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长链非编码RNA MIAT通过miR-124促进鼻咽癌细胞增殖、迁移和侵袭
引用本文:郝亚琳,金晓杰,赵辉,何平,张佳凤,董琼娜,施薇薇,赵苗苗. 长链非编码RNA MIAT通过miR-124促进鼻咽癌细胞增殖、迁移和侵袭[J]. 温州医科大学学报, 2019, 49(10): 718-723
作者姓名:郝亚琳  金晓杰  赵辉  何平  张佳凤  董琼娜  施薇薇  赵苗苗
作者单位:上海交通大学医学院附属仁济医院南院耳鼻咽喉头颈外科,上海201112
摘    要:目的:探究长链非编码RNA MIAT是否通过miR-124调节鼻咽癌细胞增殖、迁移与侵袭。方法:采用荧光定量PCR检测鼻咽癌细胞中MIAT水平,通过检测荧光素酶活性评估MIAT和miR-124之间的相互作用。随后将si-MIAT与miR-124 inhibitor分别或同时转染鼻咽癌细胞,检测其对鼻咽癌细胞生长、迁移与侵袭的影响。采用Western blot检测Wnt/β-catenin信号通路蛋白的表达情况。结果:与正常鼻咽上皮细胞NP-69相比,鼻咽癌细胞HONE-1中MIAT的表达水平显著提高。在线软件与双荧光素酶活性实验分析证实MIAT与miR-124之间存在相互作用。进一步实验表明,si-MIAT可上调miR-124水平,从而抑制鼻咽癌细胞增殖、迁移与侵袭。Western blot分析显示si-MIAT通过miR-124抑制Wnt/β-catenin信号通路在鼻咽癌细胞中发挥促癌作用。结论:MIAT通过miR-124调节Wnt/β-catenin信号通路进而影响鼻咽癌细胞增殖、迁移与侵袭。MIAT靶向调控miR-124,可作为鼻咽癌诊断与治疗的一个潜在靶点。

关 键 词:RNA  长链非编码  MIAT  miR-124  鼻咽癌  
收稿时间:2019-02-05

Long non-coding RNA MIAT in regulating cell proliferation,migration and invasion in nasopharyngeal carcinoma cells through miR-124 sponge
HAO Yalin,JIN Xiaojie,ZHAO Hui,HE Ping,ZHANG Jiafeng,DONG Qiongna,SHI Weiwei,ZHAO Miaomiao. Long non-coding RNA MIAT in regulating cell proliferation,migration and invasion in nasopharyngeal carcinoma cells through miR-124 sponge[J]. JOURNAL OF WENZHOU MEDICAL UNIVERSITY, 2019, 49(10): 718-723
Authors:HAO Yalin  JIN Xiaojie  ZHAO Hui  HE Ping  ZHANG Jiafeng  DONG Qiongna  SHI Weiwei  ZHAO Miaomiao
Affiliation:Department of Otorhinolaryngology Head and Neck Surgery, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201112, China
Abstract:Objective: To investigate whether long non-coding RNA MIAT regulates cell proliferation, migration and invasion in nasopharyngeal carcinoma cells through miR-124. Methods: qRT-qPCR was performed to detect MIAT expression in nasopharyngeal carcinoma cells. The interaction between MIAT and miR-124 was evaluated by dual luciferase reporter assay. si-MIAT and miR-124 inhibitor were transfected into nasopharyngeal carcinoma cells to detect their effects on proliferation, migration and invasion of nasopharyngeal carcinoma cells. The expression of Wnt/β-catenin signaling pathway was determined by Western blot. Results: Compared with normal nasopharyngeal epithelial cells NP-69, MIAT was significantly upregulated in nasopharyngeal carcinoma cell HONE-1. The online software and luciferase activity assay confirmed the interaction between MIAT and miR-124. Further experiments indicated that si-MIAT could increase the expression of miR-124, thus inhibiting cell proliferation, migration and invasion of nasopharyngeal carcinoma. The results of Western blot showed that MIAT functioned as an oncogene in nasopharyngeal carcinoma cell by up-regulating Wnt/β-catenin signaling pathway through miR-124. Conclusion: Our results demonstrated that MIAT affected proliferation, migration and invasion of nasopharyngeal carcinoma cells by regulating the expression of Wnt/β-catenin signaling pathway via miR-124. MIAT was a potential target for the diagnosis and treatment of nasopharyngeal carcinoma.
Keywords:RNA   long non-coding  MIAT  miR-124  nasopharyngeal carcinoma  
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