Abstract: Objective To analyze miR-125 b expression in breast cancer, specifically its effects on cell migration and invasion and to explore the mechanism of this process. Methods (1) Real-time PCR was used to detect the expression level of miR-125b and ETV6 in tumors and adjacent non-tumor breast cancer samples; (2) Real-time PCR and dual-luciferase reporter assay were used for target identification. (3) The migration and invasion ability in vitro and the change of epithelialmesenchymal transition were detected by wound healing assay, transwell migration and invasion assay and western blot respectively after instantaneously transfected with miR-125b mimics; (4) The knockdown assay was used for further confirmation. Results (1) As compared with adjacency non-tumor tissues, the expression level of miR-125b in breast cancer tissues was down-regulated (P < 0. 001) and ETV6 was up-regulated significantly (P < 0. 05); (2) ETV6 is the target gene of miR-125b; (3) Compared to control group, the migration and invasion of miR-125b overexpressing Hs578T cells was obviously inhibited in vitro (P < 0. 001), so was epithelial-mesenchymal transition; (4) The effect of ETV6 down-regulation was consistent with miR-125 b overexpression in Hs578T cells. Conclusion miR-125b was downregulated in breast cancer. It remarkably inhibited migration, invasion and EMT of Hs578 T cells by suppressing the expression of ETV6 through targeting its 3'UTR. In general, miR-125b possibly played a role as antioncogene in breast cancer.