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As influencing factors of genesis and progression in several types of human tumor, microRNAs (miRs) serves roles in the regulation of tumor cell viability, migration, and apoptosis. The present research aimed to investigate the association between the function of miR‑100‑5p and renal cell carcinoma (RCC). miR‑100‑5p expression was determined in RCC tissue and paired normal tissue samples using reverse transcription‑quantitative polymerase chain reaction. To assess the effects of miR‑100‑5p on cell viability, migration and apoptosis, multiple methods were used, including scratch wound assays, MTT assays, and flow cytometry. It was demonstrated that miR‑100‑5p was significantly upregulated in RCC tissue compared with in normal adjacent tissue samples. Furthermore, the viability and migration of 786‑O and, ACHN cells tranfected with miR‑100‑5p was significantly increased compared with the negative control group. In addition, miR‑100‑5p‑transfected 786‑O and ACHN cells demonstrated significantly reduced cellular apoptotic rates compared with the negative control group. To the best of our knowledge, the present study is the first to report an association between miR‑100‑5p and RCC. The results of the current study suggest that tumor oncogene miR‑100‑5p could be used as a diagnostic biomarker for RCC. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]