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

- MiR-29a is up-regulated in ER− breast cancer and correlated with poor survival.
- MiR-29a over-expression promotes breast cancer proliferation in vitro and in vivo.
- MiR-29a regulates cell cycle and promotes migration in breast cancer.
- TET1 is a direct target of miR-29a.
- MiR-29a targeted TET1 contributes to cell proliferation and EMT.

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.