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Biochim Biophys Acta. 2016 Nov;1862(11):2177-2185. doi: 10.1016/j.bbadis.2016.08.014. Epub 2016 Sep 16.

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

Author information

1
Department of Hepatobiliary-Pancreatic Surgery, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang Province 310014, PR China. Electronic address: professorpei@163.com.
2
Department of interventional therapy and vascular surgery, Hunan Provincial People's Hospital, Changsha, Hunan Province 410005, PR China.
3
Department of Hepatobiliary-Pancreatic Surgery, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang Province 310014, PR China. Electronic address: 416095688@qq.com.

Abstract

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 TET1 and induces cell proliferation and EMT in breast cancer.

KEYWORDS:

Breast cancer; Cell proliferation; EMT; MiR-29a; TET1

PMID:
27555295
DOI:
10.1016/j.bbadis.2016.08.014
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