Background Accumulating evidence indicates that miRNAs are involved in multiple cellular functions and participate in various cancer development and progression, including breast cancer. Methods We aimed to investigate the role of miR-381-3p in breast cancer. The expression level of miR-381-3p and EMT transcription factors was examined by quantitative real-time PCR (qRT-PCR). The effects of miR-381-3p on breast cancer proliferation and invasion were determined by Cell Counting Kit-8 (CCK-8), colony formation, and transwell assays. The regulation of miR-381-3p on its targets was determined by dual-luciferase analysis, qRT-PCR, and western blot. Results We found that the expression of miR-381-3p was significantly decreased in breast cancer tissues and cell lines. Overexpression of miR-381-3p inhibited breast cancer proliferation and invasion, whereas knockdown of miR-381-3p promoted cell proliferation and invasion in MDA-MB-231 and SKBR3 cells. Mechanistically, overexpression of miR-381-3p inhibited breast cancer epithelial–mesenchymal transition (EMT). Both Sox4 and Twist1 were confirmed as targets of miR-381-3p. Moreover, transforming growth factor-β (TGF-β) could reverse the effects of miR-381-3p on breast cancer progression. Conclusions Our observation suggests that miR-381-3p inhibits breast cancer progression and EMT by regulating the TGF-β signaling via targeting Sox4 and Twist1.

MicroRNAs are important for the regulation of multiple cellular functions and are involved in the initiation and progression of various types of cancer, including breast cancer. Although microRNA (miR)-454-3p is reported to function as an oncogene in several types of human cancer, the role of miR-454-5p in breast cancer remains unknown. The present study demonstrated that miR-454-5p was upregulated in breast cancer and was associated with a poor prognosis in patients with breast cancer. Overexpression of miR-454-5p promoted breast cancer cell viability, migration and invasion in vitro, whereas silencing of miR-454-5p inhibited breast cancer proliferation, migration and invasion in vitro and suppressed tumor growth in vivo. Mechanistically, forkhead box J2 (FoxJ2) was shown to be a target of miR-454-5p and transactivated E-cadherin expression. Moreover, silencing of miR-454-5p reversed the epithelial-mesenchymal transition phenotype through upregulation of the FoxJ2/E-cadherin axis. Collectively, the present findings suggested that miR-454-5p may serve as a novel therapeutic target and prognostic predictor for patients with breast cancer.

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