二甲双胍相关性自噬与肿瘤的关系

二甲双胍是最广泛使用的双胍类抗糖尿病药物，其通过需肝激酶B1的机制降低肝葡萄糖，该酶为控制体内代谢的要点，二甲双胍通过该机制引起蛋白合成减少、细胞增殖减慢，这激发了人们研究其在肿瘤细胞增殖、自噬和凋亡调控方面作用的兴致，其中二甲双胍相关性自噬在不同的肿瘤及其肿瘤细胞的不同时期，对肿瘤发生发展的影响并不相同。目前，已有大量的实验致力于二甲双胍能否作为抗肿瘤药物应用于临床，二甲双胍有望成为新一代抗肿瘤药物或辅助用药。

The relationship between metformin induced autophagy and tumor

Metformin was the most widely used antidiabetic drug that belongs to the biguanide class.Metformin de-creases hepatic glucose production via a mechanism requiring liver kinase B1 ,which controls the metabolic check-point.The effects of metformin on this pathway reduced protein synthesis and cell proliferation.These observations had given the impetus for many investigations on the role of metformin in the regulation of tumor cell proliferation,autoph-agy and apoptosis.In different tumors and tumor cell stages,effects of metformin induced autophagy on tumor develop-ment were different.There were numerous experiments committed to whether metformin can be used as an antitumor drug in clinical treatment.Metformin was expected to become a new antitumor drug or adjuvant drug.