miR-133b, a microRNA targeting S1PR1, suppresses nasopharyngeal carcinoma cell proliferation

被引:18
作者
Cheng, Nan [1 ]
Wang, Guang-Hui [1 ]
机构
[1] Henan Univ, Huaihe Hosp, Dept Otolaryngol, 8 Bao Bei Rd, Kaifeng 475000, Henan, Peoples R China
关键词
nasopharyngeal carcinoma; sphingosine-1-phosphate receptor 1; microRNA; miR-133b; PERSISTENT STAT3 ACTIVATION; GROWTH-FACTOR RECEPTOR; GASTRIC-CANCER; TUMOR-SUPPRESSOR; EXPRESSION; INVASION; MIGRATION; ROLES; ACTS;
D O I
10.3892/etm.2016.3043
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
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.
引用
收藏
页码:1469 / 1474
页数:6
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