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目的:探讨长链非编码RNA(lncRNA)HAGLR通过靶基因微小RNA(miR)-93-5p调控胃癌细胞增殖和迁移的分子机制。方法:采用实时定量聚合酶链式反应(qRT-PCR)检测胃癌细胞株(HS-746T、BGC823、SGC7901、MGC803)和正常胃黏膜上皮细胞(GES-1)中HAGLR的表达水平。选择HAGLR表达最低的细胞株分别转染阴性对照质粒(阴性对照组)和HAGLR高表达质粒(HAGLR组)。分别采用MTS法和划痕愈合实验检测转染后细胞的增殖情况和迁移能力。生物信息学软件miRcode数据库预测HAGLR的靶基因，双荧光素酶报告基因实验验证HAGLR与靶基因的结合。qRT-PCR检测HAGLR靶基因的表达。Western blot检测Hippo信号通路的表达。采用SPSS 21.0软件进行统计分析，组间比较应用n t检验，多组间比较应用单因素方差分析。n 结果:与GES-1细胞相比，胃癌细胞株HAGLR的表达水平均降低(均n P<0.05)，HAGLR表达最低的细胞株是SGC7901细胞(n P<0.01)。HAGLR组和阴性对照组SGC7901细胞中HAGLR表达分别为1.03±0.13和9.75±1.10，阴性对照组HAGLR的表达水平明显低于HAGLR组(n t＝7.87，n P<0.01)。与阴性对照组比较，HAGLR组SGC7901细胞的吸光度值明显降低(n P<0.05)，划痕愈合率明显减少(n P<0.01)。miRcode数据库显示HAGLR与miR-93-5p存在互补结合位点。双荧光素酶报告基因实验显示HAGLR可互补结合miR-93-5p(n P<0.01)。与阴性对照组比较，HAGLR组SGC7901细胞中miR-93-5p表达明显降低(n P<0.01)，Hippo信号通路蛋白表达明显降低(均n P<0.01)。n 结论:HAGLR在胃癌细胞株中呈低表达，HAGLR通过靶向负调控miR-93-5p抑制胃癌SGC7901细胞的增殖和迁移能力。“,”Objective:To investigate the effect of long non-coding RNA (lncRNA) HAGLR on the proliferation and migration of gastric cancer cells by inhibiting the expression of microRNA (miRNA, miR)-93-5p.Methods:Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of HAGLR in gastric cancer cell lines (HS-746T, BGC823, SGC7901, MGC803) and normal gastric mucosal epithelial cells (GES-1). Selected the cell line with the lowest HAGLR expression and transfected with the negative control plasmid (negative control group) or HAGLR-high-expression plasmid (HAGLR group) respectively. The MTS method and the scratch healing test were used to detect the proliferation and migration ability of the cells after transfection. The bioinformatics software miRcode database was used to predict the target gene of HAGLR, and the dual luciferase reporter gene experiment was used to verify the binding of HAGLR to the target gene. qRT-PCR was used to detect the expression of the target gene. Western blot was used to detect the expression of Hippo signaling pathway. The software SPSS 21.0 was used to conduct statistical analysis. The n t test was used for comparison between two groups, and the one-way analysis of variance was used for comparison between multiple groups.n Results:Compared with GES-1 cells, the expression level of HAGLR in gastric cancer cell lines was lower (all n P<0.05), and the cell line with the lowest HAGLR expression was SGC7901 cells (n P<0.01). The HAGLR expression in SGC7901 cells in the HAGLR group and the negative control group were 1.03±0.13 and 9.75±1.10, respectively. The expression level of HAGLR in the negative control group was significantly lower than that in the HAGLR group (n t=7.87, n P<0.01). Compared with the negative control group, the absorbance of SGC7901 cells in the HAGLR group was significantly reduced (n P<0.05), and the scratch healing rate was significantly reduced (n P<0.01). The miRcode database showd that HAGLR and miR-93-5p have complementary binding sites. The dual luciferase reporter gene experiment showed that HAGLR can complement miR-93-5p (n P<0.01). Compared with the negative control group, the expression of miR-93-5p in SGC7901 cells in the HAGLR group was significantly reduced (n P<0.01), and the expression of Hippo signaling pathway protein was significantly reduced (alln P<0.01).n Conclusions:HAGLR is low expressed in gastric cancer cell lines. HAGLR inhibits the proliferation and migration of gastric cancer SGC7901 cells by negatively regulating miR-93-5p.