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BioMed Research International - Volume 2017 2017, Article ID 3173547, 6 pages - https:-doi.org-10.1155-2017-3173547

Research Article

Department of Orthopaedic Surgery, Sixth People’s Hospital, Shanghai Jiao Tong University, Shanghai, China

Shanghai Key Laboratory for Bone and Joint Diseases, Shanghai Institute of Orthopaedics and Traumatology, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

Correspondence should be addressed to Changwei Li and Yang Dong

Received 15 November 2016; Revised 18 March 2017; Accepted 20 April 2017; Published 15 May 2017

Academic Editor: Natarajan Muthusamy

Copyright © 2017 Shang Sang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Giant cell tumor GCT of bone is an aggressive skeletal tumor characterized by localized bone resorption. MicroRNA-16-5p miR-16-5p has been reported to be downregulated in lesions of patients with GCT, but little is known about its role in GCT. To explore the underlying function of miR-16-5p in GCT, we first detected its expression in patients with GCT. The results showed that osteoclast formation increased, whereas miR-16-5p expression considerably decreased with the severity of bone destruction. Furthermore, we found that miR-16-5p expression considerably decreased with the progression of receptor activator of nuclear factor-κB ligand- RANKL- induced osteoclastogenesis. Functionally, miR-16-5p mimics significantly reduced RANKL-induced osteoclast formation. However, treatment with an inhibitor of miR-16-5p significantly promoted osteoclastogenesis. These findings reveal that miR-16-5p inhibits osteoclastogenesis and that it may represent a therapeutic target for giant cell tumor of bone.





Autor: Shang Sang, Zhichang Zhang, Shu Qin, Changwei Li, and Yang Dong

Fuente: https://www.hindawi.com/



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