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MicroRNA-16-5p Inhibits Osteoclastogenesis in Giant Cell Tumor of Bone.

Shang SangZhichang ZhangShu QinChangwei LiYang Dong
Published in: BioMed research international (2017)
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.
Keyphrases
  • bone loss
  • giant cell
  • nuclear factor
  • poor prognosis
  • bone mineral density
  • toll like receptor
  • diabetic rats
  • binding protein
  • high glucose
  • soft tissue
  • immune response
  • gene expression
  • drug induced
  • body composition