MiR-454 promotes the progression of human non-small cell lung cancer and directly targets PTEN

被引:62
作者
Zhu Deng-Yan [1 ]
Li Xiang-Nan [1 ]
Yu, Qi [1 ]
Liu Dong-Lei [1 ]
Yang, Yang [1 ]
Jia, Zhao [1 ]
Zhang Chun-Yang [1 ]
Kai, Wu [1 ]
Song, Zhao [1 ]
机构
[1] Zhengzhou Univ, Affiliated Hosp 1, Dept Thorac Surg, 1 East Jianshe Rd, Zhengzhou 450052, Henan, Peoples R China
关键词
MiR-454; Non-small cell lung cancer; PTEN; Prognosis; Proliferation; Apoptosis; PROLIFERATION; EXPRESSION; ONCOGENE; INVASION;
D O I
10.1016/j.biopha.2016.03.029
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Purpose: MicroRNA-454 has been proven dysregulated in some human malignancies and correlated with tumor progression. However, its expression and function in non-small cell lung cancer (NSCLC) is still unclear. Thus, the aim of this study was to explore the effects of miR-454 in NSCLC tumorigenesis and development. Methods: Using quantitative RT-PCR, we detected miR-454 expression in NSCLC cell lines and primary tumor tissues. The association of miR-454 expression with clinicopathological factors and prognosis was also analyzed. Then, the effects of miR-454 on the biological behavior of NSCLC cells were investigated. At last, the potential regulatory function of miR-454 on PTEN expression was confirmed. Results: miR-454 was found to be up-regulated in NSCLC tissues and cell lines. High miR-454 expression was closely correlated with lymph node metastasis, advanced TNM stage, and shorter overall survival. Multivariate regression analysis corroborated that miR-454 overexpression was an independent unfavourable prognostic factor for patients with NSCLC. Down-regulation of miR-454 could significantly reduce NSCLC cell proliferation, enhance cell apoptosis, and impair cell invasion and migration in vitro, while up-regulation of miR-454 showed opposite effects. Further, PTEN was confirmed as a direct target of miR-454 by using Luciferase Reporter Assay. Conclusions: These findings indicate that miR-454 may act as an oncogene in NSCLC and would serve as a potential therapy target for this disease. a 2016 Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:79 / 85
页数:7
相关论文
共 27 条
[1]  
[Anonymous], TUMOUR BIOL
[2]   MicroRNAs: Target Recognition and Regulatory Functions [J].
Bartel, David P. .
CELL, 2009, 136 (02) :215-233
[3]   MicroRNAs: Genomics, biogenesis, mechanism, and function (Reprinted from Cell, vol 116, pg 281-297, 2004) [J].
Bartel, David P. .
CELL, 2007, 131 (04) :11-29
[4]  
Bonneau D, 2000, HUM MUTAT, V16, P109, DOI 10.1002/1098-1004(200008)16:2<109::AID-HUMU3>3.0.CO
[5]  
2-0
[6]   Mechanisms of Disease: the PI3K-Akt-PTEN signaling node - an intercept point for the control of angiogenesis in brain tumors [J].
Castellino, Robert C. ;
Durden, Donald L. .
NATURE CLINICAL PRACTICE NEUROLOGY, 2007, 3 (12) :682-693
[7]   The Noncoding RNA Revolution-Trashing Old Rules to Forge New Ones [J].
Cech, Thomas R. ;
Steitz, Joan A. .
CELL, 2014, 157 (01) :77-94
[8]   MicroRNAs as oncogenes and tumor suppressors [J].
Chen, CZ .
NEW ENGLAND JOURNAL OF MEDICINE, 2005, 353 (17) :1768-1771
[9]   Over-expressing CYLD augments antitumor activity of TRAIL by inhibiting the NF-κB survival signaling in lung cancer cells [J].
Deng, L. L. ;
Shao, Y. X. ;
Lv, H. F. ;
Deng, H. B. ;
Lv, F. Z. .
NEOPLASMA, 2012, 59 (01) :18-29
[10]   MiR-454 inhibited cell proliferation of human glioblastoma cells by suppressing PDK1 expression [J].
Fang, Baojun ;
Zhu, Jianxin ;
Wang, Yunhua ;
Geng, Fengyang ;
Li, Gang .
BIOMEDICINE & PHARMACOTHERAPY, 2015, 75 :148-152