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

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 deubiquit...

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Published in:EMBO molecular medicine Vol. 8; no. 8; pp. 851 - 862
Main Authors: Engel, Katharina, Rudelius, Martina, Slawska, Jolanta, Jacobs, Laura, Ahangarian Abhari, Behnaz, Altmann, Bettina, Kurutz, Julia, Rathakrishnan, Abirami, Fernández‐Sáiz, Vanesa, Brunner, Andrä, Targosz, Bianca‐Sabrina, Loewecke, Felicia, Gloeckner, Christian Johannes, Ueffing, Marius, Fulda, Simone, Pfreundschuh, Michael, Trümper, Lorenz, Klapper, Wolfram, Keller, Ulrich, Jost, Philipp J, Rosenwald, Andreas, Peschel, Christian, Bassermann, Florian
Format: Journal Article
Language:English
Published: London Nature Publishing Group UK 01.08.2016
EMBO Press
John Wiley and Sons Inc
Springer Nature
Subjects:
Animals
Antineoplastic Agents - pharmacology
Apoptosis
B-cell lymphoma
B-Lymphocytes - drug effects
B-Lymphocytes - physiology
Cancer therapies
Cell cycle
Cell Death
Cell fate
Cells, Cultured
Chemoresistance
Chemotherapy
Chromosomes
Disease Models, Animal
Drug Resistance
EMBO03
EMBO18
Genomes
Humans
IAP protein
Lymphocytes B
Lymphoma
Lymphoma, B-Cell - pathology
Medical prognosis
Mice
Mitosis
Myc protein
Protein Processing, Post-Translational
Proteins
Therapeutic applications
Tumors
ubiquitin
Ubiquitin - metabolism
Ubiquitin Thiolesterase - metabolism
USP9X
X-Linked Inhibitor of Apoptosis Protein - metabolism
XIAP
XIAP protein
United Kingdom > UK
XIAP
mitosis
USP9X
B‐cell lymphoma
ubiquitin
ISSN:1757-4676, 1757-4684, 1757-4684
Online Access:Get full text
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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. Synopsis USP9X deubiquitylates and stabilizes anti‐apoptotic protein XIAP and promotes mitotic survival. Overexpression of USP9X/XIAP confers chemotherapy resistance and associates with decreased survival in aggressive B‐cell lymphoma patients. USP9X deubiquitylates and stabilizes XIAP in mitosis The USP9X‐XIAP pathway promotes mitotic survival USP9X and XIAP are overexpressed in Diffuse Large B Cell Lymphoma (DLBCL) The USP9X‐XIAP axis promotes lymphoma growth and resistance to spindle poisons Overexpression of USP9X and XIAP associates with chemotherapy resistance in DLBCL patients Graphical Abstract USP9X deubiquitylates and stabilizes anti‐apoptotic protein XIAP and promotes mitotic survival. Overexpression of USP9X/XIAP confers chemotherapy resistance and associates with decreased survival in aggressive B‐cell lymphoma patients.
AbstractList 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. Synopsis USP9X deubiquitylates and stabilizes anti‐apoptotic protein XIAP and promotes mitotic survival. Overexpression of USP9X/XIAP confers chemotherapy resistance and associates with decreased survival in aggressive B‐cell lymphoma patients. USP9X deubiquitylates and stabilizes XIAP in mitosis The USP9X‐XIAP pathway promotes mitotic survival USP9X and XIAP are overexpressed in Diffuse Large B Cell Lymphoma (DLBCL) The USP9X‐XIAP axis promotes lymphoma growth and resistance to spindle poisons Overexpression of USP9X and XIAP associates with chemotherapy resistance in DLBCL patients USP9X deubiquitylates and stabilizes anti‐apoptotic protein XIAP and promotes mitotic survival. Overexpression of USP9X/XIAP confers chemotherapy resistance and associates with decreased survival in aggressive B‐cell lymphoma patients.
