Document Detail


Autophagy prolongs survival after NFκB inhibition in B-cell lymphomas.
MedLine Citation:
PMID:  22361669     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Autophagy allows cells to survive under conditions of nutrient deprivation. We have demonstrated that autophagy inhibitors are synthetically lethal with NFκB inhibitors in B-cell lymphomas because the NFκB pathway promotes survival by increasing glucose import. When NFκB is inhibited in B-cell lymphoma, glucose import decreases and cells become sensitive to perturbations in mitochondrial metabolism and autophagy. Thus, combined inhibition of autophagy and NFκB drives cells into metabolic crisis accelerating cell death.
Authors:
Thomas G Sommermann; Hildegard I D Mack; Ellen Cahir-McFarland
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Publication Detail:
Type:  Journal Article     Date:  2012-02-01
Journal Detail:
Title:  Autophagy     Volume:  8     ISSN:  1554-8635     ISO Abbreviation:  Autophagy     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-03-19     Completed Date:  2012-07-13     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  101265188     Medline TA:  Autophagy     Country:  United States    
Other Details:
Languages:  eng     Pagination:  265-7     Citation Subset:  IM    
Affiliation:
Department of Medicine, Division of Infectious Diseases, Brigham and Women's Hospital, Boston, MA, USA.
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MeSH Terms
Descriptor/Qualifier:
Autophagy*
Biological Transport
Cell Membrane / metabolism
Cell Survival
Glucose / metabolism
Glucose Transporter Type 1 / metabolism
Humans
I-kappa B Kinase / metabolism
Lymphocytes / metabolism
Lymphoma, B-Cell / drug therapy,  enzymology,  metabolism*,  pathology*
Models, Biological
NF-kappa B / antagonists & inhibitors*,  metabolism
Phosphatidylinositol 3-Kinases / metabolism
Transcription, Genetic
Chemical
Reg. No./Substance:
0/Glucose Transporter Type 1; 0/NF-kappa B; 50-99-7/Glucose; EC 2.7.1.-/Phosphatidylinositol 3-Kinases; EC 2.7.11.10/I-kappa B Kinase
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