miR-362-3p targets nemo-like kinase and functions as a tumor suppressor in renal cancer cells
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Updated: Mar 29, 2026

Modeling Spontaneous Metastatic Renal Cell Carcinoma mRCC in Mice Following Nephrectomy
Published on: April 29, 2014
Xiaowen Zou1, Jianhua Zhong1, Jiaqiang Li2
1National‑Regional Key Technology Engineering Laboratory for Clinical Application of Cancer Genomics, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong 518000, P.R. China.
Abstract:
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.
Insights
MicroRNA-362-3p is downregulated in renal cell carcinoma (RCC). Upregulating this microRNA suppresses tumor growth, migration, and invasion, indicating its potential as a therapeutic target for RCC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) show altered expression in human cancers.
- Identifying novel tumor suppressors is crucial for cancer therapy.
Purpose of the Study:
- To identify a novel tumor suppressor microRNA (miR) in renal cell carcinoma (RCC).
- To investigate the physiological function and mechanism of miR-362-3p in RCC.
Main Methods:
- Quantitative reverse transcription-polymerase chain reaction to measure miR-362-3p expression in 47 RCC and normal tissue pairs.
- Transfection of miR-362-3p mimics into renal cancer cells.
- Luciferase reporter assays and western blot analysis to identify target genes.
Main Results:
- miR-362-3p expression was significantly downregulated in RCC tissues compared to normal tissues.
- Overexpression of miR-362-3p inhibited renal cancer cell proliferation, migration, and invasion.
- miR-362-3p upregulation induced apoptosis and G1 phase arrest in cancer cells.
- Nemo-like kinase was identified as a target gene suppressed by miR-362-3p.
Conclusions:
- miR-362-3p acts as a tumor suppressor in renal cell carcinoma.
- miR-362-3p may represent a potential molecular target for RCC treatment.
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