PLAGL2 regulates Wnt signaling to impede differentiation in neural stem cells and gliomas

Cancer Cell. 2010 May 18;17(5):497-509. doi: 10.1016/j.ccr.2010.03.020.

Abstract

A hallmark feature of glioblastoma is its strong self-renewal potential and immature differentiation state, which contributes to its plasticity and therapeutic resistance. Here, integrated genomic and biological analyses identified PLAGL2 as a potent protooncogene targeted for amplification/gain in malignant gliomas. Enhanced PLAGL2 expression strongly suppresses neural stem cell (NSC) and glioma-initiating cell differentiation while promoting their self-renewal capacity upon differentiation induction. Transcriptome analysis revealed that these differentiation-suppressive activities are attributable in part to PLAGL2 modulation of Wnt/beta-catenin signaling. Inhibition of Wnt signaling partially restores PLAGL2-expressing NSC differentiation capacity. The identification of PLAGL2 as a glioma oncogene highlights the importance of a growing class of cancer genes functioning to impart stem cell-like characteristics in malignant cells.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Differentiation / physiology*
  • Cell Transformation, Neoplastic
  • DNA-Binding Proteins / physiology*
  • Glioblastoma / pathology*
  • Humans
  • Mice
  • RNA-Binding Proteins / physiology*
  • Signal Transduction / physiology*
  • Stem Cells / cytology*
  • Transcription Factors / physiology*
  • Wnt Proteins / metabolism*

Substances

  • DNA-Binding Proteins
  • Plagl2 protein, mouse
  • RNA-Binding Proteins
  • Transcription Factors
  • Wnt Proteins

Associated data

  • GEO/GSE21143