Effects of miR-181a on the biological function of multiple myeloma

The present study aimed to investigate the role of miR-181a in multiple myeloma (MM) cell lines. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of microRNA (miR)-181a. The MM cell line RPMI 8226 stably transduced with miR-181a mimics or inhibitor was established via lentiviral vectors. A Cell Counting Kit-8 proliferation assay, flow cytometry and a Transwell assay were conducted to assess cell proliferation, cell cycle, apoptosis and invasion. The role of miR-181a in MM tumor formation in vivo was assessed using a SCID Berge xenograft tumor model. The potential target genes of miR-181a were predicted using bioinformatic tools, and the expression of a potential target gene of miR-181a, neuro-oncological ventral antigen-1 (NOVA1) was detected by RT-qPCR. miR-181a was determined to be significantly upregulated in MM cells (P<0.001). Following silencing of miR-181a via lentiviral-mediated transduction, RPMI 8226 cells exhibited a significant decrease in the number of S phase cells, and proliferative and invasive abilities. In addition, apoptosis was significantly promoted. A total of nine cross-target genes were pre-selected via bioinformatics software, including NOVA1. The results revealed that miR-181a inhibitor suppressed the expression of NOVA1 (t=26.951, P=0.001). In the xenograft tumor model of SCID Berge mice, miR-181a knock down significantly inhibited tumor growth. Conversely, these effects were reversed in response to miR-181 mimics. In summary, miR-181a was determined to be upregulated in MM cells, and may affect the biological function of cancer cells. The underlying mechanism may comprise the regulation of downstream target genes; however, further investigation is required.