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M2型丙酮酸激酶(PKM2)是细胞糖酵解通路的关键酶,催化磷酸烯醇丙酮酸转化为丙酮酸并产生三磷酸腺苷(ATP)。作为有氧糖酵解途径的一个重要调节因子,PKM2在肿瘤进程中发挥着举足轻重的作用。除了通过糖代谢途径促进肿瘤细胞增殖,PKM2还能够为肿瘤细胞提供中间代谢产物以支持快速分裂细胞所需的生物合成,并避免氧化应激损伤。同时,PKM2能够进入细胞核内,作为共转录因子和蛋白激酶调节基因转录。因此PKM2在氧代谢途径、核内信号转导、蛋白合成、蛋白质相互作用等多种途径行使功能。目前,针对PKM2的干扰肿瘤代谢的治疗方案正在积极地探索过程之中。现就PKM2在调控肿瘤细胞代谢的研究现状作一综述,为肿瘤的临床治疗提供新的思路。
M2 pyruvate kinase (PKM2) is a key enzyme in cellular glycolytic pathways and catalyzes the conversion of phosphoenolpyruvate to pyruvate and to adenosine triphosphate (ATP). As an important regulator of aerobic glycolysis, PKM2 plays a pivotal role in tumor progression. In addition to promoting tumor cell proliferation through the glucose metabolism pathway, PKM2 is also able to provide intermediate metabolites to tumor cells to support the biosynthesis required to rapidly divide cells and to avoid oxidative stress damage. At the same time, PKM2 is able to enter the nucleus and regulate gene transcription as a co-transcription factor and protein kinase. Therefore, PKM2 functions in various pathways such as oxygen metabolism, nuclear signal transduction, protein synthesis and protein interaction. At present, the treatment of PKM2 interfering with tumor metabolism is actively exploring the process. Now on PKM2 in the regulation of tumor cell metabolism research status to be reviewed for the clinical treatment of cancer provide a new way of thinking.