长链非编码RNA RP11-554D14.7对非小细胞肺癌细胞增殖和凋亡能力的影响

摘要

目的:研究lncRNA RP11-554D14.7在非小细胞肺癌(non-small cell lung cancer,NSCLC)中的表达情况,及其对NSCLC细胞功能的影响和分子机制.方法:实时定量PCR用于检测lncRNA RP11-554D14.7在NSCLC组织及细胞中的表达水平;CCK8、集落形成实验检测RP11-554D14.7对NSCLC细胞增殖能力的影响;流式细胞技术检测RP11-554D14.7对NSCLC细胞凋亡能力的影响;生物信息学分析和荧光素酶报告基因技术研究RP11-554D14.7对miR-21的调控.结果:RP11-554D14.7在NSCLC组织及细胞中表达下调,上调RP11-554D14.7的表达抑制NSCLC细胞增殖并诱导细胞凋亡;miR-21可直接结合到RP11-554D14.7的序列中.结论:下调的RP11-554D14.7在NSCLC的发生发展过程中可能是一个抑癌基因,可作为NSCLC一个候选的治疗靶点.%Objective:To investigate the expression pattern,biological function and underlying mechanism of an new identified lncRNA RP11-554D14.7 in NSCLC.Methods:Quantitative polymerase chain reaction (qPCR) was used to detect the RP11-554D14.7 expression level in NSCLC tissues and cells.CCK8 and colony formation assays were used to investigate the effect of RP11-554D14.7 on NSCLC cells proliferation.Flow cytometry analysis was used to determine the effect of RP11-554D14.7 on NSCLC cells apoptosis.Bioinformatics analysis and luciferase reporter assays were used to determine the RP11-554D14.7''s regulation of miR-21.Results:RP11-554D14.7 expression was downregulated in NSCLC tissues and cells compared with normal tissues and cells,and over-expression of RP11-554D14.7 could inhibit NSCLC cells proliferation and induce cell apoptosis.Moreover,miR-21 could directly bind to RP11-554D14.7 sequence.Conclusion:Downregulated RP11-554D14.7 may play critical role in NSCLC development by functioning as a tumor suppressor,which may be used as an potential therapy target for NSCLC patients.