Li Lihua, Luo Zhaohui
Department of Radiotherapy, Hunan Cancer Hospital, Changsha, Hunan 410013, P.R. China.
Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Oncol Rep. 2017 May;37(5):2679-2687. doi: 10.3892/or.2017.5544. Epub 2017 Mar 31.
miRNA-27a-3p is an important regulator of carcinogenesis and other pathological processes. However, its role in laryngeal carcinoma is still unknown. In our previous research, we found that miR-27a-3p expression was upregulated in nasopharyngeal carcinoma (NPC) using a microarray chip. In the present study, we identified miR-27a-3p as an endogenous promoter of metastatic invasion. The expression levels of miR-27a-3p were correlated with human metastatic progression outcomes and Kaplan-Meier survival. In silico database analyses revealed that Mapk10 is a potential target of miR-27a-3p, and luciferase reporter assay results revealed that miR-27a-3p directly inhibits the Mapk10 3' untranslated region (3'UTR). Real-time PCR and western blotting results ascertained that Mapk10 expression was regulated by miR‑27a-3p. In addition, miR‑27a-3p gain-of-function promoted cell proliferation, migration and invasion in 5-8 F NPC cells. These effects partially depended on Mapk10, and loss of miR‑27a-3p function had the opposite effects.
微小RNA-27a-3p是致癌作用和其他病理过程的重要调节因子。然而,其在喉癌中的作用仍不清楚。在我们之前的研究中,我们使用微阵列芯片发现鼻咽癌(NPC)中miR-27a-3p表达上调。在本研究中,我们确定miR-27a-3p是转移侵袭的内源性促进因子。miR-27a-3p的表达水平与人类转移进展结果和Kaplan-Meier生存相关。计算机数据库分析显示Mapk10是miR-27a-3p的潜在靶标,荧光素酶报告基因检测结果显示miR-27a-3p直接抑制Mapk10的3'非翻译区(3'UTR)。实时PCR和蛋白质印迹结果确定Mapk10的表达受miR-27a-3p调控。此外,miR-27a-3p功能获得促进了5-8F NPC细胞的增殖、迁移和侵袭。这些作用部分依赖于Mapk10,而miR-27a-3p功能缺失则产生相反的效果。