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Flow Cytometry-based Drug Screening System for the Identification of Small Molecules That Promote Cellular Differentiation of Glioblastoma Stem Cells
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Epigenetic-mediated dysfunction of the bone morphogenetic protein pathway inhibits differentiation of

Jeongwu Lee1, Myung Jin Son, Kevin Woolard

  • 1Neuro-Oncology Branch, National Cancer Institute, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.

Cancer Cell
|January 3, 2008
PubMed

Insights

Glioblastoma tumor-initiating cells (TICs) show impaired differentiation due to epigenetic silencing of BMPR1B. Restoring BMPR1B expression in these cancer stem cells reverses this, reducing tumor-initiating potential.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Cancer Stem Cell Biology

Background:

  • Glioblastoma tumor-initiating cells (TICs) share stem-like properties with normal neural stem cells.
  • Understanding differences in differentiation potential is crucial for glioblastoma treatment.

Purpose of the Study:

  • To investigate the mechanisms underlying impaired astroglial differentiation in glioblastoma TICs.
  • To explore the role of bone morphogenetic protein receptor 1B (BMPR1B) in glioblastoma TIC differentiation and tumorigenicity.

Main Methods:

  • Analyzing Jak/STAT-dependent astroglial differentiation pathways.
  • Investigating EZH2-mediated epigenetic silencing of BMPR1B in glioblastoma TICs.
  • Assessing the effects of forced BMPR1B expression on TIC differentiation and tumorigenicity.

Main Results:

  • EZH2-dependent epigenetic silencing of BMPR1B impairs BMP- and CNTF-mediated astroglial differentiation in a subset of glioblastoma TICs.
  • Forced expression of BMPR1B restores differentiation capabilities in these TICs.
  • Restored BMPR1B expression leads to a loss of tumorigenicity in glioblastoma TICs.

Conclusions:

  • Deregulation of the BMP developmental pathway contributes to glioblastoma TIC tumorigenicity.
  • Silencing of BMPR1B by EZH2 desensitizes TICs to differentiation cues and promotes proliferation.
  • Targeting BMPR1B epigenetic silencing may offer a therapeutic strategy for glioblastoma.

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