Yan Liang, Ma Jinzhu, Wang Yi, Zan Jiawei, Wang Zhen, Zhu Yu, Zhu Yiping, Ling Liefeng, Cao Long, Liu Xin, Li Shu, Xu Lei, Qi Zhilin, Nie Liuwang, Zhang Yao
Department of Biopharmaceuticals, College of Life Sciences, Anhui Normal University, Wuhu, Anhui 241002, P.R. China.
Department of Biochemistry, Provincial Key Laboratory of Biological Macro-molecules Research, Wannan Medical College, Wuhu, Anhui 241002, P.R. China.
Exp Ther Med. 2018 Dec;16(6):4655-4663. doi: 10.3892/etm.2018.6752. Epub 2018 Sep 18.
The mortality rate of non-small cell lung cancer (NSCLC) remains high worldwide. miR-21-5p plays an important part in many cancer types, including NSCLC. However, the effect of miR-21-5p in NSCLC tumorigenesis remains poorly understood. The present study investigated whether miR-21-5p promoted NSCLC cell proliferation . In order to study the molecular mechanism by which miR-21-5p contributes to NSCLC progression, three bioinformatics algorithms were used to predict the genes which miR-21-5p targeted. TGFBI was identfieid as a putative direct target in NSCLC cells via the luciferase reporter assay. Furthermore, miR-21-5p downregulated TGFBI protein expression by a post-transcriptional mechanism via western blotting and a reverse transcription-quantitative polymerase chain reaction analysis. Finally, TGFBI exhibited opposing effects to those of miR-21-5p on NSCLC cells, suggesting that miR-21-5p may promote cell proliferation by negative regulation of TGFBI. These results suggest miR-21-5p promote the proliferation of NSCLC cells via inhibiting TGFBI expression.
在全球范围内,非小细胞肺癌(NSCLC)的死亡率仍然很高。miR-21-5p在包括NSCLC在内的多种癌症类型中发挥着重要作用。然而,miR-21-5p在NSCLC肿瘤发生中的作用仍知之甚少。本研究调查了miR-21-5p是否促进NSCLC细胞增殖。为了研究miR-21-5p促进NSCLC进展的分子机制,使用了三种生物信息学算法来预测miR-21-5p靶向的基因。通过荧光素酶报告基因检测,TGFBI被确定为NSCLC细胞中的一个假定直接靶点。此外,通过蛋白质印迹法和逆转录-定量聚合酶链反应分析,miR-21-5p通过转录后机制下调TGFBI蛋白表达。最后,TGFBI对NSCLC细胞表现出与miR-21-5p相反的作用,表明miR-21-5p可能通过对TGFBI的负调控促进细胞增殖。这些结果表明,miR-21-5p通过抑制TGFBI表达促进NSCLC细胞的增殖。