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（ q PCR） 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.
出处
《现代肿瘤医学》
CAS
2017年第18期2869-2873,共5页
Journal of Modern Oncology
基金
国家自然科学基金资助(编号:81402554)
无锡市卫生局卫生科研项目青年基金(编号:Q201403)