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.
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.
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. Synopsis USP9X deubiquitylates and stabilizes anti‐apoptotic protein XIAP and promotes mitotic survival. Overexpression of USP9X/XIAP confers chemotherapy resistance and associates with decreased survival in aggressive B‐cell lymphoma patients. USP9X deubiquitylates and stabilizes XIAP in mitosis The USP9X‐XIAP pathway promotes mitotic survival USP9X and XIAP are overexpressed in Diffuse Large B Cell Lymphoma (DLBCL) The USP9X‐XIAP axis promotes lymphoma growth and resistance to spindle poisons Overexpression of USP9X and XIAP associates with chemotherapy resistance in DLBCL patients Graphical Abstract USP9X deubiquitylates and stabilizes anti‐apoptotic protein XIAP and promotes mitotic survival. Overexpression of USP9X/XIAP confers chemotherapy resistance and associates with decreased survival in aggressive B‐cell lymphoma patients.
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.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.
Author Engel, Katharina
Pfreundschuh, Michael
Fernández‐Sáiz, Vanesa
Brunner, Andrä
Ueffing, Marius
Ahangarian Abhari, Behnaz
Klapper, Wolfram
Fulda, Simone
Peschel, Christian
Rudelius, Martina
Gloeckner, Christian Johannes
Rathakrishnan, Abirami
Altmann, Bettina
Keller, Ulrich
Rosenwald, Andreas
Kurutz, Julia
Slawska, Jolanta
Targosz, Bianca‐Sabrina
Trümper, Lorenz
Jacobs, Laura
Loewecke, Felicia
Bassermann, Florian
Jost, Philipp J
AuthorAffiliation 7 German Center for Neurodegenerative Diseases (DZNE) Tübingen Germany
6 Eberhard‐Karls‐Universität Tübingen Institute for Ophthalmic Research Medical Proteome Center Tübingen Germany
3 Institut für Experimentelle Tumorforschung in der Pädiatrie Goethe‐Universität Frankfurt Frankfurt am Main Germany
2 Institute of Pathology and Comprehensive Cancer Center Mainfranken Universität Würzburg Würzburg Germany
8 Department of Medicine I Saarland University Medical School Homburg (Saar) Germany
10 Institute of Pathology Haematopathology Section and Lymph Node Registry Universitätsklinikum Schleswig‐Holstein Kiel Germany
4 Institute for Medical Informatics, Statistics and Epidemiology Universität Leipzig Leipzig Germany
5 German Cancer Consortium (DKTK) German Cancer Research Center (DKFZ) Heidelberg Germany
9 Department of Hematology and Oncology Georg‐August‐Universität Göttingen Göttingen Germany
1 Department of Medicine III Klinikum Rechts der Isar Technische Universität München München Germany
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/27317434$$D View this record in MEDLINE/PubMed
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Cites_doi 10.1016/S1470-2045(08)70002-0
