Document Detail


Metformin blocks the stimulative effect of a high-energy diet on colon carcinoma growth in vivo and is associated with reduced expression of fatty acid synthase.
MedLine Citation:
PMID:  20228137     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The molecular mechanisms responsible for the association of obesity with adverse colon cancer outcomes are poorly understood. We investigated the effects of a high-energy diet on growth of an in vivo colon cancer model. Seventeen days following the injection of 5x10(5) MC38 colon carcinoma cells, tumors from mice on the high-energy diet were approximately twice the volume of those of mice on the control diet. These findings were correlated with the observation that the high-energy diet led to elevated insulin levels, phosphorylated AKT, and increased expression of fatty acid synthase (FASN) by the tumor cells. Metformin, an antidiabetic drug, leads to the activation of AMPK and is currently under investigation for its antineoplastic activity. We observed that metformin blocked the effect of the high-energy diet on tumor growth, reduced insulin levels, and attenuated the effect of diet on phosphorylation of AKT and expression of FASN. Furthermore, the administration of metformin led to the activation of AMPK, the inhibitory phosphorylation of acetyl-CoA carboxylase, the upregulation of BNIP3 and increased apoptosis as estimated by poly (ADP-ribose) polymerase (PARP) cleavage. Prior work showed that activating mutations of PI3K are associated with increased AKT activation and adverse outcome in colon cancer; our results demonstrate that the aggressive tumor behavior associated with a high-energy diet has similar effects on this signaling pathway. Furthermore, metformin is demonstrated to reverse the effects of the high-energy diet, thus suggesting a potential role for this agent in the management of a metabolically defined subset of colon cancers.
Authors:
Carolyn Algire; Lilian Amrein; Mahvash Zakikhani; Lawrence Panasci; Michael Pollak
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-06-01
Journal Detail:
Title:  Endocrine-related cancer     Volume:  17     ISSN:  1479-6821     ISO Abbreviation:  Endocr. Relat. Cancer     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-03-15     Completed Date:  2010-06-24     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9436481     Medline TA:  Endocr Relat Cancer     Country:  England    
Other Details:
Languages:  eng     Pagination:  351-60     Citation Subset:  IM    
Affiliation:
Department of Experimental Medicine, McGill University, Montr?al, Qu?bec, Canada.
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MeSH Terms
Descriptor/Qualifier:
AMP-Activated Protein Kinases / metabolism
Acetyl-CoA Carboxylase / metabolism
Animals
Apoptosis / drug effects
Carcinoma / drug therapy*,  enzymology
Colonic Neoplasms / drug therapy*,  enzymology
Energy Intake / drug effects*
Fatty Acid Synthetase Complex / antagonists & inhibitors*,  biosynthesis
Hypoglycemic Agents / therapeutic use*
Insulin / blood
Male
Membrane Proteins / metabolism
Metformin / therapeutic use*
Mice
Mice, Inbred C57BL
Mitochondrial Proteins / metabolism
Protein-Serine-Threonine Kinases / metabolism
Tumor Cells, Cultured
Grant Support
ID/Acronym/Agency:
//Canadian Institutes of Health Research
Chemical
Reg. No./Substance:
0/BNip3 protein, mouse; 0/Hypoglycemic Agents; 0/Membrane Proteins; 0/Mitochondrial Proteins; 11061-68-0/Insulin; 657-24-9/Metformin; EC 2.7.11.1/AMP-Activated Protein Kinases; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 6.-/Fatty Acid Synthetase Complex; EC 6.4.1.2/Acetyl-CoA Carboxylase

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


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