Objective: The aim of this study was to explore the expression of microRNA-106a in breast cancer (BC) and to further investigate its role in BC development and the potential regulatory mechanism.
Patients and methods: 72 pairs of BC tissues and para-cancerous tissues were collected, and microRNA-106a expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between microRNA-106a expression and BC pathological parameters was analyzed. Meanwhile, the expression of microRNA-106a in BC cells was verified by qRT-PCR as well. In addition, microRNA-106a knockdown model was constructed by transfecting small interfering RNA in BC cell lines including MCF-7 and SKBR3. Subsequently, the effects of microRNA-106a on biological functions of BC cells were analyzed by cell counting kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EDU), and transwell invasion and migration assays, respectively. Finally, the underlying mechanism was explored by cellular rescue experiment.
Results: QRT-PCR results illustrated that microRNA-106a expression in BC tissues was markedly higher than that of normal tissues. Patients with high expression of microRNA-106a exhibited significantly higher tumor stage as well as higher incidence of lymph node metastasis and distant metastasis when compared with those with low expression. Cell proliferation, invasion, and migration abilities in microRNA-106a inhibitor group were markedly decreased when compared with control group. Subsequent experiments demonstrated that DAX-1 expression was reduced in BC cell lines and tissues. Moreover, DAX-1 expression was negatively correlated with microRNA-106a expression. In addition, a recovery experiment found that microRNA-106a and DAX-1 had mutual regulation, which could affect the malignant progression of BC.
Conclusions: We found that the expression of microRNA-106a was significantly increased in BC. Meanwhile, microRNA-106a expression was closely related to BC stage, distant metastasis, lymph node metastasis, and poor prognosis. Therefore, microRNA-106a promoted the invasion, migration, and proliferation of BC by targeting DAX-1.