Caspase-8 controls the secretion of inflammatory lysyl-tRNA synthetase in exosomes from cancer cells

J Cell Biol. 2017 Jul 3;216(7):2201-2216. doi: 10.1083/jcb.201605118. Epub 2017 Jun 13.

Abstract

Aminoacyl-tRNA synthetases (ARSs), enzymes that normally control protein synthesis, can be secreted and have different activities in the extracellular space, but the mechanism of their secretion is not understood. This study describes the secretion route of the ARS lysyl-tRNA synthetase (KRS) and how this process is regulated by caspase activity, which has been implicated in the unconventional secretion of other proteins. We show that KRS is secreted from colorectal carcinoma cells within the lumen of exosomes that can trigger an inflammatory response. Caspase-8 cleaved the N-terminal of KRS, thus exposing a PDZ-binding motif located in the C terminus of KRS. Syntenin bound to the exposed PDZ-binding motif of KRS and facilitated the exosomic secretion of KRS dissociated from the multi-tRNA synthetase complex. KRS-containing exosomes released by cancer cells induced macrophage migration, and their secretion of TNF-α and cleaved KRS made a significant contribution to these activities, which suggests a novel mechanism by which caspase-8 may promote inflammation.

Publication types

  • Video-Audio Media

MeSH terms

  • Animals
  • Caspase 8 / genetics
  • Caspase 8 / metabolism*
  • Chemotaxis
  • Colorectal Neoplasms / enzymology*
  • Colorectal Neoplasms / genetics
  • Colorectal Neoplasms / metabolism
  • Colorectal Neoplasms / pathology
  • Exosomes / enzymology*
  • Exosomes / genetics
  • Exosomes / metabolism
  • Exosomes / pathology
  • HCT116 Cells
  • Humans
  • Inflammation Mediators / metabolism*
  • Lysine-tRNA Ligase / genetics
  • Lysine-tRNA Ligase / metabolism*
  • Macrophages / metabolism
  • Mice
  • Multienzyme Complexes
  • PDZ Domains
  • Protein Binding
  • RAW 264.7 Cells
  • RNA Interference
  • Signal Transduction
  • Syntenins / metabolism
  • Time Factors
  • Transfection
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Inflammation Mediators
  • Multienzyme Complexes
  • Syntenins
  • Tumor Necrosis Factor-alpha
  • CASP8 protein, human
  • Caspase 8
  • KRS protein, human
  • Lysine-tRNA Ligase