[摘 要] 目的：分析整合素连接激酶（ILK）基因在食管鳞状细胞癌（ESCC）组织中的表达水平及其与患者临床病理特征之间的关系，探讨其对KYSE-150细胞增殖、凋亡和裸鼠皮下移植瘤生长的影响。方法:选取2012年1月至2014年12月手术切除并经病理证实的75例ESCC患者的癌组织和其配对的癌旁组织标本，用组织芯片技术及免疫组织化学染色法检测ESCC组织和癌旁组织中ILK的表达情况；qPCR法检测ESCC细胞ECA109、TE-1、EC9706、KYSE-150中ILK mRNA的表达，选用ILK表达最高的KYSE-150细胞进行后续细胞功能学研究。使用ILK干扰慢病毒感染KYSE-150细胞下调ILK的表达，qPCR和WB法检测ILK基因敲降效率；MTT实验、克隆形成实验和FACS检测干扰ILK表达对KYSE-150细胞增殖能力和凋亡水平的影响；裸鼠皮下成瘤实验检测干扰ILK对KYSE-150细胞移植瘤生长的影响。结果:ESCC组织中ILK蛋白阳性表达率高于癌旁组织（P<0.05），且ILK高表达与淋巴结转移有关联（P<0.05）。ILK干扰慢病毒感染的KYSE-150细胞中ILK mRNA表达明显受到抑制（P<0.05），ILK蛋白水平表达下调，以上结果提示ILK敲降成功。与感染阴性对照病毒的KYSE-150细胞相比，ILK干扰慢病毒感染的KYSE-150细胞的增殖能力、克隆形成数均显著降低（均P<0.05），但细胞凋亡率升高（P<0.05）。与对照组相比，干预组裸鼠移植瘤生长缓慢，移植瘤的质量及体积均较小（均P<0.05）。结论:ESCC组织中ILK的表达高于癌旁组织，且ILK高表达与患者发生淋巴结转移有关联；抑制ILK基因可导致KYSE-150细胞增殖能力降低，促进细胞凋亡而抑制裸鼠移植瘤生长。

【Objective】To investigate the effect of miR- 127-3p on proliferation，apoptosis，migration and invasion of uveal melanoma cells.【Methods】The expression of miR- 127- 3p and MAPK4 mRNA in human uveal melanoma tissues and cells，normal tissues and cells were detected by RT-qPCR. The mimic-NC，miR-127-3p mimic，pc-MAPK4 plasmids were transfected into SP6.5 or OM431 cells，respectively，by Lipofectamine 2000. The relationship between miR-127-3p and MAPK4 counterstaining was detected by dual luciferase assay. Cell proliferation was detected by CCK- 8 method，apoptosis was detected by flow cytometry，cell migration ability was detected by scratch test，cell invasion ability was detected by Transwell method，and relative expression level of AKT/mTOR pathway protein was detected by Western blot.【Results】In uveal melanoma tissues and cell lines，the expression of miR- 127-3p was down-regulated（P < 0.01）while that of MAPK4 expression was significantly up-regulated（P < 0.01）. The binding site of miR-127-3p and MAPK4 3′UTR region，the high expression of miR-127-3p significantly inhibited the luciferase activity of wild-type MAPK4 plasmid（P < 0.01），but the mutant MAPK4 plasmid Luciferase activity has no effect. Compared with the Control group ，the proliferation of SP6.5 cells and OM431 cells in miR- 127-3p mimic group were significantly decreased（P < 0.01），and the apoptotic rate was significantly increased（P < 0.01）. The scratch closure rate was obvious. The decrease（P < 0.01）， the number of invading cells per field was significantly decreased（P < 0.01），and the expression of p-AKT（T308）/AKT and p-mTORr（S473）/mTOR protein were significantly down-regulated（P < 0.01）. Transfection of pc-MAPK4 reversed the above changes.【Conclusion】MiR-127-3p inhibits proliferation，migration and invasion of uveal melanoma cells and induces apoptosis by down-regulating MAPK4，which may be involved in the inhibition of AKT/mTOR pathway activation.