Exosomal miR-6733-5p mediates cross-talk between glioblastoma stem cells and macrophages and promotes glioblastoma multiform progression synergistically

CNS Neurosci Ther. 2023 Dec;29(12):3756-3773. doi: 10.1111/cns.14296. Epub 2023 Jun 12.

Abstract

Aim: Exosomal miRNAs derived from glioblastoma stem cells (GSCs) are important mediators of immunosuppressive microenvironment formation in glioblastoma multiform (GBM), especially in M2-like polarization of tumor-associated macrophages (TAMs). However, the exact mechanisms by which GSCs-derived exosomes (GSCs-exo) facilitate the remodeling of the immunosuppressive microenvironment of GBM have not been elucidated.

Methods: Transmission electron microscopy (TME) and nanoparticle tracking analysis (NTA) were applied to verify the existence of GSCs-derived exosomes. Sphere formation assays, flow cytometry, and tumor xenograft transplantation assays were performed to identify the exact roles of exosomal miR-6733-5p. Then, the mechanisms of miR-6733-5p and its downstream target gene regulating crosstalk between GSCs cells and M2 macrophages were further investigated.

Results: GSCs-derived exosomal miR-6733-5p induce macrophage M2 polarization of TAMs by positively targeting IGF2BP3 to activate the AKT signaling pathway, which further facilitates the self-renewal and stemness of GSCs.

Conclusion: GSCs secrete miR-6733-5p-rich exosomes to induce M2-like polarization of macrophages, as well as enhance GSCs stemness and promote malignant behaviors of GBM through IGF2BP3 activated AKT pathway. Targeting GSCs exosomal miR-6733-5p may provide a potential new strategy against GBM.

Keywords: exosomes; glioblastoma stem cells; macrophage polarization; microRNA-6733-5p; stemness.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Glioblastoma* / pathology
  • Humans
  • Macrophages / pathology
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Stem Cells / metabolism
  • Tumor Microenvironment

Substances

  • Proto-Oncogene Proteins c-akt
  • MicroRNAs