Document Detail


The oncogene c-Myc coordinates regulation of metabolic networks to enable rapid cell cycle entry.
MedLine Citation:
PMID:  18414044     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The c-myc proto-oncogene is rapidly activated by serum and regulates genes involved in metabolism and cell cycle progression. This gene is thereby uniquely poised to coordinate both the metabolic and cell cycle regulatory events required for cell cycle entry. However, this function of Myc has not been evaluated. Using a rat fibroblast model of isogenic cell lines, myc(-/-), myc(+/-), myc(+/+) and myc(-/-) cells with an inducible c-myc transgene (mycER), we show that the Myc protein programs cells to utilize both oxidative phosphorylation and glycolysis to drive cell cycle progression. We demonstrate this coordinate regulation of metabolic networks is essential, as specific inhibitors of these pathways block Myc-induced proliferation. Metabolic events temporally correlated with cell cycle entry include increased oxygen consumption, mitochondrial function, pyruvate and lactate production, and ATP generation. Treatment of normal cells with inhibitors of oxidative phosphorylation recapitulates the myc(-/-) phenotype, resulting in impaired cell cycle entry and reduced metabolism. Combined with a kinetic expression profiling analysis of genes linked to mitochondrial function, our study indicates that Myc's ability to coordinately regulate the mitochondrial metabolic network transcriptome is required for rapid cell cycle entry. This function of Myc may underlie the pervasive presence of Myc in many human cancers.
Authors:
Fionnuala Morrish; Nicola Neretti; John M Sedivy; David M Hockenbery
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural     Date:  2008-02-08
Journal Detail:
Title:  Cell cycle (Georgetown, Tex.)     Volume:  7     ISSN:  1551-4005     ISO Abbreviation:  Cell Cycle     Publication Date:  2008 Apr 
Date Detail:
Created Date:  2008-05-29     Completed Date:  2008-09-03     Revised Date:  2011-03-09    
Medline Journal Info:
Nlm Unique ID:  101137841     Medline TA:  Cell Cycle     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1054-66     Citation Subset:  IM    
Affiliation:
Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Cell Cycle / physiology*
Cell Line
Cell Proliferation
Gene Expression Profiling
Glycolysis / physiology
Membrane Potential, Mitochondrial
Metabolic Networks and Pathways / physiology*
Microarray Analysis
Mitochondria / metabolism*
Oxidative Phosphorylation
Proto-Oncogene Proteins c-myc / genetics,  metabolism*
Rats
Reactive Oxygen Species / metabolism
Grant Support
ID/Acronym/Agency:
K25 AG028753/AG/NIA NIH HHS; K25 AG028753-01A1/AG/NIA NIH HHS; R01 CA106650-02/CA/NCI NIH HHS; R01 GM041690-18/GM/NIGMS NIH HHS; R01 GM41690/GM/NIGMS NIH HHS; R01CA106650-02/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/MYC protein, human; 0/Proto-Oncogene Proteins c-myc; 0/Reactive Oxygen Species
Comments/Corrections

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