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.