MiR-25-3p targets PTEN to regulate the migration, invasion, and apoptosis of esophageal cancer cells via the PI3K/AKT pathway

Biosci Rep. 2020 Oct 30;40(10):BSR20201901. doi: 10.1042/BSR20201901.

Abstract

Background: Esophageal cancer (EC) is one of the most common malignant tumors of the digestive system. MiR-25-3p was proved to be a biomarker for the diagnosis and treatment of many cancers. MiR-25-3p was found to be high expressed in the blood of EC patients. The aim of the present study was to explore the effect of miR-25-3p and its target gene on EC.

Methods: miR-25-3p expression in the blood of EC patients and EC cells was detected by RT-qPCR. The target of miR-25-3p was identified by bioinformatics and luciferase reporter assay. After transfection, cell viability, apoptosis, migration, and invasion were detected by MTT, flow cytometry, wound healing, and transwell assays, respectively. The expressions of PTEN, Bax, Bcl-2, cleaved Caspase-3, p-PI3K, PI3K, p-AKT, and AKT were detected by Western blot.

Results: MiR-25-3p was high expressed in the blood of EC patients and EC cells. MiR-25-3p targeted PTEN and inhibited the expression of PTEN. MiR-25-3p mimic increased the viability, migration, invasion and the expressions of Bcl-2, and inhibited the apoptosis and the expression of Bax and cleaved caspase-3 in EC cells. MiR-25-3p mimic also enhanced the expressions of p-PI3K and p-AKT and the ratios of p-PI3K/PI3K and p-AKT/AKT in EC cells. PTEN overexpression not only had an opposite effect of miR-25-3p mimic, but also reversed the effect of miR-25-3p mimic on EC cells.

Conclusion: MiR-25-3p targeted PTEN to promote the migration and invasion, and inhibit apoptosis of EC cells via the PI3K/AKT pathway, which might provide a new therapeutic target for EC treatment.

Keywords: PTEN; apoptosis; esophageal cancer; invasion; miR-25-3p; migration.

Publication types

  • Observational Study
  • Research Support, Non-U.S. Gov't
  • Retracted Publication

MeSH terms

  • Apoptosis / drug effects
  • Apoptosis / genetics
  • Case-Control Studies
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Movement / genetics
  • Cell Proliferation / drug effects
  • Cell Proliferation / genetics
  • Esophageal Neoplasms / blood
  • Esophageal Neoplasms / genetics*
  • Esophageal Neoplasms / pathology
  • Gene Expression Regulation, Neoplastic / drug effects
  • Healthy Volunteers
  • Humans
  • MicroRNAs / agonists
  • MicroRNAs / blood
  • MicroRNAs / metabolism*
  • Neoplasm Invasiveness / genetics
  • PTEN Phosphohydrolase / genetics*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction / genetics

Substances

  • MIRN25 microRNA, human
  • MicroRNAs
  • AKT1 protein, human
  • Proto-Oncogene Proteins c-akt
  • PTEN Phosphohydrolase
  • PTEN protein, human