AIM This study aims to evaluate the role of the EPHA5 mutation in the migration and invasion of non-small cell lung cancer (NSCLC) cells and in modulating the killing effect of natural killer (NK) cells to NSCLC cells. METHODS EPHA5-wt (wild type) and EPHA5-mut (mutation) plasmids were constructed. EPHA5 was silenced using si-EPHA5. NSCLC cell migration and invasion were determined using Transwell assays. NK cell proliferation and apoptosis were determined using CCK-8 assay and flow cytometry, respectively. The killing effect of NK cells to NSCLC cells was also examined. RESULTS EPHA5 mutation significantly promoted migration and invasion in NSCLC cells. Furthermore, EPHA5 mutation notably impaired the cytotoxicity of NK cells against NSCLC cells. In contrast, EPHA5-wt overexpression and EPHA5 silencing exerted the opposite effect. CONCLUSION EPHA5 mutation impairs the NK cell-mediated cytotoxicity against NSCLC cells and promotes migration and invasion in NSCLC cells.

中文翻译：

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EPHA5突变削弱了自然杀伤细胞介导的针对非小肺癌细胞的细胞毒性，并促进了癌细胞的迁移和侵袭。

目的本研究旨在评估EPHA5突变在非小细胞肺癌（NSCLC）细胞的迁移和侵袭中以及在调节自然杀伤（NK）细胞对NSCLC细胞的杀伤作用中的作用。方法构建EPHA5-wt（野生型）和EPHA5-mut（突变）质粒。使用si-EPHA5使EPHA5沉默。使用Transwell测定法确定NSCLC细胞迁移和侵袭。分别使用CCK-8分析和流式细胞仪确定NK细胞的增殖和凋亡。还检查了NK细胞对NSCLC细胞的杀伤作用。结果EPHA5突变显着促进了NSCLC细胞的迁移和侵袭。此外，EPHA5突变显着削弱了NK细胞对NSCLC细胞的细胞毒性。相反，EPHA5-wt过表达和EPHA5沉默则发挥相反的作用。