Silencing of SENP2 in Multiple Myeloma Induces Bortezomib Resistance by Activating NF-κB Through the Modulation of IκBα Sumoylation

[1]  Xiaoshan Feng,et al.  SENP2 suppresses NF-κB activation and sensitizes breast cancer cells to doxorubicin. , 2019, European journal of pharmacology.

[2]  H. Pei,et al.  SUMO-specific protease 2 (SENP2) functions as a tumor suppressor in osteosarcoma via SOX9 degradation. , 2018, Experimental and therapeutic medicine.

[3]  María Blanca Fernández-Viñéa CURRENT STATUS AND FUTURE PERSPECTIVES , 2018 .

[4]  G. Jansen,et al.  Bortezomib resistance in multiple myeloma is associated with increased serine synthesis , 2017, Cancer & metabolism.

[5]  S. Holstein,et al.  Immunomodulatory Drugs in Multiple Myeloma: Mechanisms of Action and Clinical Experience , 2017, Drugs.

[6]  A. Dejean,et al.  SUMO and the robustness of cancer , 2017, Nature Reviews Cancer.

[7]  D. Kazandjian Multiple myeloma epidemiology and survival: A unique malignancy. , 2016, Seminars in oncology.

[8]  H. Saitsu,et al.  Bortezomib-resistance is associated with increased levels of proteasome subunits and apoptosis-avoidance , 2016, Oncotarget.

[9]  H. Goldschmidt,et al.  Treatment of multiple myeloma with high-risk cytogenetics: a consensus of the International Myeloma Working Group. , 2016, Blood.

[10]  I. Coyne,et al.  Bortezomib for the treatment of multiple myeloma. , 2016, The Cochrane database of systematic reviews.

[11]  M. Nikiforov,et al.  Oxidative stress and proteasome inhibitors in multiple myeloma. , 2016, Pharmacological research.

[12]  A. Vertegaal,et al.  SUMOylation-Mediated Regulation of Cell Cycle Progression and Cancer. , 2015, Trends in biochemical sciences.

[13]  F. Aversa,et al.  Mechanism of Action of Bortezomib and the New Proteasome Inhibitors on Myeloma Cells and the Bone Microenvironment: Impact on Myeloma-Induced Alterations of Bone Remodeling , 2015, BioMed research international.

[14]  M. Gobbi,et al.  Mechanisms and Clinical Applications of Genome Instability in Multiple Myeloma , 2015, BioMed research international.

[15]  Chu-Tse Wu,et al.  SENP1 inhibition induces apoptosis and growth arrest of multiple myeloma cells through modulation of NF-κB signaling. , 2015, Biochemical and biophysical research communications.

[16]  F. Alesiani,et al.  Efficacy and tolerability of bendamustine, bortezomib and dexamethasone in patients with relapsed-refractory multiple myeloma: a phase II study , 2013, Blood Cancer Journal.

[17]  J. Keats,et al.  Xbp1s-negative tumor B cells and pre-plasmablasts mediate therapeutic proteasome inhibitor resistance in multiple myeloma. , 2013, Cancer cell.

[18]  K. O'Byrne,et al.  Targeting Nuclear Factor-Kappa B to Overcome Resistance to Chemotherapy , 2013, Front. Oncol..

[19]  D. Durocher,et al.  Regulation of DNA damage responses by ubiquitin and SUMO. , 2013, Molecular cell.

[20]  Jianmin Wang,et al.  The resistance mechanisms of proteasome inhibitor bortezomib , 2013, Biomarker Research.

[21]  P. Fraser,et al.  Heterologous SUMO-2/3-Ubiquitin Chains Optimize IκBα Degradation and NF-κB Activity , 2012, PloS one.

[22]  G. Mulligan,et al.  Sequence analysis of β-subunit genes of the 20S proteasome in patients with relapsed multiple myeloma treated with bortezomib or dexamethasone. , 2012, Blood.

[23]  J. Naval,et al.  Bortezomib resistance in a myeloma cell line is associated to PSMβ5 overexpression and polyploidy. , 2012, Leukemia research.

[24]  E. Yeh,et al.  NF-κB induction of the SUMO protease SENP2: A negative feedback loop to attenuate cell survival response to genotoxic stress. , 2011, Molecular cell.

[25]  S. Kaufmann,et al.  Noxa/Bcl-2 Protein Interactions Contribute to Bortezomib Resistance in Human Lymphoid Cells* , 2011, The Journal of Biological Chemistry.

[26]  Di Chen,et al.  Bortezomib as the first proteasome inhibitor anticancer drug: current status and future perspectives. , 2011, Current cancer drug targets.

[27]  B. Aggarwal,et al.  Inhibiting NF-κB activation by small molecules as a therapeutic strategy. , 2010, Biochimica et biophysica acta.

[28]  Bart Barlogie,et al.  The sumoylation pathway is dysregulated in multiple myeloma and is associated with adverse patient outcome. , 2010, Blood.

[29]  N. Munshi,et al.  Interactions of the Hdm2/p53 and Proteasome Pathways May Enhance the Antitumor Activity of Bortezomib , 2009, Clinical Cancer Research.

[30]  Jianmin Yang,et al.  Overexpression of the PSMB5 gene contributes to bortezomib resistance in T-lymphoblastic lymphoma/leukemia cells derived from Jurkat line. , 2008, Experimental hematology.

[31]  KyungMann Kim,et al.  Bortezomib-Resistant Nuclear Factor-κB Activity in Multiple Myeloma Cells , 2008, Molecular Cancer Research.

[32]  M. Dasso,et al.  Modification in reverse: the SUMO proteases. , 2007, Trends in biochemical sciences.

[33]  L. Boise,et al.  Proteasome inhibitors induce a terminal unfolded protein response in multiple myeloma cells. , 2006, Blood.

[34]  D. Esseltine,et al.  A phase 2 study of two doses of bortezomib in relapsed or refractory myeloma , 2004, British journal of haematology.

[35]  S. Müller,et al.  SUMO: a regulator of gene expression and genome integrity , 2004, Oncogene.

[36]  F. Melchior,et al.  SUMO: ligases, isopeptidases and nuclear pores. , 2003, Trends in biochemical sciences.

[37]  Marianne Fillet,et al.  NF-κB transcription factor induces drug resistance through MDR1 expression in cancer cells , 2003, Oncogene.

[38]  A. Baldwin Control of oncogenesis and cancer therapy resistance by the transcription factor NF-kappaB. , 2001, The Journal of clinical investigation.

[39]  R. Hay,et al.  SUMO-1 modification of IkappaBalpha inhibits NF-kappaB activation. , 1998, Molecular cell.

[40]  H. Niitani,et al.  [Phase II study]. , 1995, Gan to kagaku ryoho. Cancer & chemotherapy.