USP9X stabilizes XIAP to regulate mitotic cell death and chemoresistance in aggressive B‐cell lymphoma

Abstract The mitotic spindle assembly checkpoint (SAC) maintains genome stability and marks an important target for antineoplastic therapies. However, it has remained unclear how cells execute cell fate decisions under conditions of SAC‐induced mitotic arrest. Here, we identify USP9X as the mitotic...

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Main Authors: Katharina Engel, Martina Rudelius, Jolanta Slawska, Laura Jacobs, Behnaz Ahangarian Abhari, Bettina Altmann, Julia Kurutz, Abirami Rathakrishnan, Vanesa Fernández‐Sáiz, Andrä Brunner, Bianca‐Sabrina Targosz, Felicia Loewecke, Christian Johannes Gloeckner, Marius Ueffing, Simone Fulda, Michael Pfreundschuh, Lorenz Trümper, Wolfram Klapper, Ulrich Keller, Philipp J Jost, Andreas Rosenwald, Christian Peschel, Florian Bassermann
Format: Article
Language:English
Published: Springer Nature 2016-06-01
Series:EMBO Molecular Medicine
Subjects:
Online Access:https://doi.org/10.15252/emmm.201506047
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author Katharina Engel
Martina Rudelius
Jolanta Slawska
Laura Jacobs
Behnaz Ahangarian Abhari
Bettina Altmann
Julia Kurutz
Abirami Rathakrishnan
Vanesa Fernández‐Sáiz
Andrä Brunner
Bianca‐Sabrina Targosz
Felicia Loewecke
Christian Johannes Gloeckner
Marius Ueffing
Simone Fulda
Michael Pfreundschuh
Lorenz Trümper
Wolfram Klapper
Ulrich Keller
Philipp J Jost
Andreas Rosenwald
Christian Peschel
Florian Bassermann
author_facet Katharina Engel
Martina Rudelius
Jolanta Slawska
Laura Jacobs
Behnaz Ahangarian Abhari
Bettina Altmann
Julia Kurutz
Abirami Rathakrishnan
Vanesa Fernández‐Sáiz
Andrä Brunner
Bianca‐Sabrina Targosz
Felicia Loewecke
Christian Johannes Gloeckner
Marius Ueffing
Simone Fulda
Michael Pfreundschuh
Lorenz Trümper
Wolfram Klapper
Ulrich Keller
Philipp J Jost
Andreas Rosenwald
Christian Peschel
Florian Bassermann
author_sort Katharina Engel
collection DOAJ
description Abstract The mitotic spindle assembly checkpoint (SAC) maintains genome stability and marks an important target for antineoplastic therapies. However, it has remained unclear how cells execute cell fate decisions under conditions of SAC‐induced mitotic arrest. Here, we identify USP9X as the mitotic deubiquitinase of the X‐linked inhibitor of apoptosis protein (XIAP) and demonstrate that deubiquitylation and stabilization of XIAP by USP9X lead to increased resistance toward mitotic spindle poisons. We find that primary human aggressive B‐cell lymphoma samples exhibit high USP9X expression that correlate with XIAP overexpression. We show that high USP9X/XIAP expression is associated with shorter event‐free survival in patients treated with spindle poison‐containing chemotherapy. Accordingly, aggressive B‐cell lymphoma lines with USP9X and associated XIAP overexpression exhibit increased chemoresistance, reversed by specific inhibition of either USP9X or XIAP. Moreover, knockdown of USP9X or XIAP significantly delays lymphoma development and increases sensitivity to spindle poisons in a murine Eμ‐Myc lymphoma model. Together, we specify the USP9X–XIAP axis as a regulator of the mitotic cell fate decision and propose that USP9X and XIAP are potential prognostic biomarkers and therapeutic targets in aggressive B‐cell lymphoma.