10.1038/40901
10.1182/asheducation-2013.1.584
10.1128/MCB.21.10.3604-3608.2001
10.1038/nrm1621
10.1038/nrd3627
10.1002/iub.300
10.1038/335440a0
10.1038/emboj.2010.112
10.1177/2040620711419001
10.1056/NEJMoa0802885
10.1016/j.clim.2009.03.517
10.1126/science.1120160
10.1016/j.bbamcr.2013.02.028
10.1016/S0092-8674(01)00274-4
10.1182/blood-2005-04-1399
10.1126/science.1106114
10.1016/j.cell.2008.05.043
10.1038/nature05257
10.1002/emmm.201303090
10.1016/j.cell.2007.10.030
10.1038/nrm3143
10.1038/onc.2011.30
10.1200/JCO.2009.26.2493
10.1002/cyto.b.21166
10.1038/nature09732
10.1016/S0092-8674(00)00008-8
10.1038/nature09779
10.1016/j.molcel.2012.04.014
10.1046/j.1365-2443.1999.00297.x
10.1016/S1097-2765(03)00054-6
10.1002/cncr.22219
10.1182/blood-2013-02-483727
10.1038/nature08646
10.1038/cdd.2011.197
10.1016/S0092-8674(01)00272-0
10.1073/pnas.0907131106
10.1126/science.1098231
10.1053/j.seminhematol.2010.01.011
10.1158/0008-5472.CAN-10-1530
10.1016/j.cell.2007.10.037
10.1016/j.critrevonc.2012.12.009
10.1146/annurev-immunol-020711-075027
10.1038/ncb2651
10.1091/mbc.E03-08-0630
10.1038/sj.cdd.4401524
10.1038/nm.3740
10.1038/318533a0
10.1016/j.cub.2012.10.006
10.1101/gad.13.20.2658
10.1073/pnas.1322198111
10.1097/MOH.0b013e3283623d7f
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Issue 8
Keywords XIAP
mitosis
USP9X
B‐cell lymphoma
ubiquitin
Language English
License Attribution
http://creativecommons.org/licenses/by/4.0
2016 The Authors. Published under the terms of the CC BY 4.0 license.
This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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References 2013; 20
2008; 9
2013; 122
2010; 463
2012; 19
2011; 12
2011; 471
2013; 5
2012; 11
2001; 104
2010; 62
2003; 11
2014; 20
1997; 388
2013; 15
2013; 2013
2010; 29
2010; 28
2005; 106
2007; 131
1999; 13
2005; 307
2008; 359
2010; 70
2012; 22
2006; 444
1988; 335
2011; 2
2013; 87
2005; 310
2009; 132
2011; 30
1999; 4
2014; 111
2004; 305
2014; 1843
2012; 30
2014; 86
2001; 21
2010; 47
1985; 318
2000; 102
2004; 15
2005; 6
2008; 134
2012; 46
2006; 107
2005; 12
2009; 106
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e_1_2_8_5_1
Wilson WH (e_1_2_8_52_1) 2013; 2013
e_1_2_8_7_1
e_1_2_8_9_1
e_1_2_8_20_1
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References_xml – volume: 29
  start-page: 2407
  year: 2010
  end-page: 2420
  article-title: Phosphorylation of Mcl‐1 by CDK1‐cyclin B1 initiates its Cdc20‐dependent destruction during mitotic arrest
  publication-title: EMBO J
– volume: 471
  start-page: 104
  year: 2011
  end-page: 109
  article-title: SCF(FBW7) regulates cellular apoptosis by targeting MCL1 for ubiquitylation and destruction
  publication-title: Nature
– volume: 22
  start-page: R966
  year: 2012
  end-page: R980
  article-title: The spindle assembly checkpoint
  publication-title: Curr Biol
– volume: 20
  start-page: 336
  year: 2013
  end-page: 344
  article-title: The genetic basis of diffuse large B‐cell lymphoma
  publication-title: Curr Opin Hematol
– volume: 20
  start-page: 1401
  year: 2014
  end-page: 1409
  article-title: Disruption of the PRKCD‐FBXO25‐HAX‐1 axis attenuates the apoptotic response and drives lymphomagenesis
  publication-title: Nat Med
– volume: 86
  start-page: 263
  year: 2014
  end-page: 271
