miR-944 inhibits cell migration and invasion by targeting MACC1 in nasopharyngeal carcinoma

被引:2
|
作者
Ji, Juanjuan [1 ]
Peng, Yi [2 ]
Niu, Tao [2 ]
Lin, Yunhong [2 ]
Lin, Yan [3 ]
Li, Xudong [2 ]
Wu, Xiaoguang [3 ]
Huang, Zhiyong [2 ]
Zhong, Ling [3 ]
Zhang, Shinan [2 ]
机构
[1] Second Peoples Hosp Yunnan Prov, Kunming, Yunnan, Peoples R China
[2] Kunming Med Univ, Affiliated Stomatol Hosp, Block C 1088,Hai Yuan Rd, Kunming 650500, Yunnan, Peoples R China
[3] Kunming Med Univ, Affiliated Hosp 1, Kunming, Yunnan, Peoples R China
关键词
Nasopharyngeal carcinoma; miR-944; MACC1; cell migration; invasion; PROGNOSTIC-FACTORS; DOWN-REGULATION; POOR-PROGNOSIS; CANCER; OVEREXPRESSION; EXPRESSION; METASTASIS; MICRORNAS; PREDICTS; BREAST;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Nasopharyngeal carcinoma (NPC) is a common disease in Southern China with high prevalence. miR-944 has been reported to play a vital role in progression of a variety of cancers. The present study aimed to investigate the potential role of miR-944 in NPC cell migration and invasion through elucidating the interaction with its target genes, MACC1. Expression of miR-944 in NPC tissues and cell lines was examined with quantitative RT-PCR. Over-expressed miR-944 and suppressed miR-944 were established with miR-944 mimics and miR-944 inhibitor, respectively. The effect of miR-944 on cell migration and invasion was determined using Transwell cell migration and Matrigel invasion assay. Luciferase assay was used to determine the target of miR-944. Knocked down of MACC1 was done by MACC1 siRNA. Expression of MET related-markers was examined using Western blot analysis. The expression level of miR-944 was downregulated in NPC tissues and cell lines. Overexpression of miR-944 significantly inhibited the cell migration and invasion in NPC 6-10B cells. In contrast, suppression of miR-944 promoted cell migration and invasion in NPC C-6661 cells. MACC1 is a direct target of miR-944. MACC1 expression was repressed in miR-944 mimic transfected cells while it was enhanced in miR-944 inhibitor transfected cells. MACC1 knock down inhibited cell migration and invasion. Either miR-944 restoration or MACC1 knockdown caused enhanced E-cadherin, reduced N-cadherin, and vimentin expression. In conclusion, miR-944 could inhibit MET and metastasis of NPC by targeting MACC1. This study suggests that miR-944 has anti-tumor and anti-metastatic properties and could thus be a novel therapeutic agent for NPC treatment.
引用
收藏
页码:1167 / 1174
页数:8
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