MicroRNA-93 promotes cell growth and invasion in nasopharyngeal carcinoma by targeting disabled homolog-2
MicroRNA-93 promotes cell growth and invasion in nasopharyngeal carcinoma by targeting disabled homolog-2
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MicroRNA-93通过靶向Disabledhomolog-2促进鼻咽癌细胞生长和侵袭
DOI：
10.1016/j.canlet.2015.04.006
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发表时间：
2015-07-28
期刊：
影响因子：
9.7
通讯作者：
Ma, Jun
中科院分区：
文献类型：
--
作者：
Xu, Ya-Fei;Mao, Yan-Ping;Ma, Jun
微小RNA（microRNAs，miRNAs）的异常调控与鼻咽癌的恶性进展密切相关。我们以前报道过，基于微阵列分析，miR-93在NPC中显著上调。然而，miR-93在NPC的发生和发展中的潜在作用和作用机制仍不清楚。定量RT-PCR结果显示，miR-93在鼻咽癌细胞系和临床标本中表达显著上调。MTT法、集落形成法、非贴壁依赖性生长法、Transwell迁移和侵袭法显示，去除miR-93后，体外抑制鼻咽癌细胞生长、侵袭和迁移，体内抑制肿瘤生长。荧光素酶报告基因检测、定量RT-PCR和Western blotting证实Dab 2是miR-93的靶基因，参与miR-93调控的NPC细胞生长、侵袭和迁移。这些结果表明，miR-93通过靶向Dab 2在鼻咽癌的发生和发展中起重要作用，miR-93/Dab 2通路可能为今后开发新的鼻咽癌治疗策略提供新的思路。(C)2015爱思唯尔爱尔兰有限公司版权所有。
Dysregulation of microRNAs (miRNAs) has been demonstrated to contribute to malignant progression in nasopharyngeal carcinoma (NPC). We previously reported that miR-93 was significantly upregulated in NPC based on a microarray analysis. However, the potential role and mechanism of action of miR-93 in the initiation and progression of NPC remain largely unknown. Quantitative RT-PCR demonstrated that miR-93 was significantly upregulated in NPC cell lines and clinical specimens. The MTT assay, colony formation assay, anchorage-independent growth, and Transwell migration and invasion assays showed that depletion of miR-93 inhibited NPC cell growth, invasion and migration in vitro and suppressed tumor growth in vivo. Disabled homolog-2 (Dab2) was verified as a miR-93 target gene using Luciferase reporter assays, quantitative RT-PCR and Western blotting and was involved in miR-93-regulated NPC cell growth, invasion and migration. These results indicated that miR-93 plays an important role in the initiation and progression of NPC by targeting Dab2 and the miR-93/Dab2 pathway may contribute to the development of novel therapeutic strategies for NPC in the future. (C) 2015 Elsevier Ireland Ltd. All rights reserved.