Related Experiment Video

Updated: Jul 6, 2025

A Preclinical Mouse Model of Osteosarcoma to Define the Extracellular Vesicle-mediated Communication Between Tumor and Mesenchymal Stem Cells
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A Preclinical Mouse Model of Osteosarcoma to Define the Extracellular Vesicle-mediated Communication Between Tumor and Mesenchymal Stem Cells

Published on: May 6, 2018

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Exosome microRNA-22 inhibiting proliferation, migration and invasion through regulating Twist1/CADM1 axis in

Qing Ruan1, Cuijie Wang2, Yuntao Wu1

  • 1Department of Orthopedics of the China-Japan Union Hospital of Jilin University, Sendai Street 126, Changchun, 130033, Jilin, China.

Scientific Reports
|January 9, 2024
PubMed

Insights

MicroRNA-22 (miR-22) delivered by mesenchymal stem cell (MSC) exosomes inhibits osteosarcoma (OS) growth and spread by targeting Twist1. This exosome-based therapy offers a promising strategy for OS treatment.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Biotechnology

Background:

  • Osteosarcoma (OS) is a primary bone malignancy with high metastatic potential.
  • MicroRNAs (miRNAs) play crucial roles in cancer development and progression.
  • Mesenchymal stem cells (MSCs) and their exosomes are emerging as potential therapeutic delivery vehicles.

Purpose of the Study:

  • To investigate the function of miR-22 from MSCs in regulating osteosarcoma (OS) cell proliferation, migration, and invasion.
  • To explore the therapeutic potential of exosome-delivered miR-22 in OS treatment.
  • To elucidate the molecular mechanism involving miR-22, Twist1, and CADM1 in OS.

Main Methods:

  • Bioinformatic analyses (GEO2R, Gene Ontology) to identify target genes.
  • RT-qPCR and Western blotting to assess gene and protein expression.
  • Cell proliferation assays (MTS, CCK8, colony formation, EdU).
  • Cell migration and invasion assays (Transwell, wound healing).
  • Luciferase reporter assays to confirm miRNA-target interactions.
  • Exosome isolation, labeling (PKH-26), and cellular uptake studies.

Main Results:

  • miR-22 and CADM1 were downregulated, while Twist1 was upregulated in OS tissues and cell lines.
  • Overexpression of miR-22 in OS cells significantly inhibited proliferation, migration, and invasion.
  • Twist1 was confirmed as a direct target of miR-22.
  • Exosomes derived from MSCs (exo-MSC) loaded with miR-22 mimic demonstrated enhanced inhibition of OS cell behaviors compared to unmodified exo-MSC.
  • Uptake of miR-22 by OS cells via exo-MSC effectively suppressed tumor progression by targeting Twist1.

Conclusions:

  • miR-22 acts as a tumor suppressor in osteosarcoma by inhibiting proliferation, migration, and invasion.
  • Exosome-mediated delivery of miR-22 represents a potent therapeutic strategy for osteosarcoma.
  • Targeting the miR-22/Twist1 axis offers a novel approach for osteosarcoma treatment.

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