Open AccessmiR-362-3p targets nemo-like kinase and functions as a tumor suppressor in renal cancer cells
Author(s) -
Xiaowen Zou,
Jian Zhong,
Jiaqiang Li,
Zhengming Su,
Yan Chen,
WanXin Deng,
Yuchi Li,
Siheng Lu,
You-Cheng Lin,
Liya Luo,
Zesong Li,
Zhiming Cai,
Aifa Tang
Publication year - 2015
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2015.4632
Subject(s) - oncogene , cell cycle , microrna , cancer research , biology , cancer , apoptosis , cell growth , tumor suppressor gene , transfection , renal cell carcinoma , cell , molecular medicine , a431 cells , cancer cell , suppressor , kinase , microbiology and biotechnology , cell culture , carcinogenesis , pathology , medicine , gene , genetics
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.