Abstract：
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It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.
摘要：
背景：长非编码RNA（lncRNA）MCM3AP-AS1的功能已在几种类型的癌症中报道，而其在非小细胞肺癌（NSCLC）中的参与尚不清楚。
目的：本研究旨在探讨MCM3AP-AS1在非小细胞肺癌中的作用。
方法：在肿瘤细胞中实现MCM3AP-AS1的沉默或过表达，以构建荷瘤小鼠模型，以评估MCM3AP-AS1对肿瘤生长的影响。
结果：结果显示MCM3AP-AS1在非小细胞肺癌中上调，并与较差的生存率相关。在NSCLC组织中，MCM3AP-AS1与microRNA(miR)-34a呈负相关。MCM3AP-AS1导致增强的NSCLC细胞运动和增殖。miR-34a的过表达拯救了MCM3AP-AS1过表达对细胞运动的影响。异种移植实验显示，si-MCM3AP-AS1组和miR-34a组的肿瘤重量和体积显着减少。MCM3AP-AS1增加肿瘤重量和体积，和miR-34a部分减弱MCM3AP-AS1诱导的促进肿瘤生长。
结论：MCM3AP-AS1可能增强细胞侵袭能力，迁移,通过调节NSCLC细胞中的miR-34a和肿瘤形成能力。
目的：本研究旨在探讨MCM3AP-AS1在非小细胞肺癌中的作用。
方法：在肿瘤细胞中实现MCM3AP-AS1的沉默或过表达，以构建荷瘤小鼠模型，以评估MCM3AP-AS1对肿瘤生长的影响。
结果：结果显示MCM3AP-AS1在非小细胞肺癌中上调，并与较差的生存率相关。
结论：MCM3AP-AS1可能增强细胞侵袭能力，
