MicroRNA-150 suppresses triple-negative breast cancer metastasis through targeting HMGA2

Abstract

Wentao Tang,1,* Pingping Xu,1,* Hong Wang,1,* Zhengchuan Niu,1 Dexiang Zhu,1 Qi Lin,1 Liming Tang,2 Li Ren1 1Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China; 2Department of General Surgery, Affiliated Changzhou No 2 People’s Hospital, Nanjing Medical University, Changzhou, China *These authors contributed equally to this work 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

Keywords

• miR-150
• HMGA2
• triple negative breast cancer
• metastasis