  article-title: Clinical flow cytometric screening of SAP and XIAP expression accurately identifies patients with SH2D1A and XIAP/BIRC4 mutations
  publication-title: Cytometry B Clin Cytom
– volume: 70
  start-page: 9265
  year: 2010
  end-page: 9276
  article-title: Deubiquitinase inhibition by small‐molecule WP1130 triggers aggresome formation and tumor cell apoptosis
  publication-title: Cancer Res
– volume: 9
  start-page: 105
  year: 2008
  end-page: 116
  article-title: Six versus eight cycles of bi‐weekly CHOP‐14 with or without rituximab in elderly patients with aggressive CD20+ B‐cell lymphomas: a randomised controlled trial (RICOVER‐60)
  publication-title: Lancet Oncol
– volume: 359
  start-page: 2313
  year: 2008
  end-page: 2323
  article-title: Stromal gene signatures in large‐B‐cell lymphomas
  publication-title: N Engl J Med
– volume: 46
  start-page: 746
  year: 2012
  end-page: 758
  article-title: The ubiquitin ligase XIAP recruits LUBAC for NOD2 signaling in inflammation and innate immunity
  publication-title: Mol Cell
– volume: 132
  start-page: 116
  year: 2009
  end-page: 123
  article-title: Patients with X‐linked lymphoproliferative disease due to BIRC4 mutation have normal invariant natural killer T‐cell populations
  publication-title: Clin Immunol
– volume: 471
  start-page: 110
  year: 2011
  end-page: 114
  article-title: Sensitivity to antitubulin chemotherapeutics is regulated by MCL1 and FBW7
  publication-title: Nature
– volume: 318
  start-page: 533
  year: 1985
  end-page: 538
  article-title: The c‐myc oncogene driven by immunoglobulin enhancers induces lymphoid malignancy in transgenic mice
  publication-title: Nature
– volume: 21
  start-page: 3604
  year: 2001
  end-page: 3608
  article-title: Characterization of XIAP‐deficient mice
  publication-title: Mol Cell Biol
– volume: 104
  start-page: 791
  year: 2001
  end-page: 800
  article-title: Structural basis for the inhibition of caspase‐3 by XIAP
  publication-title: Cell
– volume: 107
  start-page: 1844
  year: 2006
  end-page: 1851
  article-title: Expression of inhibitor of apoptosis proteins in B‐cell non‐Hodgkin and Hodgkin lymphomas
  publication-title: Cancer
– volume: 11
  start-page: 519
  year: 2003
  end-page: 527
  article-title: Mechanism of XIAP‐mediated inhibition of caspase‐9
  publication-title: Mol Cell
– volume: 131
  start-page: 669
  year: 2007
  end-page: 681
  article-title: IAP antagonists induce autoubiquitination of c‐IAPs, NF‐kappaB activation, and TNFalpha‐dependent apoptosis
  publication-title: Cell
– volume: 87
  start-page: 146
  year: 2013
  end-page: 171
  article-title: Diffuse large B‐cell lymphoma
  publication-title: Crit Rev Oncol Hematol
– volume: 12
  start-page: 439
  year: 2011
  end-page: 452
  article-title: Ubiquitylation in apoptosis: a post‐translational modification at the edge of life and death
  publication-title: Nat Rev Mol Cell Biol
– volume: 28
  start-page: 2373
  year: 2010
  end-page: 2380
  article-title: Standard International prognostic index remains a valid predictor of outcome for patients with aggressive CD20+ B‐cell lymphoma in the rituximab era
  publication-title: J Clin Oncol
– volume: 131
  start-page: 682
  year: 2007
  end-page: 693
  article-title: IAP antagonists target cIAP1 to induce TNFalpha‐dependent apoptosis
