Long non-coding RNAs (lncRNAs) are proved to perform critical function in regulating cancer cell behavior. It is reported that LINC00324 promotes lung adenocarcinoma development by regulating miR-615-5p/AKT1 axis. This study aimed to demonstrate whether LINC00324 participates in non-small cell lung cancer (NSCLC) pathogenesis through other molecular mechanism. Relative mRNA, lncRNA, and microRNA levels were analyzed using quantitative real-time–polymerase chain reaction (qRT-PCR). Western blot was used to detect protein level. MTT assay shown proliferation ability and transwell assay shown invasive ability. Luciferase reporter assay illustrated the interaction between RNA molecules. In NSCLC, the high expression of LINC00324 had correlation with the poor prognosis. LINC00324 promoted the proliferation and invasion of NSCLC cells while miR-139-5p inhibited these behaviors. LINC00324 overexpression promoted insulin-like growth factor 1 receptor (IGF1R) expression via absorbing miR-139-5p. The tumor-promoting effects of LINC00324 were attenuated through miR-139-5p overexpression. Highly expressed LINC00324 in NSCLC through sponged miR-139-5p to elevate IGF1R expression and promoted cell proliferation and invasion. This research demonstrated that LINC00324 is a potential NSCLC diagnosis and therapy target.

长非编码RNA（lncRNA）被证明在调节癌细胞行为中起关键作用。据报道，LINC00324通过调节miR-615-5p / AKT1轴促进肺腺癌的发展。这项研究旨在证明LINC00324是否通过其他分子机制参与非小细胞肺癌（NSCLC）发病机制。使用定量实时聚合酶链反应（qRT-PCR）分析了相对mRNA，lncRNA和microRNA的水平。使用蛋白质印迹法检测蛋白质水平。MTT法显示增殖能力，transwell法显示侵袭能力。萤光素酶报告基因检测说明了RNA分子之间的相互作用。在NSCLC中，LINC00324的高表达与不良预后相关。LINC00324促进了NSCLC细胞的增殖和侵袭，而miR-139-5p抑制了这些行为。LINC00324过表达通过吸收miR-139-5p促进了胰岛素样生长因子1受体（IGF1R）的表达。LINC00324的促肿瘤作用通过miR-139-5p过表达而减弱。通过海绵状miR-139-5p在NSCLC中高表达LINC00324，以提高IGF1R表达并促进细胞增殖和侵袭。这项研究表明，LINC00324是潜在的NSCLC诊断和治疗目标。通过海绵状miR-139-5p在NSCLC中高表达LINC00324，以提高IGF1R表达并促进细胞增殖和侵袭。这项研究表明，LINC00324是潜在的NSCLC诊断和治疗目标。通过海绵状miR-139-5p在NSCLC中高表达LINC00324，以提高IGF1R表达并促进细胞增殖和侵袭。这项研究表明，LINC00324是潜在的NSCLC诊断和治疗目标。