Platelets promote tumour metastasis via interaction between TLR4 and tumour cell-released high-mobility group box1 protein

Nat Commun. 2014 Oct 28:5:5256. doi: 10.1038/ncomms6256.

Abstract

Increasing evidence suggests that TLR4 expression by tumour cells promotes tumour progression, but it is unclear whether TLR4 is involved in metastasis. Here we show that TLR4 deficiency significantly diminishes experimental lung metastasis without affecting primary tumour growth. Bone marrow transplantation experiment and application of antiplatelet agents in mice demonstrate that TLR4 on platelets plays an important role in metastasis. TLR4 is critical for platelet-tumour cell interaction in vitro. Furthermore, high-mobility group box1 (HMGB1) neutralization attenuates platelet-tumour cell interaction in vitro and metastasis in vivo in a TLR4-dependent manner, indicating that tumour cell-released HMGB1 is the key factor that interacts with TLR4 on platelets and mediates platelet-tumour cell interaction, which promotes metastasis. These findings demonstrate a mechanism by which platelets promote tumour cell metastasis and suggest TLR4, and its endogenous ligand HMGB1 as targets for antimetastatic therapies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Platelets / metabolism*
  • Carcinoma, Lewis Lung / pathology*
  • Cell Communication* / drug effects
  • Cell Line, Tumor
  • Enzyme-Linked Immunosorbent Assay
  • HMGB1 Protein / metabolism*
  • Hematopoiesis / drug effects
  • Male
  • Melanoma, Experimental / pathology*
  • Mice, Inbred C57BL
  • Neoplasm Metastasis
  • Platelet Adhesiveness / drug effects
  • Platelet Aggregation Inhibitors / pharmacology
  • Protein Binding / drug effects
  • Toll-Like Receptor 4 / deficiency
  • Toll-Like Receptor 4 / metabolism*

Substances

  • HMGB1 Protein
  • Platelet Aggregation Inhibitors
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4