  publication-title: Cell
– volume: 305
  start-page: 1471
  year: 2004
  end-page: 1474
  article-title: A small molecule Smac mimic potentiates TRAIL‐ and TNFalpha‐mediated cell death
  publication-title: Science
– volume: 307
  start-page: 1101
  year: 2005
  end-page: 1104
  article-title: Obligate role of anti‐apoptotic MCL‐1 in the survival of hematopoietic stem cells
  publication-title: Science
– volume: 310
  start-page: 1499
  year: 2005
  end-page: 1504
  article-title: Chromosome alignment and segregation regulated by ubiquitination of survivin
  publication-title: Science
– volume: 122
  start-page: 1256
  year: 2013
  end-page: 1265
  article-title: Mutational and structural analysis of diffuse large B‐cell lymphoma using whole‐genome sequencing
  publication-title: Blood
– volume: 15
  start-page: 72
  year: 2013
  end-page: 81
  article-title: SCFFbxo9 and CK2 direct the cellular response to growth factor withdrawal via Tel2/Tti1 degradation and promote survival in multiple myeloma
  publication-title: Nat Cell Biol
– volume: 104
  start-page: 769
  year: 2001
  end-page: 780
  article-title: Structural basis of caspase‐7 inhibition by XIAP
  publication-title: Cell
– volume: 106
  start-page: 3183
  year: 2005
  end-page: 3190
  article-title: Diffuse large B‐cell lymphoma subgroups have distinct genetic profiles that influence tumor biology and improve gene‐expression‐based survival prediction
  publication-title: Blood
– volume: 388
  start-page: 300
  year: 1997
  end-page: 304
  article-title: X‐linked IAP is a direct inhibitor of cell‐death proteases
  publication-title: Nature
– volume: 47
  start-page: 115
  year: 2010
  end-page: 123
  article-title: Rituximab: mechanism of action
  publication-title: Semin Hematol
– volume: 15
  start-page: 1591
  year: 2004
  end-page: 1599
  article-title: The FAM deubiquitylating enzyme localizes to multiple points of protein trafficking in epithelia, where it associates with E‐cadherin and beta‐catenin
  publication-title: Mol Biol Cell
– volume: 106
  start-page: 14524
  year: 2009
  end-page: 14529
  article-title: XIAP mediates NOD signaling via interaction with RIP2
  publication-title: Proc Natl Acad Sci USA
– volume: 2013
  start-page: 584
  year: 2013
  end-page: 590
  article-title: Treatment strategies for aggressive lymphomas: what works?
  publication-title: Hematology Am Soc Hematol Educ Program
– volume: 30
  start-page: 565
  year: 2012
  end-page: 610
  article-title: Pathogenesis of human B cell lymphomas
  publication-title: Annu Rev Immunol
– volume: 11
  start-page: 109
  year: 2012
  end-page: 124
  article-title: Targeting IAP proteins for therapeutic intervention in cancer
  publication-title: Nat Rev Drug Discov
– volume: 1843
  start-page: 150
  year: 2014
  end-page: 162
  article-title: The ubiquitin proteasome system – implications for cell cycle control and the targeted treatment of cancer
  publication-title: Biochim Biophys Acta
– volume: 6
  start-page: 287
  year: 2005
  end-page: 297
  article-title: IAPs, RINGs and ubiquitylation
  publication-title: Nat Rev Mol Cell Biol
– volume: 12
  start-page: 87
  year: 2005
  end-page: 90
  article-title: XIAP‐deficiency leads to delayed lobuloalveolar development in the mammary gland
  publication-title: Cell Death Differ
– volume: 111
