ITGB3-mediated uptake of small extracellular vesicles facilitates intercellular communication in breast cancer cells

Nat Commun. 2020 Aug 26;11(1):4261. doi: 10.1038/s41467-020-18081-9.

Abstract

Metastasis, the spread of malignant cells from a primary tumour to distant sites, causes 90% of cancer-related deaths. The integrin ITGB3 has been previously described to play an essential role in breast cancer metastasis, but the precise mechanisms remain undefined. We have now uncovered essential and thus far unknown roles of ITGB3 in vesicle uptake. The functional requirement for ITGB3 derives from its interactions with heparan sulfate proteoglycans (HSPGs) and the process of integrin endocytosis, allowing the capture of extracellular vesicles and their endocytosis-mediated internalization. Key for the function of ITGB3 is the interaction and activation of focal adhesion kinase (FAK), which is required for endocytosis of these vesicles. Thus, ITGB3 has a central role in intracellular communication via extracellular vesicles, proposed to be critical for cancer metastasis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Cell Communication / physiology*
  • Cell Line, Tumor
  • Culture Media, Conditioned
  • Endocytosis
  • Extracellular Vesicles / metabolism*
  • Female
  • Focal Adhesion Kinase 1 / metabolism
  • Heparan Sulfate Proteoglycans / metabolism
  • Heterografts
  • Humans
  • Integrin beta3 / metabolism*
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / pathology
  • Lung Neoplasms / secondary
  • MCF-7 Cells
  • Mice
  • Mice, Nude
  • Models, Biological
  • Neoplasm Metastasis / pathology
  • Neoplasm Transplantation

Substances

  • Culture Media, Conditioned
  • Heparan Sulfate Proteoglycans
  • ITGB3 protein, human
  • Integrin beta3
  • Focal Adhesion Kinase 1
  • PTK2 protein, human