This study aimed to investigate the role of lncRNA MAGI2-AS3 in non-small cell lung cancer (NSCLC). Expression levels of MAGI2-AS3 and RECK mRNA in two types of tissues (non-tumor and NCSLC) were measured by qPCR. To further investigate the interaction between MAGI2-AS3 and RECK, MAGI2-AS3 and RECK expression vectors were transfected into H1993 cells. We found that MAGI2-AS3 and RECK were upregulated and positively correlated in NSCLC. In NSCLC cells, MAGI2-AS3 overexpression led to upregulated RECK. Bioinformatics analysis showed that MAGI2-AS3 may bind miR-25, which can directly target RECK. In NSCLC cells, miR-25 overexpression led to downregulated RECK and attenuated the effects of MAGI2-AS3 overexpression, while MAGI2-AS3 and miR-25 failed to affect each other. Cell invasion and migration analysis showed decreased NSCLC cell invasion and migration rates after MAGI2-AS3 and RECK overexpression. MiR-25 showed opposite role and reduced the effects of MAGI2-AS3 overexpression. Therefore, MAGI2-AS3 may sponge miR-25 to upregulate RECK, thereby inhibiting NSCLC cell invasion and migration. HLJCM20163358592, registered by First Affiliated Hospital, Heilongjiang University of Chinese Medicine at March 3, 2016, prospectively.

中文翻译：

---

LncRNA MAGI2-AS3在非小细胞肺癌中下调，可能是miR-25的海绵

本研究旨在探讨lncRNA MAGI2-AS3在非小细胞肺癌（NSCLC）中的作用。通过 qPCR 测量两种类型组织（非肿瘤组织和 NCSLC）中 MAGI2-AS3 和 RECK mRNA 的表达水平。为了进一步研究MAGI2-AS3和RECK之间的相互作用，将MAGI2-AS3和RECK表达载体转染到H1993细胞中。我们发现 MAGI2-AS3 和 RECK 在 NSCLC 中表达上调且呈正相关。在 NSCLC 细胞中，MAGI2-AS3 过表达导致 RECK 上调。生物信息学分析表明MAGI2-AS3可能结合miR-25，从而直接靶向RECK。在NSCLC细胞中，miR-25过表达导致RECK下调并减弱MAGI2-AS3过表达的作用，而MAGI2-AS3和miR-25未能相互影响。细胞侵袭和迁移分析显示，MAGI2-AS3和RECK过表达后，NSCLC细胞侵袭和迁移率降低。MiR-25 显示相反的作用并降低 MAGI2-AS3 过表达的影响。因此，MAGI2-AS3可能通过海绵miR-25来上调RECK，从而抑制NSCLC细胞的侵袭和迁移。HLJCM20163358592，2016年3月3日在黑龙江中医药大学第一附属医院注册，前瞻性。