miR-100 inhibits the migration and invasion of nasopharyngeal carcinoma by targeting IGF1R

被引:26
作者
Sun, Xiaoyan [1 ]
Liu, Xiaoying [1 ]
Wang, Yanmei [1 ]
Yang, Shuqin [1 ]
Chen, Yao [1 ]
Yuan, Tiejun [1 ]
机构
[1] Weifang Peoples Hosp, Dept Otorhinolaryngol, 151 Guangwen St, Weifang 261041, Shandong, Peoples R China
关键词
IGF1R; invasion; migration; miR-100; TUMOR-SUPPRESSOR; GROWTH; EXPRESSION; MICRORNA; RBSP3;
D O I
10.3892/ol.2018.8420
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Nasopharyngeal carcinoma (NPC) is a cancer pattern that often develops in the epithelial cells of the nasopharynx. miR-100 is a miRNA that has been identified in a number of cancers. The aim of the present study was to investigate whether miR-100 can affect cell migration and proliferation of NPC by targeting insulin-like growth factor 1 receptor (IGF1R). Western blot analysis was used to determine the protein levels of genes. The reverse transcription-quantitative PCR (RT-qPCR) was used to detect the expression level of miR-100 and IGF1R. Transwell assay was used to detect the migration and invasion of cell lines. The luciferase reporter assay was employed to confirm the target gene of miR-100. miR-100 expression was highly reduced in NPC tissues compared with non-cancerous tissues. Overexpression of miR-100 significantly inhibited the migration and invasion of NPC cell lines C666-1 and SUNE1. IGF1R was a downstream target of miR-100 and was downregulated by miR-100. Knockdown of IGF1R by siRNA suppressed cell proliferation of the C666-1 cell line. The newly identified miR-100/IGF1R axis offers novel biomarkers for the therapeutic intervention of NPC treatment. As a result, our findings suggest that miR-100 plays an important role in suppressing migration and invasion of NPC cells and suppresses IGF1R expression by directly targeting its 3'-UTR. It is suggested that miR-100 may be a novel therapeutic target of microRNA-mediated suppression of cell migration and invasion in NPC. However, the role of the miR-100/IGF1R axis in NPC progression needs further investigation.
引用
收藏
页码:8333 / 8338
页数:6
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