MiR-29a promotes cell proliferation and EMT in breast cancer by targeting ten eleven translocation 1

被引:75
作者
Pei, Yao-fei [1 ]
Lei, Yao [2 ]
Liu, Xi-qiang [1 ]
机构
[1] Zhejiang Prov Peoples Hosp, Dept Hepatobiliary Pancreat Surg, Hangzhou 310014, Zhejiang, Peoples R China
[2] Hunan Prov Peoples Hosp, Dept Intervent Therapy & Vasc Surg, Changsha 410005, Hunan, Peoples R China
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2016年 / 1862卷 / 11期
关键词
Breast cancer; Cell proliferation; EMT; MiR-29a; TET1; TUMOR-SUPPRESSOR; EXPRESSION; 5-HYDROXYMETHYLCYTOSINE; MICRORNA-148B; REGULATOR; CARCINOMA; MIRNAS;
D O I
10.1016/j.bbadis.2016.08.014
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Increasing evidence has shown that microRNAs played an important role in regulating carcinogenesis. However, the role of miR-29a in breast cancer is still unclear. Herein, we showed that miR-29a was significantly up-regulated in breast cancer as compared with non-tumor tissues. Moreover, the up-regulation of miR-29a was significantly correlated with tumor metastasis and shorter overall survival in breast cancer patients. Knockdown of miR-29a in breast cancer cell lines inhibited cell proliferation and migration. Furthermore, data from bioinformatic analysis validated by dual-luciferase reporter gene assay showed that ten eleven translocation 1 (TET1) was a direct target of miR-29a, and over-expression of TET1 inhibited cell proliferation and migration which could be induced by the up-regulation of miR-29a. TET1 silencing promoted cell growth and migration in breast cancer. MiR-29a over-expression had the same effect. MiR-29a targets TET1, down regulates its expression and thus promotes EMT in breast cancer. Altogether, we demonstrate that miR-29a acts as a tumor activator by targeting TETI and induces cell proliferation and EMT in breast cancer. (C) 2016 Elsevier B.V. All rights reserved.
引用
收藏
页码:2177 / 2185
页数:9
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