miR-362-3p targets nemo-like kinase and functions as a tumor suppressor in renal cancer cells

作者：Xiaowen Zou, Jianhua Zhong, Jiaqiang Li, ZHENGMING SU, Yan Chen, WanXin Deng, Yu‐Chi Li, Siheng Lu, You-Cheng Lin, Liya Luo, Zesong Li, Zhiming Cai, Aifa Tang · 发表于：Molecular Medicine Reports · 年份：2015 · DOI：10.3892/mmr.2015.4632 · 被引用次数：37 · 研究领域：MicroRNA in disease regulation、Circular RNAs in diseases、Cancer-related molecular mechanisms research

MicroRNAs (miRNAs) have been demonstrated to exhibit abnormal expression patterns in various types of human cancer. The aim of the present study was to identify a novel tumor suppressor microRNA (miR) and investigate its physiological function and mechanism in renal cell carcinoma (RCC). The expression levels of miRNA (miR)‑362‑3p expres were measured in 47 pairs of RCC and adjacent normal tissue samples, using reverse transcription-quantitative polymerase chain reaction analysis. In addition, miR‑362‑3p was transfected into renal cancer cells to investigate its role in the regulation of cell proliferation, migration, invasion, apoptosis and cell cycle. Identification of the target gene of miR‑362‑3p was performed using luciferase reporter assays and western blot analyses. The results demonstrated that the expression levels of miR‑362‑3p were downregulated in the RCC tissue samples, compared with the adjacent normal tissue samples. The upregulation of miR‑362‑3p using a synthesized mimic suppressed the proliferation, migration and invasion of the renal cancer cells, and induced cell apoptosis and G1 phase arrest. Further experiments demonstrated that the overexpression of miR‑362‑3p resulted in decrease expression levels of nemo-like kinase. These results suggested that miR-362-3p functions as a tumor suppressor in RCC, and may serve as a potential molecular target in the treatment of RCC.