miR‑505 suppresses prostate cancer progression by targeting NRCAM Corrigendum in /10.3892/or.2020.7696

Ling,Xiao‑Hui; Fu,Hao; Chen,Zhi‑Yun; Lu,Jian‑Ming; Zhuo,Yang‑Jia; Chen,Jia‑Hong; Zhong,Wei‑De; Jia,Zhenyu

doi:10.3892/or.2019.7231

miR‑505 suppresses prostate cancer progression by targeting NRCAM

Corrigendum in: /10.3892/or.2020.7696

Authors:
- Xiao‑Hui Ling
- Hao Fu
- Zhi‑Yun Chen
- Jian‑Ming Lu
- Yang‑Jia Zhuo
- Jia‑Hong Chen
- Wei‑De Zhong
- Zhenyu Jia
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Affiliations: Guangdong Provincial Institute of Nephrology, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China, Department of Urology, Nanhua Affiliated Hospital, University of South China, Hengyang, Hunan 421001, P.R. China, Reproductive Medicine Centre, Huizhou Central People's Hospital, Guangdong Medical University, Huizhou, Guangdong 516001, P.R. China , Department of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China , Department of Botany and Plant Sciences, University of California, Riverside, CA 92521, USA
Published online on: July 11, 2019 https://doi.org/10.3892/or.2019.7231
Pages: 991-1004
Copyright: © Ling et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Previous researchers have demonstrated that microRNA‑505 (miR‑505) is negatively correlated with progression in various malignancies. However, the detailed function and molecular mechanisms of miR‑505 have yet to be completely elucidated in prostate cancer (PCa). The present study initially identified the potential role of miR‑505 in PCa using in vitro experiments, and demonstrated that restoration of miR‑505 inhibited proliferation, invasion and migration, yet induced cell cycle arrest and promoted apoptosis in PCa cells. The present study also demonstrated that the expression of neuron‑glial‑related cell adhesion molecule (NRCAM) was markedly upregulated in PCa cells when compared with benign prostate epithelium. A luciferase reporter assay demonstrated that miR‑505 directly targeted NRCAM in PCa cells. In addition, NRCAM stimulation antagonized the inhibitory effects of miR‑505 on the proliferation, migration, and invasion of PCa cells. Furthermore, lower levels of miR‑505 and higher levels of NRCAM may serve as a predictor of worse biochemical recurrence‑free survival or disease‑free survival in patients with PCa. In conclusion, the present study revealed the inhibitory effects of miR‑505 on PCa tumorigenesis, which potentially occur by targeting NRCAM. The combined analysis of NRCAM and miR‑505 may predict disease progression in patients with PCa following radical prostatectomy.

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