miR-96/HBP1/Wnt/β-catenin regulatory circuitry promotes glioma growth

FEBS Lett. 2014 Aug 25;588(17):3038-46. doi: 10.1016/j.febslet.2014.06.017. Epub 2014 Jun 12.

Abstract

We found that miR-96 is overexpressed in glioma, and its level inversely correlates with the survival of patients. The reduction in miR-96 abundance suppresses the proliferation and colony formation of glioma cells. The tumorigenicity of U-87 MG cells is reduced by miR-96 silencing. miR-96 contributes to the activation of Wnt/β-catenin pathway in glioma cells. HMG-box transcription factor 1 (HBP-1), a Wnt/β-catenin pathway inhibitor, is suppressed by miR-96. The reactivation of Wnt/β-catenin signaling causes an increase in the proliferation of glioma cells, and a decrease in miR-96 expression. On the other hand, HBP1 silencing promotes miR-96 expression. Collectively, miR-96 contributes to the progression of glioma by enhancing the activation of the Wnt/β-catenin pathway, and the miR-96/HBP1/Wnt/β-catenin regulatory circuitry promotes the proliferation of glioma cells.

Keywords: Glioma; HMG-box transcription factor 1; Proliferation; Wnt/β-catenin; miR-96.

Publication types

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

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Cell Proliferation
  • DNA-Binding Proteins / metabolism*
  • Gene Expression Regulation, Neoplastic
  • Gene Silencing
  • Glioma / genetics
  • Glioma / pathology*
  • Humans
  • Male
  • Mice
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Nuclear Proteins / metabolism*
  • Survival Analysis
  • Wnt Proteins / metabolism*
  • Wnt Signaling Pathway
  • beta Catenin / metabolism*

Substances

  • DNA-Binding Proteins
  • MIRN96 microRNA, human
  • MicroRNAs
  • Nuclear Proteins
  • Wnt Proteins
  • beta Catenin
  • histone DNA binding protein-1