Antitumor Mechanism of Metformin via Adenosine Monophosphate-activated 
Protein Kinase (AMPK) Activation

Metformin, as a traditional oral hypoglycemic agent, is commonly used in the clinical treatment for type 2 diabetes. Recently, a large number of epidemiological researches have shown that metformin could reduce the tumor morbidity of type 2 diabetes, moreover, it has also been indicated that metform...

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Main Authors: Zhaoyu CHEN, Liantang WANG, Yanyang CHEN
Format: Article
Language:zho
Published: Chinese Anti-Cancer Association; Chinese Antituberculosis Association 2013-08-01
Series:Chinese Journal of Lung Cancer
Subjects:
Online Access:http://dx.doi.org/10.3779/j.issn.1009-3419.2013.08.07
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author Zhaoyu CHEN
Liantang WANG
Yanyang CHEN
author_facet Zhaoyu CHEN
Liantang WANG
Yanyang CHEN
author_sort Zhaoyu CHEN
collection DOAJ
description Metformin, as a traditional oral hypoglycemic agent, is commonly used in the clinical treatment for type 2 diabetes. Recently, a large number of epidemiological researches have shown that metformin could reduce the tumor morbidity of type 2 diabetes, moreover, it has also been indicated that metformin could inhibit the growth, proliferation and transformation of cancer cells in metabolic pathways, cell cycle, oxidative stress and cancer/tumor stem cells transformation via AMPK pathway activation. But the antitumor effect of metformin via AMPK activation still exists arguments, and the definite mechanism remains to be further investigated and confirmed by extensive clinical trials.
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spelling doaj.art-e68a6b71e17548bc8b51217de4a54ece2022-12-22T00:42:34ZzhoChinese Anti-Cancer Association; Chinese Antituberculosis AssociationChinese Journal of Lung Cancer1009-34191999-61872013-08-0116842743210.3779/j.issn.1009-3419.2013.08.07Antitumor Mechanism of Metformin via Adenosine Monophosphate-activated 
Protein Kinase (AMPK) ActivationZhaoyu CHENLiantang WANGYanyang CHENMetformin, as a traditional oral hypoglycemic agent, is commonly used in the clinical treatment for type 2 diabetes. Recently, a large number of epidemiological researches have shown that metformin could reduce the tumor morbidity of type 2 diabetes, moreover, it has also been indicated that metformin could inhibit the growth, proliferation and transformation of cancer cells in metabolic pathways, cell cycle, oxidative stress and cancer/tumor stem cells transformation via AMPK pathway activation. But the antitumor effect of metformin via AMPK activation still exists arguments, and the definite mechanism remains to be further investigated and confirmed by extensive clinical trials.http://dx.doi.org/10.3779/j.issn.1009-3419.2013.08.07MetforminAntitumor mechanismAdenosine monophosphate-activated protein kinase (AMPK)MetabolismCell cycle arrestOxidative stressTransformation of cancer/tumor stem cells
spellingShingle Zhaoyu CHEN
Liantang WANG
Yanyang CHEN
Antitumor Mechanism of Metformin via Adenosine Monophosphate-activated 
Protein Kinase (AMPK) Activation
Chinese Journal of Lung Cancer
Metformin
Antitumor mechanism
Adenosine monophosphate-activated protein kinase (AMPK)
Metabolism
Cell cycle arrest
Oxidative stress
Transformation of cancer/tumor stem cells
title Antitumor Mechanism of Metformin via Adenosine Monophosphate-activated 
Protein Kinase (AMPK) Activation
title_full Antitumor Mechanism of Metformin via Adenosine Monophosphate-activated 
Protein Kinase (AMPK) Activation
title_fullStr Antitumor Mechanism of Metformin via Adenosine Monophosphate-activated 
Protein Kinase (AMPK) Activation
title_full_unstemmed Antitumor Mechanism of Metformin via Adenosine Monophosphate-activated 
Protein Kinase (AMPK) Activation
title_short Antitumor Mechanism of Metformin via Adenosine Monophosphate-activated 
Protein Kinase (AMPK) Activation
title_sort antitumor mechanism of metformin via adenosine monophosphate activated 
protein kinase ampk activation
topic Metformin
Antitumor mechanism
Adenosine monophosphate-activated protein kinase (AMPK)
Metabolism
Cell cycle arrest
Oxidative stress
Transformation of cancer/tumor stem cells
url http://dx.doi.org/10.3779/j.issn.1009-3419.2013.08.07
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