二甲双胍通过激活腺苷酸活化蛋白激酶(AMPK)的抗肿瘤机制  

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

作　　者：陈兆煜[1] 王连唐[2] 陈雁扬[2] 

机构地区：[1]中山大学中山医学院,广州510080 [2]中山大学附属第一医院病理科,广州510080

出　　处：《中国肺癌杂志》2013年第8期427-432,共6页Chinese Journal of Lung Cancer

基　　金：国家自然科学基金(No.81172232/H1615)资助~~

摘　　要：二甲双胍是一种传统的口服降糖药,临床上普遍用于2型糖尿病的治疗。近年来大量流行病学研究报道二甲双胍能够降低2型糖尿病患者的肿瘤发病率,亦有研究发现二甲双胍能在代谢途径、细胞周期、氧化应激、肿瘤干细胞转化等方面通过激活腺苷酸活化蛋白激酶(adenosin emonophosphate-activated protein kinase,AMPK)信号通路,从而抑制肿瘤细胞的生长、增殖以及转化。但二甲双胍通过激活AMPK的抗肿瘤机制仍存在着争议,其确切的作用机制有待进一步深入的研究,同时亟需大规模的临床试验来证实。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 mefformin 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 ofmetformin via AMPK activation still exists arguments, and the definite mechanism remains to be further investigated and confirmed by extensive clinical trials.

关 键 词：二甲双胍 抗肿瘤机制 腺苷酸活化蛋白激酶(AMPK) 代谢 细胞周期阻滞 氧化应激 肿瘤干细胞转化 

分 类 号：R734.2[医药卫生—肿瘤]