PC-3-Derived Exosomes Inhibit Osteoclast Differentiation by Downregulating miR-214 and Blocking NF- κ B Signaling Pathway

Biomed Res Int. 2019 Apr 1:2019:8650846. doi: 10.1155/2019/8650846. eCollection 2019.

Abstract

Prostate cancer is a serious disease that can invade bone tissues. These bone metastases can greatly decrease a patient's quality of life, pose a financial burden, and even result in death. In recent years, tumor cell-secreted microvesicles have been identified and proposed to be a key factor in cell interaction. However, the impact of cancer-derived exosomes on bone cells remains unclear. Herein, we isolated exosomes from prostate cancer cell line PC-3 and investigated their effects on human osteoclast differentiation by tartrate-resistant acid phosphatase (TRAP) staining. The potential mechanism was evaluated by qRT-PCR, western blotting, and microRNA transfection experiments. The results showed that PC-3-derived exosomes dramatically inhibited osteoclast differentiation. Marker genes of mature osteoclasts, including CTSK, NFATc1, ACP5, and miR-214, were all downregulated in the presence of PC-3 exosomes. Furthermore, transfection experiments showed that miR-214 downregulation severely impaired osteoclast differentiation, whereas overexpression of miR-214 promoted differentiation. Furthermore, we demonstrated that PC-3-derived exosomes block the NF-κB signaling pathway. Our study suggested that PC-3-derived exosomes inhibit osteoclast differentiation by downregulating miR-214 and blocking the NF-κB signaling pathway. Therefore, elevating miR-214 levels in the bone metastatic site may attenuate the invasion of prostate cancer.

MeSH terms

  • Animals
  • Bone Neoplasms / genetics*
  • Bone Neoplasms / pathology
  • Bone Neoplasms / secondary
  • Cathepsin K / genetics
  • Cell Differentiation / genetics
  • Exosomes / metabolism
  • Exosomes / pathology
  • Gene Expression Regulation, Neoplastic / genetics
  • Healthy Volunteers
  • Humans
  • Male
  • Mice
  • MicroRNAs / genetics*
  • NFATC Transcription Factors / genetics
  • Neoplasm Invasiveness / genetics
  • Neoplasm Invasiveness / pathology
  • Neoplasm Metastasis
  • Osteoclasts / pathology
  • Osteogenesis / genetics*
  • PC-3 Cells
  • Prostatic Neoplasms / genetics*
  • Prostatic Neoplasms / pathology
  • Signal Transduction / genetics
  • Tartrate-Resistant Acid Phosphatase / chemistry
  • Tartrate-Resistant Acid Phosphatase / genetics

Substances

  • MIRN214 microRNA, human
  • MicroRNAs
  • NFATC Transcription Factors
  • ACP5 protein, human
  • Tartrate-Resistant Acid Phosphatase
  • CTSK protein, human
  • Cathepsin K