suppresses triple-negative breast cancer metastasis through targeting HMGA2.

BACKGROUND

Growing evidence suggests that plays an inhibitory role in various types of cancer. However, the function and underlying mechanisms of in triple-negative breast cancer (TNBC) remain unknown.

PATIENTS AND METHODS

expression was detected by qRT-PCR and ISH in TNBC tumor and adjacent normal breast tissues. 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 . HMGA2 over-expression plasmid was co-transfected with to study the role of through regulating HMGA2.

RESULTS

We found that 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 suppressed TNBC cell migration in vitro and metastasis in vivo. Mechanistic study revealed that down-regulates HMGA2 by directly targeting its mRNA. Moreover, the suppression of cell migration caused by is relieved by over-expression of HMGA2, suggesting that inhibits migration of TNBC cells by down-regulating HMGA2.

CONCLUSION

This work indicates that the /HMGA2 axis may serve as a treatment marker in TNBC.