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

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

卷:1862

Article

Pei, Yao-fei¹  Lei, Yao²  Liu, Xi-qiang¹ 

[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

关键词: Breast cancer;    Cell proliferation;    EMT;    MiR-29a;    TET1;   

DOI  :  10.1016/j.bbadis.2016.08.014

来源: Elsevier

【 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.

【 授权许可】

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