  start-page: 4251
  year: 2014
  end-page: 4256
  article-title: Ablation of the oncogenic transcription factor ERG by deubiquitinase inhibition in prostate cancer
  publication-title: Proc Natl Acad Sci USA
– volume: 2
  start-page: 369
  year: 2011
  end-page: 379
  article-title: The molecular biology of diffuse large B‐cell lymphoma
  publication-title: Ther Adv Hematol
– volume: 5
  start-page: 1278
  year: 2013
  end-page: 1295
  article-title: Disease‐causing mutations in the XIAP BIR2 domain impair NOD2‐dependent immune signalling
  publication-title: EMBO Mol Med
– volume: 444
  start-page: 110
  year: 2006
  end-page: 114
  article-title: XIAP deficiency in humans causes an X‐linked lymphoproliferative syndrome
  publication-title: Nature
– volume: 13
  start-page: 2658
  year: 1999
  end-page: 2669
  article-title: Disruption of the ARF‐Mdm2‐p53 tumor suppressor pathway in Myc‐induced lymphomagenesis
  publication-title: Genes Dev
– volume: 134
  start-page: 256
  year: 2008
  end-page: 267
  article-title: The Cdc14B‐Cdh1‐Plk1 axis controls the G2 DNA‐damage‐response checkpoint
  publication-title: Cell
– volume: 4
  start-page: 757
  year: 1999
  end-page: 767
  article-title: The deubiquitinating enzyme Fam interacts with and stabilizes beta‐catenin
  publication-title: Genes Cells
– volume: 30
  start-page: 2799
  year: 2011
  end-page: 2809
  article-title: Mitosis as an anti‐cancer target
  publication-title: Oncogene
– volume: 19
  start-page: 369
  year: 2012
  end-page: 377
  article-title: Killing cells by targeting mitosis
  publication-title: Cell Death Differ
– volume: 463
  start-page: 103
  year: 2010
  end-page: 107
  article-title: Deubiquitinase USP9X stabilizes MCL1 and promotes tumour cell survival
  publication-title: Nature
– volume: 62
  start-page: 140
  year: 2010
  end-page: 157
  article-title: Emerging roles of deubiquitinases in cancer‐associated pathways
  publication-title: IUBMB Life
– volume: 335
  start-page: 440
  year: 1988
  end-page: 442
  article-title: Bcl‐2 gene promotes haemopoietic cell survival and cooperates with c‐myc to immortalize pre‐B cells
  publication-title: Nature
– volume: 102
  start-page: 33
  year: 2000
  end-page: 42
  article-title: Smac, a mitochondrial protein that promotes cytochrome c‐dependent caspase activation by eliminating IAP inhibition
  publication-title: Cell
– ident: e_1_2_8_35_1
  doi: 10.1016/S1470-2045(08)70002-0
– ident: e_1_2_8_11_1
  doi: 10.1038/40901
– volume: 2013
  start-page: 584
  year: 2013
  ident: e_1_2_8_52_1
  article-title: Treatment strategies for aggressive lymphomas: what works?
  publication-title: Hematology Am Soc Hematol Educ Program
  doi: 10.1182/asheducation-2013.1.584
– ident: e_1_2_8_19_1
  doi: 10.1128/MCB.21.10.3604-3608.2001
– ident: e_1_2_8_45_1
  doi: 10.1038/nrm1621
– ident: e_1_2_8_16_1
  doi: 10.1038/nrd3627
– ident: e_1_2_8_38_1
  doi: 10.1002/iub.300
– ident: e_1_2_8_44_1
  doi: 10.1038/335440a0
– ident: e_1_2_8_18_1
  doi: 10.1038/emboj.2010.112
– ident: e_1_2_8_15_1
  doi: 10.1177/2040620711419001
– ident: e_1_2_8_25_1
  doi: 10.1056/NEJMoa0802885
– ident: e_1_2_8_28_1
  doi: 10.1016/j.clim.2009.03.517
– ident: e_1_2_8_47_1
  doi: 10.1126/science.1120160
– ident: e_1_2_8_5_1
  doi: 10.1016/j.bbamcr.2013.02.028
– ident: e_1_2_8_36_1