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spelling doaj-art-b5cf9b3c87fb41cfa1b6fcd1a47c21bb2025-08-20T04:03:06ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842016-06-018885186210.15252/emmm.201506047USP9X stabilizes XIAP to regulate mitotic cell death and chemoresistance in aggressive B‐cell lymphomaKatharina Engel0Martina Rudelius1Jolanta Slawska2Laura Jacobs3Behnaz Ahangarian Abhari4Bettina Altmann5Julia Kurutz6Abirami Rathakrishnan7Vanesa Fernández‐Sáiz8Andrä Brunner9Bianca‐Sabrina Targosz10Felicia Loewecke11Christian Johannes Gloeckner12Marius Ueffing13Simone Fulda14Michael Pfreundschuh15Lorenz Trümper16Wolfram Klapper17Ulrich Keller18Philipp J Jost19Andreas Rosenwald20Christian Peschel21Florian Bassermann22Department of Medicine III, Klinikum Rechts der Isar, Technische Universität MünchenInstitute of Pathology and Comprehensive Cancer Center Mainfranken, Universität WürzburgDepartment of Medicine III, Klinikum Rechts der Isar, Technische Universität MünchenDepartment of Medicine III, Klinikum Rechts der Isar, Technische Universität MünchenInstitut für Experimentelle Tumorforschung in der Pädiatrie, Goethe‐Universität FrankfurtInstitute for Medical Informatics, Statistics and Epidemiology, Universität LeipzigDepartment of Medicine III, Klinikum Rechts der Isar, Technische Universität MünchenDepartment of Medicine III, Klinikum Rechts der Isar, Technische Universität MünchenDepartment of Medicine III, Klinikum Rechts der Isar, Technische Universität MünchenDepartment of Medicine III, Klinikum Rechts der Isar, Technische Universität MünchenDepartment of Medicine III, Klinikum Rechts der Isar, Technische Universität MünchenDepartment of Medicine III, Klinikum Rechts der Isar, Technische Universität MünchenEberhard‐Karls‐Universität Tübingen, Institute for Ophthalmic Research, Medical Proteome CenterEberhard‐Karls‐Universität Tübingen, Institute for Ophthalmic Research, Medical Proteome CenterInstitut für Experimentelle Tumorforschung in der Pädiatrie, Goethe‐Universität FrankfurtDepartment of Medicine I, Saarland University Medical SchoolDepartment of Hematology and Oncology, Georg‐August‐Universität GöttingenInstitute of Pathology, Haematopathology Section and Lymph Node Registry, Universitätsklinikum Schleswig‐HolsteinDepartment of Medicine III, Klinikum Rechts der Isar, Technische Universität MünchenDepartment of Medicine III, Klinikum Rechts der Isar, Technische Universität MünchenInstitute of Pathology and Comprehensive Cancer Center Mainfranken, Universität WürzburgDepartment of Medicine III, Klinikum Rechts der Isar, Technische Universität MünchenDepartment of Medicine III, Klinikum Rechts der Isar, Technische Universität MünchenAbstract The mitotic spindle assembly checkpoint (SAC) maintains genome stability and marks an important target for antineoplastic therapies. However, it has remained unclear how cells execute cell fate decisions under conditions of SAC‐induced mitotic arrest. Here, we identify USP9X as the mitotic deubiquitinase of the X‐linked inhibitor of apoptosis protein (XIAP) and demonstrate that deubiquitylation and stabilization of XIAP by USP9X lead to increased resistance toward mitotic spindle poisons. We find that primary human aggressive B‐cell lymphoma samples exhibit high USP9X expression that correlate with XIAP overexpression. We show that high USP9X/XIAP expression is associated with shorter event‐free survival in patients treated with spindle poison‐containing chemotherapy. Accordingly, aggressive B‐cell lymphoma lines with USP9X and associated XIAP overexpression exhibit increased chemoresistance, reversed by specific inhibition of either USP9X or XIAP. Moreover, knockdown of USP9X or XIAP significantly delays lymphoma development and increases sensitivity to spindle poisons in a murine Eμ‐Myc lymphoma model. Together, we specify the USP9X–XIAP axis as a regulator of the mitotic cell fate decision and propose that USP9X and XIAP are potential prognostic biomarkers and therapeutic targets in aggressive B‐cell lymphoma.https://doi.org/10.15252/emmm.201506047B‐cell lymphomamitosisubiquitinUSP9XXIAP
spellingShingle Katharina Engel
Martina Rudelius
Jolanta Slawska
Laura Jacobs
Behnaz Ahangarian Abhari
Bettina Altmann
Julia Kurutz
Abirami Rathakrishnan
Vanesa Fernández‐Sáiz
Andrä Brunner
Bianca‐Sabrina Targosz
Felicia Loewecke
Christian Johannes Gloeckner
Marius Ueffing
Simone Fulda
Michael Pfreundschuh
Lorenz Trümper
Wolfram Klapper
Ulrich Keller
Philipp J Jost
Andreas Rosenwald
Christian Peschel
Florian Bassermann
USP9X stabilizes XIAP to regulate mitotic cell death and chemoresistance in aggressive B‐cell lymphoma
EMBO Molecular Medicine
B‐cell lymphoma
mitosis
ubiquitin
USP9X
XIAP
title USP9X stabilizes XIAP to regulate mitotic cell death and chemoresistance in aggressive B‐cell lymphoma
title_full USP9X stabilizes XIAP to regulate mitotic cell death and chemoresistance in aggressive B‐cell lymphoma
title_fullStr USP9X stabilizes XIAP to regulate mitotic cell death and chemoresistance in aggressive B‐cell lymphoma
title_full_unstemmed USP9X stabilizes XIAP to regulate mitotic cell death and chemoresistance in aggressive B‐cell lymphoma
title_short USP9X stabilizes XIAP to regulate mitotic cell death and chemoresistance in aggressive B‐cell lymphoma
title_sort usp9x stabilizes xiap to regulate mitotic cell death and chemoresistance in aggressive b cell lymphoma
topic B‐cell lymphoma
mitosis
ubiquitin
USP9X
XIAP
url https://doi.org/10.15252/emmm.201506047
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