5-Fluoruracil blocked giant cell tumor progression by suppressing osteoclastogenesis through NF-kappaB signals and blocking angiogenesis

Bone. 2015 Sep:78:46-54. doi: 10.1016/j.bone.2015.04.047. Epub 2015 May 5.

Abstract

Giant cell tumor of bone (GCTB) is a bone destroying tumor comprised of spindle-like stromal cells and monocytes of myeloid lineage that are differentiated into osteoclast-like multinucleated giant cells. Nuclear factor-Kappa B (NF-κB) has been identified to be essential for GCT progression. Herein, we found that 5-Fluorouracil (5-FU), a widely used chemotherapeutics, is a promising anticancer agent for GCT both targeting spindle-like stromal cells and osteoclast giant cells through NF-κB pathway. In this study, in vitro 5-FU not only directly blocked both stromal cell- and RANKL-induced osteoclastogenesis through NF-κB pathway, but also indirectly inhibited osteoclast formation and angiogenesis by suppressing the expression of osteoclast-activating factors including IL-1β, MCP-1 and tumor angiogenesis factor VEGF in stromal cells. In vivo, we found that 5-FU blocked GCT progression through NF-κB pathway by utilizing our chick embryo chorioallantoic membrane (CAM) model. Taken together, our results suggest that 5-FU can inhibit GCT development by suppressing osteoclast formation through NF-κB pathway and blocking angiogenesis, and may serve as a novel agent in the treatment of GCT.

Keywords: 5-FU; Angiogenesis; Giant cell tumor; NF-κB pathway; Osteoclastgenesis.

MeSH terms

  • Animals
  • Antimetabolites, Antineoplastic / therapeutic use
  • Bone Resorption
  • Cell Differentiation
  • Cell Lineage
  • Chemokine CCL2 / metabolism
  • Chick Embryo
  • Chorioallantoic Membrane / drug effects
  • Endothelial Cells / cytology
  • Fluorouracil / therapeutic use*
  • Giant Cell Tumor of Bone / drug therapy*
  • Giant Cell Tumor of Bone / pathology*
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Interleukin-1beta / metabolism
  • Leukocytes, Mononuclear / cytology
  • Mice
  • Mice, Inbred C57BL
  • Monocytes / cytology
  • NF-kappa B / metabolism*
  • Neovascularization, Pathologic / drug therapy*
  • Osteoclasts / cytology*
  • Osteoclasts / drug effects
  • RANK Ligand / metabolism
  • Signal Transduction / drug effects
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Antimetabolites, Antineoplastic
  • CCL2 protein, human
  • Chemokine CCL2
  • Interleukin-1beta
  • NF-kappa B
  • RANK Ligand
  • Vascular Endothelial Growth Factor A
  • Fluorouracil