一磷酸腺苷激酶(AMPK)以异质三联体形式存在于所有真核细胞内,是维持机体能量稳态的感受器。AMPK的激活主要来自avicinD、LKB1等,而AMPK主要激活底物是TSC2、p53和p27kip1,其中TSC2是mTOR的负性调控元件,它的激活可以间接地抑制细胞增殖;p53也可抑制mTOR通路,中断细胞增殖;活化的p27kip1可以诱导自噬,促进细胞死亡,抑制肿瘤生长。这些都表明AMPK在肿瘤细胞增殖和自噬中发挥作用。由于在许多肿瘤细胞中可以发现失活的AMPK,因而研究AMPK与肿瘤发展及细胞自噬的关系,将可能为肿瘤治疗找到新靶点。 Adenosine monophosphate kinase (AMPK) in the form of heterogeneous triplet in all eukaryotic cells, is to maintain the body’s energy homeostasis receptors. AMPK activation mainly from avicinD, LKB1, etc., and AMPK main activation substrates are TSC2, p53 and p27kip1, of which TSC2 is a negative regulatory element of mTOR, its activation can indirectly inhibit cell proliferation; p53 can inhibit the mTOR pathway, Interruption of cell proliferation; activated p27kip1 can induce autophagy, promote cell death, inhibit tumor growth. All of these show that AMPK plays a role in tumor cell proliferation and autophagy. As AMPK can be found in many tumor cells, studying the relationship between AMPK and tumor development and autophagy may find a new target for tumor therapy.