M1 macrophage-derived exosomes containing miR-150 inhibit glioma progression by targeting MMP16

Cell Signal. 2023 Aug:108:110731. doi: 10.1016/j.cellsig.2023.110731. Epub 2023 May 26.

Abstract

A large amount of clinical and experimental evidence indicates that M1 macrophages can inhibit tumor progression and expansion; however, the molecular mechanism by which macrophage-derived exosomes inhibit the proliferation of glioblastoma cells has not yet been elucidated. Here, we used M1 macrophage exosomes encapsulating microRNAs to inhibit the proliferation of glioma cells. Exosomes derived from M1 macrophages exhibited high expression levels of miR-150, and the inhibition of glioma cell proliferation mediated by exosomes derived from M1 macrophages was dependent on this microRNA. Mechanistically, miR-150 is transferred to glioblastoma cells through M1 macrophages and binds to MMP16, downregulating its expression and inhibiting glioma progression. Overall, these findings indicate that M1 macrophage-derived exosomes carrying miR-150 inhibit the proliferation of glioblastoma cells through targeted binding to MMP16. This dynamic mutual influence between glioblastoma cells and M1 macrophages provides new opportunities for the treatment of glioma.

Keywords: Glioblastoma; Glioma; M1 macrophage; Tumor- associated macrophage; microRNA-150.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Exosomes* / metabolism
  • Glioblastoma* / metabolism
  • Glioma* / metabolism
  • Humans
  • Macrophages / metabolism
  • Matrix Metalloproteinase 16 / metabolism
  • MicroRNAs* / metabolism

Substances

  • Matrix Metalloproteinase 16
  • MicroRNAs
  • MMP16 protein, human
  • MIRN150 microRNA, human