Document Detail


Molecular mechanisms of nutlin-induced apoptosis in multiple myeloma: evidence for p53-transcription-dependent and -independent pathways.
MedLine Citation:
PMID:  20595817     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Multiple myeloma (MM) is an incurable plasma cell malignancy in which p53 is rarely mutated. Thus, activation of the p53 pathway by a small molecule inhibitor of the p53-MDM2 interaction, nutlin, in MM cells retaining wild type p53 is an attractive therapeutic strategy. Recently we reported that nutlin plus velcade (a proteasome inhibitor) displayed a synergistic response in MM. However, the mechanism of the p53-mediated apoptosis in MM has not been fully understood. Our data show that nutlin-induced apoptosis correlated with reduction in cell viability, upregulation of p53, p21 and MDM2 protein levels with a simultaneous increase in pro-apoptotic targets PUMA, Bax and Bak and downregulation of anti-apoptotic targets Bcl2 and survivin and activation of caspase in MM cells harboring wild type p53. Nutlin-induced apoptosis was inhibited when activation of caspase was blocked by the caspase inhibitor. Nutlin caused mitochondrial translocation of p53 where it binds with Bcl2, leading to cytochrome C release. Moreover, blocking the transcriptional arm of p53 by the p53-specific transcriptional inhibitor, pifithrin-α, not only inhibited nutlin-induced upregulation of p53-transcriptional targets but also augmented apoptosis in MM cells, suggesting an association of transcription-independent pathway of apoptosis. However, inhibitor of mitochondrial translocation of p53, PFT-μ, did not prevent nutlin-induced apoptosis, suggesting that the p53 transcription-dependent pathway was also operational in nutlin-induced apoptosis in MM. Our study provides the evidence that nutlin-induced apoptosis in MM cells is mediated by transcription-dependent and -independent pathways and supports further clinical evaluation of nutlin as a novel therapeutic agent in MM.
Authors:
Manujendra N Saha; Hua Jiang; Hong Chang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-10-01
Journal Detail:
Title:  Cancer biology & therapy     Volume:  10     ISSN:  1555-8576     ISO Abbreviation:  Cancer Biol. Ther.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-11-18     Completed Date:  2011-04-18     Revised Date:  2012-04-26    
Medline Journal Info:
Nlm Unique ID:  101137842     Medline TA:  Cancer Biol Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  567-78     Citation Subset:  IM    
Affiliation:
Division of Molecular and Cellular Biology, Toronto General Hospital Research Institute, Dept of Laboratory Medicine and Pathobiology, University of Toronto, Ontario, Canada.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects*
Apoptosis Regulatory Proteins / genetics,  metabolism
Benzothiazoles / pharmacology
Cell Line, Tumor
Cell Proliferation / drug effects
Cell Survival / drug effects
Cyclin-Dependent Kinase Inhibitor p21 / genetics,  metabolism
Dose-Response Relationship, Drug
Flow Cytometry
Gene Expression Profiling
Gene Expression Regulation, Neoplastic / drug effects
Humans
Imidazoles / pharmacology*
Immunoblotting
Multiple Myeloma / genetics,  metabolism,  pathology
Piperazines / pharmacology*
Protein Binding / drug effects
Protein Transport / drug effects
Proto-Oncogene Proteins c-bcl-2 / genetics,  metabolism
Proto-Oncogene Proteins c-mdm2 / genetics,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction / drug effects
Sulfonamides / pharmacology
Toluene / analogs & derivatives,  pharmacology
Transcription, Genetic / drug effects
Tumor Suppressor Protein p53 / genetics,  metabolism*
Grant Support
ID/Acronym/Agency:
//Canadian Institutes of Health Research
Chemical
Reg. No./Substance:
0/2-phenylacetylenesulfonamide; 0/Apoptosis Regulatory Proteins; 0/Benzothiazoles; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Imidazoles; 0/Piperazines; 0/Proto-Oncogene Proteins c-bcl-2; 0/Sulfonamides; 0/Tumor Suppressor Protein p53; 0/nutlin 3; 0/pifithrin; 108-88-3/Toluene; EC 6.3.2.19/MDM2 protein, human; EC 6.3.2.19/Proto-Oncogene Proteins c-mdm2
Comments/Corrections
Comment In:
Cancer Biol Ther. 2010 Sep;10(6):579-81   [PMID:  20716967 ]

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