miR-4792 inhibits epithelial-mesenchymal transition and invasion in nasopharyngeal carcinoma by targeting FOXC1
miR-4792 inhibits epithelial-mesenchymal transition and invasion in nasopharyngeal carcinoma by targeting FOXC1
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DOI：
10.1016/j.bbrc.2015.11.045
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发表时间：
2015-12-25
影响因子：
3.1
通讯作者：
Chen, Xiangdong
中科院分区：
文献类型：
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作者：
Li, Ying;Chen, Xiangdong
通过分析已发表的基于微阵列的高通量评估，我们发现miR-4792在鼻咽癌（NPC）组织中显著下调。然而，其在鼻咽癌发生发展中的作用及机制尚不清楚。在此，我们报道了miR-4792在NPC上皮间质转化（EMT）和侵袭中的作用。我们发现miR-4792的表达水平与鼻咽癌细胞的EMT和侵袭呈负相关，miR-4792的上调抑制了鼻咽癌细胞的EMT和侵袭。此外，我们还鉴定并验证了FOXC 1是miR-4792的直接靶点，miR-4792通过直接作用于FOXC 1 mRNA的3 'UTR来调节NPC中的EMT和侵袭。我们还进行了动物实验来探讨miR-4792的抗肿瘤作用，发现miR-4792的过表达抑制了体内鼻咽肿瘤的生长。这些结果提示miR-4792通过靶向FOXC 1在鼻咽癌的发生发展中发挥抑癌作用，可能成为鼻咽癌治疗的新靶点，我们研究的miR-4792/FOXC 1通路可能在未来用于鼻咽癌的治疗。(C)2015爱思唯尔公司All rights reserved.
Through analysis of a published micro-array-based high-throughput assessment, we discovered that miR-4792 was markedly down-regulated in nasopharyngeal carcinoma (NPC) tissues. However, little is known about its effect and mechanism involved in NPC development and progression. Here, we reported the role of miR-4792 in epithelial mesenchymal transition (EMT) and invasion in NPC. We identified an inverse correlation between miR-4792 expression level and NPC cell EMT and invasion, and up-regulation of miR-4792 inhibited NPC cell EMT and invasion. Moreover, we identified and validated that FOXC1 was a direct target of miR-4792, and miR-4792 regulated EMT and invasion in NPC by acting directly on the 3'UTR of FOXC1 mRNA. We also performed the animal experiments to explore the antitumor effect of miR-4792, and found that overexpression of miR-4792 inhibited the growth of nasopharyngeal tumors in vivo. These findings suggest that miR-4792 functions as a tumor suppressor in NPC development and progression by targeting FOXC1, which could act as a novel potential therapeutic target for NPC treatment, and miR-4792/FOXC1 pathway that we studied might be used for NPC treatment in future. (C) 2015 Elsevier Inc. All rights reserved.