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 by 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). The miR-9 expression was examined by quantitative real-time polymerase chain reaction 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, I kappa B alpha, and p-I kappa B alpha. The potential target of miR-9 was confirmed by luciferase reporter assay. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) assay, colony formation assay, and 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, nuclear factor-kappa B (NF-kappa B) 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-kappa B pathway, thereby providing a potential microRNA-based target for MM therapy.