MicroRNA-365 inhibits the progression of lung adenocarcinoma through targeting ETS1 and inactivating AKT/mTOR pathway

Eur Rev Med Pharmacol Sci. 2020 May;24(9):4836-4845. doi: 10.26355/eurrev_202005_21172.

Abstract

Objective: MicroRNAs (miRNAs) act as important regulators in human cancers by regulating the gene expression. The dysregulation of miR-365 has been investigated in many cancers. However, the function of miR-365 remains unknown in lung adenocarcinoma. Therefore, the regulatory mechanism of miR-365 was explored in lung adenocarcinoma.

Patients and methods: The expression of miR-365 was detected in cell lines and 67 lung adenocarcinoma tissues using qRT-PCR. The Kaplan-Meier analysis was used to determine the association between miR-365 expressions and the survival rate in patients with lung adenocarcinoma. Transwell assay was then performed to investigate the effect of miR-365 on invasion and migration of lung adenocarcinoma cells.

Results: Downregulation of miR-365 and upregulation of ETS1 were identified in lung adenocarcinoma. Furthermore, miR-365 reversely regulated ETS1 expression in lung adenocarcinoma. Functionally, the overexpression of miR-365 inhibited proliferation, migration, and invasion of lung adenocarcinoma cells. However, the upregulation of ETS1 lessened the inhibitory effect of miR-365 in lung adenocarcinoma. In addition, miR-365 inhibited EMT and inactivated AKT/mTOR pathway in lung adenocarcinoma.

Conclusions: MiR-365 inhibits the progression of lung adenocarcinoma by targeting ETS1 and inactivating the AKT/mTOR pathway.

MeSH terms

  • Adenocarcinoma of Lung / metabolism*
  • Adenocarcinoma of Lung / pathology*
  • Cell Movement
  • Cell Proliferation
  • Cells, Cultured
  • Disease Progression
  • Female
  • Humans
  • Lung Neoplasms / metabolism*
  • Lung Neoplasms / pathology
  • Male
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Middle Aged
  • Proto-Oncogene Protein c-ets-1 / metabolism*
  • Proto-Oncogene Proteins c-akt / metabolism*
  • TOR Serine-Threonine Kinases / metabolism*

Substances

  • ETS1 protein, human
  • MIRN365 microRNA, human
  • MicroRNAs
  • Proto-Oncogene Protein c-ets-1
  • MTOR protein, human
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases