二甲双胍是治疗2型糖尿病药物（T2DM）的一线药物，近年来，其也作为潜在的抗肿瘤药物，被人们进行了广泛的研究。目前了解的二甲双胍抗肿瘤机制多种多样，二甲双胍可以通过AMPK直接或间接调节LKB1/AMPK/mTOR信号通路，诱导ACC磷酸化。也可以通过AMPK的非依赖机制抑制胰岛素受体/IGF-IR信号通路、诱导细胞自噬和凋亡、上调Micro RNAs，以及调节P53/REDD1通路、免疫作用、氧化作用、协同药物治疗等多种机制抑制肿瘤生长。本文将对近年来二甲双胍可能产生的抗肿瘤机制进行分类综述，为其日后相关研究奠定理论基础。

Metformin is a first-line drug for the treatment of type 2 diabetes mellitus (T2DM). In recent years, it has been widely studied as a potential anti-tumor drug. There are various anti-tumor mechanisms currently known for metformin. Metformin can directly or indirectly regulate the LKB1/AMPK/mTOR signaling pathway via AMPK to and induce ACC phosphorylation. Metformin can also inhibit the insulin receptor/IGF-IR signaling pathway via an AMPK-independent mechanism, induce autophagy and apoptosis, up-regulate Micro RNAs, and suppress tumor growth through regulating the P53/REDD1 pathway, exerting immune function, undergoing oxidation, and acting as a synergistic drug therapy. In this paper, the possible anti-tumor mechanisms of metformin in recent years are classified and summarized, which lays a good theoretical foundation for related research in the future.

黑龙江省留学回国人员择优资助项目（18930101）；哈尔滨商业大学青年创新人才项目（17XN031）；哈尔滨商业大学博士科研启动项目（2019DS116）