Oncogenic miR-23a-5p is associated with cellular function in RCC.

Abstract

In recent years, accumulating evidence has demonstrated that microRNAs (miRs, miRNAs) may serve an important role in the occurrence and development of tumors. miR‑23a‑5p has been confirmed as an oncogene in numerous diseases through gene chip analysis. However, as the most common type of renal tumor, the expression and function of miR‑23a‑5p in renal cell carcinoma (RCC) remains unclear. In the present study, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis, and Cell Counting Kit‑8 (CCK‑8), wound scratch, Transwell, MTT and flow cytometry assays were performed to investigate the role of miR‑23a‑5p in RCC. The expression of miR‑23a‑5p in RCC tissue samples was significantly higher compared with that in normal tissue samples (P<0.01). Furthermore, the expression of miR‑23a‑5p in RCC cell lines (786O, ACHN and Caki‑1) was significantly higher compared with that in the human embryo kidney 293T cell line, as determined using RT‑qPCR (P<0.001). In addition, the results revealed that the upregulation of miR‑23a‑5p promoted the proliferation, migration and invasion of RCC cells, and inhibited RCC cell apoptosis. The downregulation of miR‑23a‑5p resulted in the reversal of the results described above. Additionally, it was observed that the downregulation of miR‑23a‑5p significantly promoted ACHN and 786O cell viability (P<0.001). The results of the present study suggest that miR-23a-5p is an oncogene in the occurrence and development of RCC and may be a novel therapeutic target for RCC.