Exosomes derived from human mesenchymal stem cells promote gastric cancer cell growth and migration via the activation of the Akt pathway

Mol Med Rep. 2016 Oct;14(4):3452-8. doi: 10.3892/mmr.2016.5625. Epub 2016 Aug 11.

Abstract

Mesenchymal stem cells (MSCs) are a component of the tumor microenvironment and can promote the development of gastric cancer through paracrine mechanism. However, the effects of MSC‑exosomes (MSC‑ex) on gastric cancer are less clear. The present study reported that MSC‑ex promoted the proliferative and metastatic potential of gastric cancer cells ex vivo. It was found that MSC‑ex enhanced the migration and invasion of HGC‑27 cells via the induction of the epithelial‑mesenchymal transition. MSC‑ex increased the expression of mesenchymal markers and reduced the expression of epithelial markers in gastric cancer cells. MSC‑ex also enhanced the tumorigenicity of gastric cancer cells ex vivo. MSC‑ex induced the stemness of gastric cancer cells. The expression of octamer‑binding transcription factor 4, ex determining region Y‑box 2 and Lin28B significantly increased in gastric cancer cells treated with MSC‑ex. The present study further demonstrated that MSC‑ex elicited these biological effects predominantly via the activation of the protein kinase B signaling pathway. Taken together, the present findings provided novel evidence for the role of MSC‑ex in gastric cancer and a new opportunity for improving the efficiency of gastric cancer treatment by targeting MSC‑ex.

MeSH terms

  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation*
  • Cells, Cultured
  • Epithelial-Mesenchymal Transition*
  • Exosomes / metabolism
  • Exosomes / pathology*
  • Gastric Mucosa / metabolism
  • Humans
  • Mesenchymal Stem Cells / metabolism
  • Mesenchymal Stem Cells / pathology*
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Signal Transduction
  • Stomach / cytology
  • Stomach / pathology
  • Stomach Neoplasms / metabolism
  • Stomach Neoplasms / pathology*
  • Tumor Microenvironment*

Substances

  • Proto-Oncogene Proteins c-akt