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Background  MicroRNAs can act as both tumor suppressor genes and oncogenes and participate in cell proliferation, metastasis, and apoptosis. Low levels of  miR‐577  are found in several cancers, for example, thyroid carcinoma, glioblastoma, and hepatocellular carcinoma. The aim of this study was to investigate the effect of  miR‐577  on breast cancer (BC).    Methods  The relative level of  miR‐577  in 120 BC tissues and cells was detected by real‐time PCR. MDA‐MB‐231 cells with upregulated  miR‐577  and MCF‐7 cells with downregulated  miR‐577  were established. Transwell invasion assays were used to examine the invasiveness of cells. Epithelial‐mesenchymal transition (EMT) markers were evaluated by immunofluorescence and Western blot. Targeted combinations of  miR‐577  and Rab25 were analyzed by luciferase assays. Xenograft models were used to examine the effect of  miR‐577  on BC metastasis.    Results   MiR‐577  expression was significantly suppressed in BC tissues. Tumor size, tumor stage, and lymphatic metastasis were attributed to  miR‐577  expression. Moreover,  miR‐577  overexpression strongly inhibited the invasiveness and EMT of BC cells in vitro.  MiR‐577  directly regulated Rab25 in BC. Rab25 upregulation by  miR‐577  decreased the levels of E‐cadherin and increased the levels of Vimentin. Notably, Rab25 knockdown inhibited BC invasion; however, an increase in Rab25 counteracted the invasive effect of  miR‐577  in BC.    Conclusion  Results indicated that  miR‐577  suppressed EMT by inhibiting Rab25 expression in BC.  MiR‐577  and Rab25 are considered potential targets of BC treatment.

MiR‐577 suppresses epithelial‐mesenchymal transition and metastasis of breast cancer by targeting Rab25