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目的:探讨长链非编码RNA(lncRNA)X染色体失活特异转录本(XIST)对胰腺癌PANC1细胞增殖和迁移能力的影响，明确lncRNA XIST与miR-101/zeste基因增强子同源物2(EZH2)的靶向关系。方法:收集2010年7月至2018年9月间浙江省嘉兴市第一医院行手术切除并经病理学确诊的90例胰腺癌及其对应的癌旁正常组织；选取PANC1细胞将其分为sh-XIST组、sh-control组、miR-control组和miR-101组。采用荧光定量PCR法检测胰腺癌组织和各组PANC1细胞lncRNA XIST、miR-101的表达，分析lncRNA XIST和miR-101的表达与肿瘤临床病理参数的关系。采用CCK-8法和Transwell小室检测各组PANC1细胞的增殖和迁移能力，蛋白质免疫印迹法检测各组PANC1细胞的EZH2表达水平。将各组PANC1细胞以3×10n 6个/100 μl密度分别接种于Balb/c裸鼠，检测种植瘤体积。采用生物信息学和双荧光素酶报告基因分析lncRNA XIST与miR-101及其下游靶基因EZH2的关系。n 结果:与癌旁组织比，胰腺癌组织lncRNA XIST表达量显著上调(2.89±0.42比1.12±0.22，n P<0.05)，miR-101水平显著下调(0.32±0.12比1.25±0.22)，差异均有统计学意义(n P值均<0.05)。胰腺癌的分化程度越高、TNM分期越高、淋巴结转移的癌组织lncRNA XIST水平显著升高，miR-101水平显著降低。sh-XIST组PANC1细胞lncRNA XIST表达水平较sh-control组显著下调(0.34±0.18比1.21±0.27)，miR-101组PANC1细胞miR-101表达水平较miR-control组显著上调(2.94±0.31比1.54±0.29)，差异均有统计学意义(n P值均<0.05)。培养72 h的sh-control组、sh-XIST组、miR-control组和miR-101组450 nm处吸光度值(n A450值)分别为1.98±0.24、1.21±0.20、1.87±0.21、1.11±0.17，穿膜细胞数分别为(74.25±6.79)、(29.11±5.17)、(61.27±5.19)、(20.47±4.58)个细胞/200倍视野，sh-XIST组较sh-control组、miR-101组较miR-control组细胞增殖活力和迁移能力均显著下降，种植瘤生长明显缓慢，差异均有统计学意义(n P值均<0.05)。n 结论:lncRNA XIST可靶向结合miR-101/EZH2调节胰腺癌PANC1细胞的增殖和迁移能力，促进胰腺癌的发生和发展。“,”Objective:To investigate the effects of long-chain non coding RNA (lncRNA) XIST on the proliferation and migration of pancreatic cancer PANC1 cells, and clarify the targeting relationship between lncRNA XIST and miR-101/enhancer of zeste homologz(EZH2).Methods:Ninety cases of pancreatic cancer surgically resected and pathologically confirmed in the first hospital of Jiaxing city from July 2010 to September 2018 and its corresponding paracarcinoma normal tissue were collected. PANC1 cells were divided into sh-XIST group, SH control group, MiR control group and miR-101 group. The expression of LncRNA XIST and miR-101 in pancreatic cancer tissue and PANC1 cells in each group were detected by fluorescence quantitative PCR. The relationship between the expression of LncRNA XIST and miR-101 and the clinicopathological parameters of tumor was analyzed. The proliferation and migration ability of PANC1 cells in each group were analyzed by CCK8 method and transwell chamber test. The EZH2 expression level of PANC1 cells in each group were analyzed by western blot. PANC1 cells in each group was inoculated into BALB/C nude mice with a cell density of 3×10n 6 cells/100 μl and the tumor volume was measured. The relationship between LncRNA XIST and its miR-101 and targeting gene EZH2 were analyzed by bioinformatics and double luciferase reporter genes.n Results:Compared with the paracancerous tissues, the level of LncRNA XIST in pancreatic cancer tissue was significantly increased 2.89±0.42 n vs (1.12±0.22, n P<0.05), and the level of miR-101 was significantly decreased 0.32±0.12n vs (1.25±0.22, n P<0.05), and the differences were statistically significant (n P<0.05). LncRNA XIST expression in pancreatic cancer tissue was obviously increased along with higher differentiation degree, advanced TNM stage and lymph node metastasis, while miR-101 was greatly decreased. Compared with the cells in the sh-control group, the expression level of LncRNA XIST in the sh-XIST group was significantly decreased (0.34±0.18n vs 1.21±0.27). Compared with miR-control cells, the level of miR-101 cells in miR-101 group significantly increased (2.94±0.31 n vs 1.54±0.29 ), and the differences were statistically significant (n P<0.05). After 72 h cell culture, the light absorption value at 450 nm in sh-control group, sh-XIST group, miR-control group and miR-101 group was 1.98±0.24, 1.21±0.20, 1.87±0.21 and 1.11±0.17; the number of transmembrane cells were (74.25±6.79 ), (29.11±5.17), (61.27±5.19) and (20.47±4.58)per 200 times visual field; the cell proliferation activity and migration ability in sh-XIST group were significantly decreased than sh-control group, miR-101 group and miR-control group and the xenograft tumor grew obviously slowly, all the differences were statistically significant (alln P<0.05).n Conclusions:LncRNA XIST can target miR-101/EZH2, regulating the proliferation and migration of pancreatic cancer cells, which promotes the occurrence and development of pancreatic cancer.