Transferred by exosomes-derived MiR-19b-3p targets PTEN to regulate esophageal cancer cell apoptosis, migration and invasion

Biosci Rep. 2020 Nov 27;40(11):BSR20201858. doi: 10.1042/BSR20201858.

Abstract

The present study aims to investigate the relationship between miR-19b-3p and esophageal cancer (ESCA), and to detect the effects of miR-19b-3p transferred by exosomes on the phenotype of EC9706 cells. The expression of miR-19b-3p was detected by starBase analysis and real-time quantitative PCR (RT-qPCR). The target genes of miR-19b-3p were predicted by TargetScan and further verified by luciferase analysis. The mRNA and protein expression levels of PTEN and EMT-related genes were detected by RT-qPCR and Western blotting. The effects of miR-19b-3p transferred by exosomes and its target genes on the apoptosis, migration and invasion of EC9706 cells were studied by establishing a co-culture model of donor cells. The expression of miR-19b-3p in ESCA plasma, cells and exosomes was significantly up-regulated. miR-19b-3p transferred by exosomes could significantly reduce EC9706 cells apoptosis rate, promote cell migration and invasion, and could target the inhibition of PTEN expression. PTEN overexpression promoted apoptosis, inhibited cell migration and invasion, down-regulated the expression of MMP-2 and vimentin, and up-regulated E-cadherin expression; however, these effects could be partially reversed by miR-19b-3p. In summary, our results reveal that miR-19b-3p transferred by exosomes can target PTEN to regulate ESCA biological functions in the receptor EC9706 cells.

Keywords: PTEN pathway; esophageal cancer; exosomes; miR-19b-3p; migration.

MeSH terms

  • Antigens, CD / genetics
  • Antigens, CD / metabolism
  • Apoptosis*
  • Cadherins / genetics
  • Cadherins / metabolism
  • Case-Control Studies
  • Cell Line, Tumor
  • Cell Movement*
  • Coculture Techniques
  • Epithelial-Mesenchymal Transition
  • Esophageal Neoplasms / enzymology
  • Esophageal Neoplasms / genetics
  • Esophageal Neoplasms / pathology
  • Esophageal Neoplasms / therapy*
  • Exosomes / genetics*
  • Exosomes / metabolism
  • Gene Expression Regulation, Neoplastic
  • Genetic Therapy*
  • Humans
  • Matrix Metalloproteinase 2 / genetics
  • Matrix Metalloproteinase 2 / metabolism
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Neoplasm Invasiveness
  • PTEN Phosphohydrolase / genetics
  • PTEN Phosphohydrolase / metabolism*
  • Signal Transduction
  • Vimentin / genetics
  • Vimentin / metabolism

Substances

  • Antigens, CD
  • CDH1 protein, human
  • Cadherins
  • MIRN19 microRNA, human
  • MicroRNAs
  • VIM protein, human
  • Vimentin
  • PTEN Phosphohydrolase
  • PTEN protein, human
  • MMP2 protein, human
  • Matrix Metalloproteinase 2