MiR-548b-3p inhibits proliferation and migration of breast cancer cells by targeting MDM2.

OBJECTIVE: The aim of this study was to explore the expression and biological functions of micro ribonucleic acid (miR)-548b-3p in breast cancer (BC), and to investigate its potential molecular mechanism. PATIENTS AND METHODS: The expression level of miR-548b-3p in BC tissues and cells was detected by quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). Subsequently, the impacts of miR-548b-3p on the proliferation, apoptosis, and cycle, as well as migration and invasion of BC cells, were explored using colony formation assay and 5-ethynyl-2'-deoxyuridine (EdU) staining, flow cytometry, and transwell assay, respectively. The possible downstream target genes of miR-548b-3p were predicted via bioinformatics and verified through qRT-PCR and Western blotting. Furthermore, Dual-Luciferase reporter gene assay was employed to confirm whether miR-548b-3p could directly bind to murine double minute 2 (MDM2). RESULTS: QRT-PCR results showed that miR-548b-3p expression was significantly downregulated in 37 out of 43 BC tissues. Subsequent in-vitro experiments indicated that the overexpression of miR-548b-3p significantly inhibited the proliferation and metastasis, whereas promoted the apoptosis of BC cells. Bioinformatics predicted that MDM2 was the downstream target gene of miR-548b-3p. After overexpression of miR-548b-3p, qRT-PCR, and Western blotting results revealed that the expression of MDM2 was remarkably downregulated. Dual-Luciferase reporter gene assay further confirmed that miR-548b-3p could directly bind to MDM2. CONCLUSIONS: MiR-548b-3p expression was significantly downregulated in BC. In addition, lowly expressed miR-548b-3p repressed the proliferation and metastasis of BC cells through targeted regulation of MDM2.