MiR-21 modulates hTERT through a STAT3-dependent manner on glioblastoma cell growth

CNS Neurosci Ther. 2012 Sep;18(9):722-8. doi: 10.1111/j.1755-5949.2012.00349.x. Epub 2012 Jun 18.

Abstract

Background and purpose: As an important oncogenic miRNA, miR-21 has been reported to play crucial roles in glioblastoma (GBM) carcinogenesis. However, the precise biological function and molecular mechanism of miR-21 in GBM remain elusive. This study is designed to explore the mechanism of miR-21 involved in the control of GBM cell growth.

Methods and results: MTT assay, cell cycle analysis, and apoptosis analysis showed that reduction of miR-21 inhibited cell growth in U87 and LN229 GBM cells. Further, reduction of miR-21 decreased the expression of human telomerase reverse transcriptase (hTERT) and repressed STAT3 expression and STAT3 phosphorylation. STAT3 inhibition led to a remarkable depletion of hTERT at both mRNA and protein levels by binding to the hTERT gene promoter by performing luciferase reporter assay and chromatin Immunoprecipitation PCR. Finally, knockdown of miR-21 considerably inhibited tumor growth and diminished the expression of STAT3 and hTERT in xenograft model.

Conclusion: Our findings indicate that miR-21 regulates hTERT expression mediated by STAT3, therefore controlling GBM cell growth.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Brain Neoplasms / genetics
  • Brain Neoplasms / metabolism*
  • Brain Neoplasms / pathology
  • Cell Line, Tumor
  • Cell Proliferation
  • Gene Expression Regulation, Neoplastic / physiology*
  • Glioblastoma / genetics
  • Glioblastoma / metabolism*
  • Glioblastoma / pathology
  • Humans
  • MicroRNAs / metabolism*
  • STAT3 Transcription Factor / metabolism*
  • Telomerase / metabolism*

Substances

  • MIRN21 microRNA, human
  • MicroRNAs
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Telomerase