  doi: 10.1016/S0092-8674(01)00274-4
– ident: e_1_2_8_7_1
  doi: 10.1182/blood-2005-04-1399
– ident: e_1_2_8_33_1
  doi: 10.1126/science.1106114
– ident: e_1_2_8_4_1
  doi: 10.1016/j.cell.2008.05.043
– ident: e_1_2_8_37_1
  doi: 10.1038/nature05257
– ident: e_1_2_8_10_1
  doi: 10.1002/emmm.201303090
– ident: e_1_2_8_43_1
  doi: 10.1016/j.cell.2007.10.030
– ident: e_1_2_8_48_1
  doi: 10.1038/nrm3143
– ident: e_1_2_8_21_1
  doi: 10.1038/onc.2011.30
– ident: e_1_2_8_53_1
  doi: 10.1200/JCO.2009.26.2493
– ident: e_1_2_8_17_1
  doi: 10.1002/cyto.b.21166
– ident: e_1_2_8_20_1
  doi: 10.1038/nature09732
– ident: e_1_2_8_12_1
  doi: 10.1016/S0092-8674(00)00008-8
– ident: e_1_2_8_51_1
  doi: 10.1038/nature09779
– ident: e_1_2_8_9_1
  doi: 10.1016/j.molcel.2012.04.014
– ident: e_1_2_8_42_1
  doi: 10.1046/j.1365-2443.1999.00297.x
– ident: e_1_2_8_41_1
  doi: 10.1016/S1097-2765(03)00054-6
– ident: e_1_2_8_3_1
  doi: 10.1002/cncr.22219
– ident: e_1_2_8_30_1
  doi: 10.1182/blood-2013-02-483727
– ident: e_1_2_8_39_1
  doi: 10.1038/nature08646
– ident: e_1_2_8_27_1
  doi: 10.1038/cdd.2011.197
– ident: e_1_2_8_8_1
  doi: 10.1016/S0092-8674(01)00272-0
– ident: e_1_2_8_23_1
  doi: 10.1073/pnas.0907131106
– ident: e_1_2_8_26_1
  doi: 10.1126/science.1098231
– ident: e_1_2_8_50_1
  doi: 10.1053/j.seminhematol.2010.01.011
– ident: e_1_2_8_22_1
  doi: 10.1158/0008-5472.CAN-10-1530
– ident: e_1_2_8_46_1
  doi: 10.1016/j.cell.2007.10.037
– ident: e_1_2_8_29_1
  doi: 10.1016/j.critrevonc.2012.12.009
– ident: e_1_2_8_40_1
  doi: 10.1146/annurev-immunol-020711-075027
– ident: e_1_2_8_14_1
  doi: 10.1038/ncb2651
– ident: e_1_2_8_31_1
  doi: 10.1091/mbc.E03-08-0630
– ident: e_1_2_8_32_1
  doi: 10.1038/sj.cdd.4401524
– ident: e_1_2_8_6_1
  doi: 10.1038/nm.3740
– ident: e_1_2_8_2_1
  doi: 10.1038/318533a0
– ident: e_1_2_8_24_1
  doi: 10.1016/j.cub.2012.10.006
– ident: e_1_2_8_13_1
  doi: 10.1101/gad.13.20.2658
– ident: e_1_2_8_49_1
  doi: 10.1073/pnas.1322198111
– ident: e_1_2_8_34_1
  doi: 10.1097/MOH.0b013e3283623d7f
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Snippet The mitotic spindle assembly checkpoint (SAC) maintains genome stability and marks an important target for antineoplastic therapies. However, it has remained...
Abstract The mitotic spindle assembly checkpoint (SAC) maintains genome stability and marks an important target for antineoplastic therapies. However, it has...
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SubjectTerms Animals
Antineoplastic Agents - pharmacology
Apoptosis
B-cell lymphoma
B-Lymphocytes - drug effects
B-Lymphocytes - physiology
Cancer therapies
Cell cycle
Cell Death
Cell fate
Cells, Cultured
Chemoresistance
Chemotherapy
Chromosomes
Disease Models, Animal
Drug Resistance
EMBO03
EMBO18
Genomes
Humans
IAP protein
Lymphocytes B
Lymphoma
Lymphoma, B-Cell - pathology
Medical prognosis
Mice
Mitosis
Myc protein
Protein Processing, Post-Translational
Proteins
Therapeutic applications
Tumors
ubiquitin
Ubiquitin - metabolism
Ubiquitin Thiolesterase - metabolism
USP9X
X-Linked Inhibitor of Apoptosis Protein - metabolism
XIAP
XIAP protein
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Title USP9X stabilizes XIAP to regulate mitotic cell death and chemoresistance in aggressive B‐cell lymphoma
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