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

Abstract

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.

Keywords

• Metformin
• Antitumor mechanism
• Adenosine monophosphate-activated protein kinase (AMPK)
• Metabolism
• Cell cycle arrest
• Oxidative stress
• Transformation of cancer/tumor stem cells