Cheng Nan, Wang Guang-Hui
Department of Otolaryngology, Huaihe Hospital, Henan University, Kaifeng, Henan 475000, P.R. China.
Exp Ther Med. 2016 Apr;11(4):1469-1474. doi: 10.3892/etm.2016.3043. Epub 2016 Feb 1.
MicroRNAs (miRs) are a class of short and non-coding RNA molecules, which function as either oncogenes or tumor suppressors in the development of various human cancers, including nasopharyngeal carcinoma (NPC). The aim of the present study was to investigate the expression of miR-133b in NPC tissue samples, as compared with adjacent normal tissues, and to examine its roles and underlying mechanisms. Analysis using reverse transcription-quantitative polymerase chain reaction demonstrated that miR-133b was downregulated in NPC tissue samples, as compared with adjacent tissues. experiments using NPC cell lines transfected with miR-133b mimics or antisense oligonucleotides further demonstrated that the overexpression of miR-133b mimics impaired, whereas knockdown of its expression promoted, the proliferation of NPC cells. Sphingosine-1-phosphate receptor 1 (S1PR1) was predicted to be a target of miR-133b. Luciferase reporter assays showed that miR-133b inhibited the protein expression of S1PR1 by targeting its 3'-untranslated region. Furthermore, western blot analysis demonstrated that miR-133B altered the regulation of the signal transducer and activator of transcription-3 (STAT3) signaling pathway and the expression of downstream proteins in NPC cells. Therefore, the results of the present study suggested that a previously unknown miR-133b/S1PR1 molecular network may regulate NPC progression.
微小RNA(miR)是一类短链非编码RNA分子,在包括鼻咽癌(NPC)在内的多种人类癌症发生过程中,既可以作为癌基因发挥作用,也可以作为肿瘤抑制因子发挥作用。本研究旨在探讨miR-133b在NPC组织样本中的表达情况,并与相邻正常组织进行比较,同时研究其作用及潜在机制。逆转录定量聚合酶链反应分析表明,与相邻组织相比,NPC组织样本中miR-133b表达下调。使用转染了miR-133b模拟物或反义寡核苷酸的NPC细胞系进行的实验进一步表明,miR-133b模拟物的过表达会损害NPC细胞的增殖,而其表达的敲低则会促进NPC细胞的增殖。鞘氨醇-1-磷酸受体1(S1PR1)被预测为miR-133b的一个靶点。荧光素酶报告基因检测表明,miR-133b通过靶向S1PR1的3'-非翻译区来抑制其蛋白表达。此外,蛋白质印迹分析表明,miR-133b改变了NPC细胞中信号转导和转录激活因子3(STAT3)信号通路的调控以及下游蛋白的表达。因此,本研究结果表明,一个此前未知的miR-133b/S1PR1分子网络可能调控NPC的进展。