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Research Paper|Volume 13, Issue 7|pp 9911—9926

Exosomes derived from microRNA-512-5p-transfected bone mesenchymal stem cells inhibit glioblastoma progression by targeting JAG1

Tengfeng Yan1, Miaojing Wu1, Shigang Lv1,3, Qing Hu1, Wenhua Xu2, Ailiang Zeng3, Kai Huang1, Xingen Zhu1
  • 1Department of Neurosurgery, The Second Affiliated Hospital, Nanchang University, Nanchang, P.R. China
  • 2Department of Neurosurgery, Jiujiang No.1 People’s Hospital, Jiujiang, P.R. China
  • 3Department of Neurosurgery, The First Affiliated Hospital, Nanjing Medical University, Nanjing, P.R. China
* Equal contribution
Received: November 21, 2020Accepted: January 22, 2021Published: March 26, 2021
https://doi.org/10.18632/aging.202747

Copyright: © 2021 Yan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

In this study, we demonstrate that bone mesenchymal stem cell (BMSC)-derived exosomes alter tumor phenotypes by delivering miR-512-5p. miR-512-5p was downregulated in glioblastoma tissues and cells, and Jagged 1 (JAG1) was the target gene of miR-512-5p. We clarified the expression patterns of miR-512-5p and JAG1 along with their interactions in glioblastoma. Additionally, we observed that BMSC-derived exosomes could contain and transport miR-512-5p to glioblastoma cells in vitro. BMSC-derived exosomal miR-512-5p inhibited glioblastoma cell proliferation and induced cell cycle arrest by suppressing JAG1 expression. In vivo assays validated the in vitro findings, with BMSC-exosomal miR-512-5p inhibiting glioblastoma growth and prolonging survival in mice. These results suggest that BMSC-derived exosomes transport miR-512-5p into glioblastoma and slow its progression by targeting JAG1. This study reveals a new molecular mechanism for glioblastoma treatment and validates miRNA packaging into exosomes for glioblastoma cell communication.