Transcription factors FOXG1 and Groucho/TLE promote glioblastoma growth

Nat Commun. 2013:4:2956. doi: 10.1038/ncomms3956.

Abstract

Glioblastoma (GBM) is the most common and deadly malignant brain cancer, with a median survival of <2 years. GBM displays a cellular complexity that includes brain tumour-initiating cells (BTICs), which are considered as potential key targets for GBM therapies. Here we show that the transcription factors FOXG1 and Groucho/TLE are expressed in poorly differentiated astroglial cells in human GBM specimens and in primary cultures of GBM-derived BTICs, where they form a complex. FOXG1 knockdown in BTICs causes downregulation of neural stem/progenitor and proliferation markers, increased replicative senescence, upregulation of astroglial differentiation genes and decreased BTIC-initiated tumour growth after intracranial transplantation into host mice. These effects are phenocopied by Groucho/TLE knockdown or dominant inhibition of the FOXG1:Groucho/TLE complex. These results provide evidence that transcriptional programmes regulated by FOXG1 and Groucho/TLE are important for BTIC-initiated brain tumour growth, implicating FOXG1 and Groucho/TLE in GBM tumourigenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / metabolism
  • Brain Neoplasms / metabolism*
  • Cell Differentiation
  • Cell Line, Tumor
  • Cell Proliferation
  • Co-Repressor Proteins
  • Forkhead Transcription Factors / physiology*
  • Gene Expression Regulation, Neoplastic*
  • Gene Silencing
  • Glioblastoma / metabolism*
  • HEK293 Cells
  • Humans
  • Immunohistochemistry
  • Male
  • Mice
  • Mice, SCID
  • Microscopy, Fluorescence
  • Neoplasm Transplantation
  • Nerve Tissue Proteins / physiology*
  • Oligonucleotide Array Sequence Analysis
  • Prognosis
  • Transcription Factors / physiology*
  • Tumor Cells, Cultured

Substances

  • Co-Repressor Proteins
  • FOXG1 protein, human
  • Forkhead Transcription Factors
  • Nerve Tissue Proteins
  • Tle6 protein, human
  • Transcription Factors