Hematology · 2018 · 54 citations · 20 references
MedicineBioinformaticsOncologyApoptosisMolecular OncologyTumor ProgressionCancer ProgressionCancer TranscriptomicsMalignant NeoplasmsMolecular Tumor ProfilingMultiple MyelomaCell Cycle Arrest MechanismsCell Proliferation IndicesDual-luciferase AssaysLuciferase Reporter AssaysLuciferase ReportersMicrorna In CancerMicrorna Regulation In CancerMyeloma Pathogenesis
BACKGROUND: Increasing evidence has suggested that miR-29b plays an antitumor effect in multiple malignancies via the regulation of cell proliferation, apoptosis, invasion and migration. In the present study, we aimed to explore the underlying function and mechanism of miR-29b in multiple myeloma (MM). METHODS: The expression of miR-29b in MM cell lines and tissues was detected by quantitative real-time PCR (qRT-PCR). CCK-8 and flow cytometry analyses were performed to assess cell proliferation, cycles and apoptosis. Bioinformatics, Dual-Luciferase reporter and qRT-PCR assays were employed to explore the possible correlation between miR-29b and FOXP1. Xenograft model was established to confirm the role of miR-29b on tumor growth in vivo. RESULTS: miR-29b expression was markedly decreased in MM cell lines and tissues and downregulated miR-29b was closely related to International Staging System (ISS) stages. Exogenous overexpression of miR-29b inhibited the proliferation but induced MM cell cycle arrest and apoptosis. FOXP1 was identified as a direct target gene for miR-29b, and restoration of FOXP1 weakened miR-29b-induced anti-proliferation and pro-apoptosis in MM cell lines. Finally, the inhibitory effects of miR-29b on the growth of MM tumors were validated in mice. CONCLUSIONS: miR-29b recedes the progression of MM via downregulating FOXP1, which may provide a potential biological target for MM treatment.
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