IGFBP2 is overexpressed by pediatric malignant astrocytomas and induces the repair enzyme DNA-PK

J Child Neurol. 2008 Oct;23(10):1205-13. doi: 10.1177/0883073808321766.

Abstract

To identify targets critical to malignant childhood astrocytoma, we compared the expression of receptor tyrosine kinase- associated genes between low-grade and high-grade pediatric astrocytomas. The highest differentially overexpressed gene in high-grade astrocytoma is insulin-like growth factor- binding protein-2 (P = .0006). Immunohistochemistry confirmed overexpression of insulin-like growth factor-binding protein-2 protein (P = .027). Insulin-like growth factor- binding protein-2 stimulation had no effect on astrocytoma cell growth and migration, and minimally inhibited insulin-like growth factor-1-mediated migration, but not insulin-like growth factor-2-mediated migration. However, insulin-like growth factor-binding protein-2 stimulation significantly upregulated the major DNA repair enzyme gene, DNA-PKcs, and induced DNA-dependent protein kinase catalytic subunit protein expression in a time-dependent and dose-dependent manner, whereas insulin-like growth factor-1 had no effect. DNA-PKcs is also highly overexpressed by high-grade astrocytomas. These findings suggest insulin-like growth factor-binding protein-2 plays a role in astrocytoma progression by promoting DNA-damage repair and therapeutic resistance.

Publication types

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

MeSH terms

  • Astrocytoma / genetics*
  • Astrocytoma / metabolism
  • Astrocytoma / physiopathology
  • Biomarkers, Tumor / genetics
  • Brain Neoplasms / genetics*
  • Brain Neoplasms / metabolism
  • Brain Neoplasms / physiopathology
  • Catalytic Domain / drug effects
  • Catalytic Domain / genetics
  • Cell Line, Tumor
  • Cell Transformation, Neoplastic / genetics
  • Child
  • DNA Repair / drug effects
  • DNA Repair / genetics*
  • DNA-Activated Protein Kinase / chemistry
  • DNA-Activated Protein Kinase / genetics*
  • DNA-Activated Protein Kinase / metabolism
  • Drug Resistance, Neoplasm / drug effects
  • Drug Resistance, Neoplasm / genetics
  • Gene Expression Regulation, Neoplastic / genetics*
  • Humans
  • Insulin-Like Growth Factor Binding Protein 2 / genetics*
  • Insulin-Like Growth Factor Binding Protein 2 / metabolism
  • Insulin-Like Growth Factor Binding Protein 2 / pharmacology
  • Neoplasm Invasiveness / genetics
  • Neoplasm Metastasis / genetics
  • Nuclear Proteins / chemistry
  • Nuclear Proteins / genetics*
  • Nuclear Proteins / metabolism
  • Receptor Protein-Tyrosine Kinases / genetics
  • Receptor Protein-Tyrosine Kinases / metabolism
  • