Chinese Journal of Tissue Engineering Research ›› 2020, Vol. 24 ›› Issue (23): 3723-3729.doi: 10.3969/j.issn.2095-4344.2694

Previous Articles     Next Articles

The role of OPG/RANKL/RANK signaling pathway in the pathogenesis of giant-cell tumor of bone

Liang Chenliang1, Zhao Zhenqun2, Liu Wanlin2   

  1. 1Graduate School of Inner Mongolia Medical University, Hohhot 010000, Inner Mongolia Autonomous Region, China; 2Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010030, Inner Mongolia Autonomous Region, China
  • Received:2019-07-18 Revised:2019-12-06 Accepted:2020-01-08 Online:2020-08-18 Published:2020-07-30
  • Contact: Zhao Zhenqun, Chief physician, Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010030, Inner Mongolia Autonomous Region, China Liu Wanlin, Professor, Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010030, Inner Mongolia Autonomous Region, China
  • About author:Liang Chenliang, Master candidate, Graduate School of Inner Mongolia Medical University, Hohhot 010000, Inner Mongolia Autonomous Region, China
  • Supported by:

    the National Natural Science Foundation of China, No. 8166110173

Abstract:

BACKGROUND: Studies have shown that osteoprotegerin/receptor activator of nuclear factor κB ligand/nuclear factor κB receptor activator (OPG/RANKL/RANK) signaling pathway has a certain correlation with the pathogenesis of giant-cell tumor. Controlling the OPG/RANKL/RANK signaling pathway to affect the interaction between osteoblasts and osteoclasts can play a certain therapeutic role in giant-cell tumor of bone.

OBJECTIVE: Ton introduce the relationship between the OPG/RANKL/RANK signaling pathway and the pathogenesis of giant-cell tumor of bone, and to summarize and discuss the new advances of the OPG/RANKL/RANK signaling pathway in the pathogenesis of giant-cell tumor of bone.

METHODS: PubMed, Web of Science, and WanFang databases were searched for relevant articles published from 2001 to 2019 using the keywords of “OPG/RANKL/RANK, giant cell tumor of bone, pathogenesis, signal pathway, bone metabolism" in English and Chinese, respectively. A total of 53 articles were finally included for analysis and discussion after removal of old and repeated literatures.

RESULTS AND CONCLUSION: OPG inhibits the proliferation and differentiation of osteoclasts, reduces the activity of mature osteoclasts, and blocks the binding of RANKL to RANK. RANKL binds to RANK on the surface of osteoclast progenitor cells to promote the differentiation and proliferation of osteoclast progenitor cells, thus accelerating osteoclast progression. After binding to RANKL receptor, RANKL activates signal factors such as nuclear factor-κB to promote the proliferation, differentiation and activation of osteoclasts, and to regulate the transcription and expression of related genes. Therefore, the OPG/RANKL/RANK is associated with the pathogenesis of giant-cell tumor.

Key words: giant-cell tumor of bone, pathogenesis, signaling pathway, OPG/RANKL/RANK, National Natural Science Foundation of China

CLC Number: