ABSTRACT
The function of miR-592 has been investigated in many types of cancer, however its roles in breast cancer remain unclear. We therefore investigated the biological function and underlying mechanism of miR-592 in breast cancer. In the present study, a marked downregulation of miR-592 was observed in breast cancer tissues and cell lines compared to the matched adjacent non-tumor tissues and normal breast cell line. Statistical analysis revealed that decreased miR-592 was negatively associated with advanced clinical stage, distant metastasis and lymph node metastases. Function analysis demonstrated that overexpression of miR-592 significantly inhibited cell proliferation, clone formation, migration and invasion in breast cancer cells in vitro, as well as suppressed tumor growth in vivo. Furthermore, transforming growth factor ß-2 (TGFß-2), a known oncogene, was identified as a direct target of miR-592, and its mRNA expression level was inversely correlated with the expression level of miR-592 in human breast cancer specimens. Restoration of TGFß-2 expression rescued the inhibitory effect in breast cancer cells caused by miR-592. Collectively, these data suggest that miR-592 may exert it suppressive role in breast cancer, at least in part, by targeting TGFß-2, and that miR-592 may be a novel target for breast cancer treatment.
