Ye Ying, Zhuang Juhua, Wang Guoyu, He Saifei, Ni Jing, Xia Wei, Wang Jiening
Department of Nuclear Medicine, The Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai 200137, P.R. China.
Exp Ther Med. 2017 Jul;14(1):867-873. doi: 10.3892/etm.2017.4538. Epub 2017 Jun 1.
Lung cancer is the most common cause of cancer- associated mortality for men and women worldwide. An increasing number of studies have reported that the abnormal expression of microRNAs contributes to the pathogenesis of the majority of human cancer types, including non-small cell lung cancer (NSCLC). The present study aimed to measure microRNA-650 (miR-650) expression in NSCLC and evaluate its function in NSCLC cells. Reverse transcription-quantitative polymerase chain reaction was used to determine miR-650 expression in NSCLC tissue samples and cell lines. Assays for cell proliferation, migration and invasion were performed to investigate the roles of miR-650 on NSCLC progression. Furthermore, the mechanisms underlying the effects of miR-650 on NSCLC cell growth and metastasis were determined. In the current study, miR-650 was demonstrated to be highly expressed in NSCLC tissue samples and cell lines. Inhibition of expression of miR-650 suppressed NSCLC cell proliferation, migration and invasion . Additionally, large tumor suppressor kinase 2 (LATS2) was identified as a direct target gene of miR-650 in NSCLC. LATS2 was revealed to be significantly downregulated in NSCLC tissues and was negatively correlated with miR-650 expression. Notably, LATS2 re-expression decreased NSCLC cell proliferation, migration and invasion; similar to the effects induced by miR-650 underexpression. In conclusion, the results of the current study suggest that miR-650 may serve as an oncogene by direct targeting LATS2 in NSCLC formation and progression.
肺癌是全球男性和女性癌症相关死亡的最常见原因。越来越多的研究报告称，微小RNA的异常表达促成了包括非小细胞肺癌（NSCLC）在内的大多数人类癌症类型的发病机制。本研究旨在检测NSCLC中微小RNA-650（miR-650）的表达，并评估其在NSCLC细胞中的功能。采用逆转录-定量聚合酶链反应来测定NSCLC组织样本和细胞系中miR-650的表达。进行细胞增殖、迁移和侵袭检测以研究miR-650在NSCLC进展中的作用。此外，还确定了miR-650对NSCLC细胞生长和转移影响的潜在机制。在本研究中，miR-650在NSCLC组织样本和细胞系中被证明高表达。抑制miR-650的表达可抑制NSCLC细胞的增殖、迁移和侵袭。此外，大肿瘤抑制激酶2（LATS2）被确定为NSCLC中miR-650的直接靶基因。LATS2在NSCLC组织中显著下调，并与miR-650的表达呈负相关。值得注意的是，LATS2的重新表达降低了NSCLC细胞的增殖、迁移和侵袭；类似于miR-650低表达所诱导的效果。总之，本研究结果表明，在NSCLC的形成和进展中，miR-650可能通过直接靶向LATS2而作为一种癌基因发挥作用。
