基于lncRNA-ANRIL/miR-125a/AKT轴研究益气解毒方调控鼻咽癌细胞糖代谢重编程的作用与机制

糖代谢重编程是肿瘤细胞的重要特征。益气解毒方是治疗鼻咽癌的一个有效方药，但其作用机制仍不清。前期研究发现该方可抑制鼻咽癌细胞增殖、诱导凋亡、降低乳酸产量，影响糖代谢限速酶和lncRNA-ANRIL/miR-125a/AKT轴关键分子的表达。由此，本项目提出假说“益气解毒方可通过lncRNA-ANRIL/miR-125a/AKT轴调控糖代谢重编程，发挥抗鼻咽癌的作用”。我们拟选择在体、离体实验，结合lncRNA过表达/干扰、miRNA拮抗、糖酵解激活剂/抑制剂、AKT激活剂等多种诱导/抑制手段，从以下3个方面进行研究来验证这一假说：1）益气解毒方对鼻咽癌细胞糖代谢重编程的影响；2）糖代谢重编程在益气解毒方抗鼻咽癌中的作用；3）基于lncRNA-ANRIL/miR-125a/AKT轴研究益气解毒方调控糖代谢重编程的分子机制。该研究可丰富益气解毒理论的科学内涵，为益气解毒方的广泛应用奠定基础。

Glucose metabolic reprogramming is a major characteristic of tumor. Yiqi Jiedu formula (YQJDF) is an empirical prescription for nasopharyngeal carcinoma（NPC) , but its specific molecular mechanism is still unclear. In the previous study, we found that YQJDF can inhibit the proliferation , induce apoptosis and reduce lactate production of NPC cells, as well as effect the expression of rate limiting enzyme of glucose metabolism and key molecules of lncRNA-ANRIL/miR-125a/AKT axis . Therefore, we put forward the hypothesis that "YQJDF regulates the reprogramming of glucose metabolism and finally plays an anti NPC role through lncRNA-ANRIL/miR-125a/AKT axis". We plan to select in vivo and in vitro experiments, combined with induction/inhibition means, such as lncRNA overexpression/konckdown, miRNA inhibitor, glycolysis activator/inhibitor and AKT activator, to verify the hypothesis from the following three aspects: 1) the effects of YQJDF on the reprogramming of glucose metabolism of NPC; 2) the role of the reprogramming of glucose metabolism in YQJDF anti NPC; and 3) study on the molecular mechanism of YQJDF regulating the reprogramming of glucose metabolism based on lncRNA-ANRIL/miR-125a/AKT axis. This research can enrich the scientific connotation of the theory of "Qi-Boosting and Toxin-Resolving", and lay a foundation for further application of YQJDF.