[摘要] 目的：探索血小板反应蛋白2（thrombospondin 2，THBS2）表达对胰腺癌患者的预后意义及对胰腺癌ASPC-1 细胞增殖和迁移的影响，并探讨可能的分子机制。方法：利用数据库分析THBS2 在胰腺癌组织中的表达情况及其对患者整体生存率的影响。Wb实验检测THBS2 在胰腺癌ASPC-1 细胞中的表达，RNA干扰技术敲低ASPC-1 细胞中THBS2 的表达后，采用MTT实验以及Transwell 实验检测敲低THBS2 对于细胞增殖和迁移能力的影响；Wb技术检测对ASPC-1 细胞中MMP、E-钙黏蛋白、AKT以及PI3K蛋白表达的影响。结果：THBS2 在胰腺癌组织中的表达显著高于正常胰腺组织中的表达(P<0.01)，且THBS2 的高表达会导致胰腺癌患者整体生存率的下降。THBS2 在ASPC-1 细胞中表达上调，干扰THBS2 的表达后ASPC-1 细胞的增殖(P<0.01)和迁移能力(P<0.01)均显著下降，细胞内AKT以及PI3K的表达显著下调(P<0.01)。结论：THBS2 在胰腺癌组织和细胞中高表达，且与患者的预后情况呈负相关，其机制可能是通过调控AKT/PI3K信号通路而调节ASPC-1细胞的增殖和迁移。

[Abstract] Objective:To explore the prognostic significance of thrombospondin 2 (THBS2) expression and its effects on the proliferation and migration of pancreatic cancer ASPC-1 cells for patients with pancreatic cancer, and to investigate its possible molecular mechanism. Methods: The expression of THBS2 in pancreatic cancer tissues and its effects on overall survival rate in patients were analyzed by online database. THBS2 expression in pancreatic cancer ASPC-1 cells was detected by Western Blotting; RNA interference was used to knockdown the expression of THBS2 in ASPC-1 cells, and then the effects of THBS2 knockdown on cell proliferation and migration were detected by MTT and Transwell assays, while its effects on protein expression levels (MMP, E-cadherin, AKT and PI3K) were detected by Wb. Results: Expression of THBS2 in pancreatic cancer tissues was significantly higher than that in normal pancreatic tissues (P<0.01), and the high expression of THBS2 could lead to the decrease of overall survival rate in pancreatic cancer patients. The expression of THBS2 in pancreatic cancer cell lines was significantly up-regulated; however, after interference on the expression of THBS2,the proliferation (P<0.01) and migration ability (P<0.01) of ASPC-1 cells were significantly decreased, and the expression of AKT and PI3K in cells was significantly down-regulated (P<0.01). Conclusion: THBS2 is highly expressed in pancreatic cancer tissues and cells,and is negatively correlated with the prognosis of patients. The mechanism is possibly related with the proliferation and migration of ASPC-1 cells that regulated by AKT/PI3K signaling pathway.