding, and transcriptome analyses, we found that SPIN1 directly enhances expression of GDNF, an activator of the RET signaling pathway, in cooperation with the transcription factor MAZ. Accordingly, knockdown of SPIN1 or MAZ results in reduced levels of GDNF and activated RET explaining diminished liposarcoma cell proliferation and survival. In line with these observations, levels of SPIN1, GDNF, activated RET, and MAZ are increased in human liposarcoma compared to normal adipose tissue or lipoma. Importantly, a mutation of SPIN1 within the reader domain interfering with chromatin binding reduces liposarcoma cell proliferation and survival. Together, our data describe a molecular mechanism for SPIN1 function in liposarcoma and suggest that targeting SPIN1 chromatin association with small molecule inhibitors may represent a novel therapeutic strategy." @default.
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• W1559920963 date "2015-03-05" @default.
• W1559920963 modified "2023-10-18" @default.
• W1559920963 title "The histone code reader SPIN1 controls RET signaling in liposarcoma" @default.
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• W1559920963 doi "https://doi.org/10.18632/oncotarget.3000" @default.
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