Background: Growing evidence suggests that miR-150  plays an inhibitory role in various types of cancer. However, the function and underlying mechanisms of miR-150  in triple-negative breast cancer (TNBC) remain unknown. 
Patients and methods: miR-150  expression was detected by qRT-PCR and ISH in TNBC tumor and adjacent normal breast tissues. miR-150  function was analyzed by wound healing and transwell assay in vitro and mouse lung metastasis model in vivo. mRNA microarray, qRT-PCR, western blotting and luciferase assay were used to identify the target gene of miR-150 . HMGA2 over-expression plasmid was co-transfected with miR-150  to study the role of miR-150  through regulating HMGA2.
Results: We found that miR-150  was down-regulated in TNBC tumor tissues compared to corresponding adjacent, normal breast tissues, and was correlated with decreased lymph-node metastasis. Ectopic expression of miR-150  suppressed TNBC cell migration in vitro and metastasis in vivo. Mechanistic study revealed that miR-150  down-regulates HMGA2 by directly targeting its mRNA. Moreover, the suppression of cell migration caused by miR-150  is relieved by over-expression of HMGA2, suggesting that miR-150  inhibits migration of TNBC cells by down-regulating HMGA2. 
Conclusion: This work indicates that the miR-150 /HMGA2 axis may serve as a treatment marker in TNBC.
Keywords: miR-150 , HMGA2, triple-negative breast cancer, metastasis