Document Detail


Inhibition of the MUC1-C oncoprotein induces multiple myeloma cell death by down-regulating TIGAR expression and depleting NADPH.
MedLine Citation:
PMID:  22117045     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The MUC1-C oncoprotein is aberrantly expressed in most multiple myeloma cells. However, the functional significance of MUC1-C expression in multiple myeloma is not known. The present studies demonstrate that treatment of multiple myeloma cells with a MUC1-C inhibitor is associated with increases in reactive oxygen species (ROS), oxidation of mitochondrial cardiolipin, and loss of the mitochondrial transmembrane potential. The MUC1-C inhibitor-induced increases in ROS were also associated with down-regulation of the p53-inducible regulator of glycolysis and apoptosis (TIGAR). In concert with the decrease in TIGAR expression, which regulates the pentose phosphate pathway, treatment with the MUC1-C inhibitor reduced production of NADPH, and in turn glutathione (GSH) levels. TIGAR protects against oxidative stress-induced apoptosis. The suppression of TIGAR and NADPH levels thus contributed to ROS-mediated late apoptosis/necrosis of multiple myeloma cells. These findings indicate that multiple myeloma cells are dependent on MUC1-C and TIGAR for maintenance of redox balance and that targeting MUC1-C activates a cascade involving TIGAR suppression that contributes to multiple myeloma cell death.
Authors:
Li Yin; Michio Kosugi; Donald Kufe
Related Documents :
21807025 - Allosteric modulation of caspases.
17904265 - Protective effects of total saponins from stem and leaf of panax ginseng against cyclop...
15961255 - A novel theory: biological processes mostly involve two types of mediators, namely gene...
8168145 - Glutathione reverses the inhibition of t cell responses by superoptimal numbers of "non...
16568325 - The vagal nerve as a link between the nervous and immune system in the instance of poly...
12540195 - Biochemistry and molecular biology of gelatinase b or matrix metalloproteinase-9 (mmp-9).
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-11-23
Journal Detail:
Title:  Blood     Volume:  119     ISSN:  1528-0020     ISO Abbreviation:  Blood     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2012-01-20     Completed Date:  2012-03-13     Revised Date:  2012-04-16    
Medline Journal Info:
Nlm Unique ID:  7603509     Medline TA:  Blood     Country:  United States    
Other Details:
Languages:  eng     Pagination:  810-6     Citation Subset:  AIM; IM    
Affiliation:
Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism
Apoptosis*
Blotting, Western
Cardiolipins / metabolism
Cell Line, Tumor
Down-Regulation
Humans
Intracellular Signaling Peptides and Proteins / antagonists & inhibitors,  genetics,  metabolism*
Membrane Potential, Mitochondrial
Mitochondria / metabolism
Mucin-1 / chemistry*,  genetics,  metabolism*
Multiple Myeloma / metabolism*,  pathology*
NADP / metabolism*
Necrosis
Oxidation-Reduction
Oxidative Stress
RNA, Messenger / genetics
RNA, Small Interfering / genetics
Reactive Oxygen Species / metabolism
Real-Time Polymerase Chain Reaction
Reverse Transcriptase Polymerase Chain Reaction
Grant Support
ID/Acronym/Agency:
CA42802/CA/NCI NIH HHS; R01 CA042802-25/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/C12orf5 protein, human; 0/Cardiolipins; 0/Intracellular Signaling Peptides and Proteins; 0/MUC1 protein, human; 0/Mucin-1; 0/RNA, Messenger; 0/RNA, Small Interfering; 0/Reactive Oxygen Species; 53-59-8/NADP; 56-65-5/Adenosine Triphosphate

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Sequential mutations in Notch1, Fbxw7, and Tp53 in radiation-induced mouse thymic lymphomas.
Next Document:  Inhibition of histone methylation arrests ongoing graft-versus-host disease in mice by selectively i...