microRNAs (miRs) have been investigated as a novel class of regulators of cellular processes, including proliferation, apoptosis and metabolism. In particular, miR-30b has been demonstrated to be deregulated in certain types of cancer, including lung, colorectal and gastric cancer. Previous studies of miR-30b in renal clear cell carcinoma demonstrated that the expression level of miR-30b was associated with distant metastasis. However, the function of miR-30b in renal cell carcinoma (RCC) remained to be elucidated. In the present study, the expression of miR-30b in 31 paired RCC tissues from four cell lines (786-O, 769-P, ACHN and 293T) was detected by reverse transcription-quantitative polymerase chain reaction. In addition, the effect of miR-30b on cell proliferation in RCC cells was also determined using MTT and Cell Counting Kit-8 assay analyses. Furthermore, the function of miR-30b in cell migration and invasion was determined by wound scratch and Transwell assays. Flow cytometry was also performed to quantify the effect of miR-30b on cell apoptosis. The results of the current study indicated that miR-30b was upregulated in RCC tissues from affected cell lines when compared with adjacent normal tissues and a normal kidney cell line, which is different to the downregulation of miR-30b as observed in other types of cancer. miR-30b is associated with RCC cell proliferation, invasion, migration and apoptosis, which indicated that miR-30b acts as an oncogene in RCC. To the best of our knowledge, the present study is the first to demonstrate the upregulation of miR-30b in RCC tissues and describe miR-30b as an oncogene in RCC in the regulation of cell proliferation, migration, invasion and apoptosis. Further studies will define the target gene of miR-30b in RCC and investigate the potential role of miR-30b as a biomarker for RCC.
CITATION STYLE
Jin, L., Li, Y., He, T., Hu, J., Liu, J., Chen, M., … Lai, Y. (2017). Identification of miR-30b as an oncogene in renal cell carcinoma. Molecular Medicine Reports, 15(4), 1837–1846. https://doi.org/10.3892/mmr.2017.6197
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