目的：探讨lncRNA MAFG-AS1/miR-11181-3p/GLG1分子轴对胃癌（gastric cancer，GC）细胞迁移、侵袭和有氧糖酵解的影响及其可能的机制。方法：选取 MAFG-AS1 相对高表达的 GC 细胞系 AGS 作为研究对象，采用 qPCR 法检测其 MAFGAS1、miR-11181-3p、GLG1的RNA表达水平，Transwell实验、糖酵解分析等检测细胞迁移、侵袭和有氧糖酵解的变化，利用生物信息学分析及双荧光素酶报告基因验证MAFG-AS1、miR-11181-3p、GLG1之间的相互作用关系。结果：敲减MAFG-AS1显著上调miR-11181-3p及下调GLG1的表达（均P<0.01），并可显著抑制GC细胞迁移、侵袭和有氧糖酵解（均P<0.01）；荧光素酶报告基因证实MAFG-AS1竞争性吸附miR-11181-3p（P<0.01）；抑制miR-11181-3p或过表达GLG1可部分逆转敲减MAFG-AS1对GC细胞迁移、侵袭和有氧糖酵解的抑制作用（均P<0.05或P<0.01）。结论：MAFG-AS1通过miR-11181-3p/GLG1分子轴增强GC迁移、侵袭和有氧糖酵解，可能是GC诊疗的潜在分子靶点。

Objective: To investigate the effect of lncRNA MAFG-AS1/ miR-11181-3p/GLG1 axis on cell migration, invasion and aerobic glycolysis of gastric cancer (GC) cells and its possible mechanism. Methods: AGS, a GC cell line with relatively high expression of MAFG-AS1, was selected as the study object. qPCR was used to detect RNA expression levels of MAFG-AS1,miR-11181-3p and GLG1. Transwell and glycolysis analysis were used to investigate cell migration, invasion and aerobic glycolysis.Bioinformatics analysis and Dual luciferase reporter gene assay were used to analyze the interaction among MAFG-AS1, miR-11181-3p and GLG1. Results: Knockdown of MAFG-AS1 significantly up-regulated miR-11181-3p and down-regulated GLG1 expression (both P<0.01), and significantly inhibited migration, invasion and aerobic glycolysis of GC cells (all P<0.01). Luciferase reporter gene assay confirmed that MAFG-AS1 competitively sponged miR-11181-3p (P<0.01). Inhibition of miR-11181-3p or overexpression of GLG1 partially reversed the inhibitory effect of MAFG-AS1 knockdown on GC cell migration, invasion, and aerobic glycolysis (all P<0.05 or P<0.01). Conclusion: MAFG-AS1 promotes cell migration, invasion and aerobic glycolysis of GC cells via miR-11181-3p/GLG1 axis, and may be a potential molecular target for GC diagnosis and therapy.

浙江省自然科学基金资助项目（No. LY16H160033）；浙江省医药卫生科技计划资助项目（No. 2019RC314）；国家级大学生创新创业训练计划项目（No.201910350008）；台州市科技计划项目（No. 20ywa61）