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失调的miR-27a-3p通过靶向Mapk10促进鼻咽癌细胞的增殖和迁移。

Dysregulated miR-27a-3p promotes nasopharyngeal carcinoma cell proliferation and migration by targeting Mapk10.

作者信息

Li Lihua, Luo Zhaohui

机构信息

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.

出版信息

Oncol Rep. 2017 May;37(5):2679-2687. doi: 10.3892/or.2017.5544. Epub 2017 Mar 31.

Abstract

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.

摘要

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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6965/5428281/782229723d91/OR-37-05-2679-g00.jpg

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