miR-92b regulates glioma cells proliferation, migration, invasion, and apoptosis via PTEN/Akt signaling pathway

J Physiol Biochem. 2016 Jun;72(2):201-11. doi: 10.1007/s13105-016-0470-z. Epub 2016 Feb 18.

Abstract

Glioblastoma (GBM) is a highly invasive malignant primary brain tumor with neoplastic growth. Despite the progresses made in surgery, chemotherapy, and radiation in recent decade, the prognosis of patients with gliomas remains poor and the average survival time of patients suffering from glioblastoma is still short. As a potential therapy strategy, microRNAs have been considered as new targets for possible cancer treatment. In this study, we found that the miR-92b inhibitors (miR-92b-I) could inhibit the proliferation, migration, invasion, and promote the apoptosis of glioma cells. As a predicted target of miR-92b, phosphatase and tensin homolog (PTEN), also elevated at both mRNA and protein levels. Moreover, the Akt phosphorylation was consistently inhibited. The rescue experiment with miR-92b and PTEN double knockdown resulted in partial reversion of miR-92b-I-induced phenotypes. Taken together, our findings indicated that miR-92b-I could restrain the proliferation, invasion, migration, and stimulate apoptosis of glioma cells by targeting PTEN/Akt signaling pathway. Further investigations will focus on antitumor effect of miR‑92b-I in glioma treatment.

Keywords: Akt; Carcinogenesis; Glioblastomas; PTEN; miR-92b.

MeSH terms

  • 3' Untranslated Regions / drug effects
  • Antagomirs / pharmacology*
  • Antimetabolites, Antineoplastic / pharmacology*
  • Apoptosis / drug effects*
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Proliferation / drug effects
  • Computational Biology
  • Gene Expression Regulation, Neoplastic / drug effects
  • Genes, Reporter / drug effects
  • Glioma / drug therapy*
  • Glioma / metabolism
  • Glioma / pathology
  • Humans
  • MicroRNAs / antagonists & inhibitors*
  • MicroRNAs / metabolism
  • Mutation
  • PTEN Phosphohydrolase / antagonists & inhibitors
  • PTEN Phosphohydrolase / genetics
  • PTEN Phosphohydrolase / metabolism*
  • Phosphorylation / drug effects
  • Protein Processing, Post-Translational / drug effects
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA Interference
  • RNA, Messenger / antagonists & inhibitors
  • RNA, Messenger / metabolism
  • RNA, Neoplasm / antagonists & inhibitors
  • RNA, Neoplasm / metabolism
  • Signal Transduction / drug effects*

Substances

  • 3' Untranslated Regions
  • Antagomirs
  • Antimetabolites, Antineoplastic
  • MIRN92 microRNA, human
  • MicroRNAs
  • RNA, Messenger
  • RNA, Neoplasm
  • AKT1 protein, human
  • Proto-Oncogene Proteins c-akt
  • PTEN Phosphohydrolase
  • PTEN protein, human