MicroRNA (miR)-125b has been identified as deregulated in a number of types of cancer. Previous studies have detected the expression of miR-125b in clear cell renal cell carcinoma (ccRCC) tissues by in situ hybridization and revealed that miR-125b was upregulated in ccRCC tissues, and was associated with recurrence and survival of patients with ccRCC. However, the function of miR-125b in RCC remains unclear. Thus, the expression of miR-125b was detected with quantitative polymerase chain reaction (qPCR) in 24 paired RCC and adjacent normal tissues. The result of qPCR showed that miR-125b was upregulated in RCC tissues. Furthermore, the function of miR-125b in RCC (786-O and ACHN) cells was detected by transfecting miR-125 mimic or inhibitor to upregulate or downregulate miR-125b expression. Cell proliferation assays (MTT and Cell Counting Kit-8), cell mobility assays (cell scratch and Transwell assay) and a cell apoptotic assay (flow cytometry assay) were performed to assess the function of miR-125b on RCC cells. Results from the assays demonstrated that overexpression of miR-125b could promote cell migration and invasion, and reduce the cell apoptotic rate. It was also revealed that downregulation of miR-125b could reduce cell migration and invasion, and induce cell apoptosis. However, the results of the cell proliferation assay revealed that miR-125b had no significant effect on cell proliferation. Not only could miR-125b predict recurrence and survival of ccRCC; the present study revealed that miR-125b could regulate RCC cell migration, invasion and apoptosis. Additional studies are required to determine the mechanism of miR-125b in RCC cells and define the target genes of miR-125b in RCC.
Keywords: miR-125b; microRNA; oncogene; renal cell carcinoma.