miR-133b, a microRNA targeting S1PR1, suppresses nasopharyngeal carcinoma cell proliferation
miR-133b, a microRNA targeting S1PR1, suppresses nasopharyngeal carcinoma cell proliferation
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DOI：
10.3892/etm.2016.3043
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发表时间：
2016-04-01
影响因子：
2.7
通讯作者：
Wang, Guang-Hui
中科院分区：
文献类型：
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作者：
Cheng, Nan;Wang, Guang-Hui
microRNA（miRs）是一类短的非编码RNA分子，在包括鼻咽癌（NPC）在内的多种人类癌症的发生发展中起着癌基因或肿瘤抑制因子的作用。本研究的目的是研究miR-133 b在鼻咽癌组织中的表达，并与癌旁正常组织进行比较，探讨其作用和机制。逆转录-定量聚合酶链反应分析表明，miR-133 b在NPC组织样本中表达下调，与邻近组织相比。使用miR-133 b模拟物或反义寡核苷酸转染的NPC细胞系的体外实验进一步证明，miR-133 b模拟物的过表达损害NPC细胞的增殖，而其表达的敲低促进NPC细胞的增殖。鞘氨醇-1-磷酸受体1（S1 PR 1）被预测为miR-133 b的靶点。荧光素酶报告基因分析表明，miR-133 b通过靶向S1 PR 1的3 '端非翻译区抑制其蛋白表达。Western blot结果显示，miR-133 B改变了鼻咽癌细胞信号转导和转录激活因子-3（STAT 3）信号通路的调控及下游蛋白的表达。因此，本研究的结果表明，以前未知的miR-133 b/S1 PR 1分子网络可能调控NPC的进展。
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. In vitro 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.