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MiR-9 promotes multiple myeloma progression by regulating TRIM56/NF-κB pathway.

MiR-9 has been reported to play a pivotal role in multiple human cancers through acting as an oncogene or tumor suppressor. In this study, we explored the possible role and molecular mechanism of miR-9 in multiple myeloma (MM). MiR-9 expression was examined by qRT-PCR assay. Transfection with miR-9-mimics, miR-9-inhibitor, pcDNA-TRIM56 or si-TRIM56 into cells was used to change the expression levels of miR-9 and TRIM56. Western blot analysis was used to detect the expression of TRIM56, p65, p-p65, IκBα and p-IκBα. The potential target of miR-9 was confirmed by luciferase reporter assay. MTT assay, colony formation assay, flow cytometry were used to assess the abilities of cell proliferation and apoptosis. MiR-9 was upregulated in MM patients and cell lines, and miR-9 overexpression promoted proliferation and repressed apoptosis in MM cell lines. TRIM56 was confirmed as a target of miR-9. Moreover, TRIM56 reversed miR-9-mediated pro-proliferation and anti-apoptosis effect on MM cell lines. Furthermore, NF-κB pathway was involved in miR-9/TRIM56-mediated regulation on MM cell lines. MiR-9 promoted the development and progression of MM by regulating TRIM56/NF-κB pathway, providing a potential miRNA-based target of MM therapy.

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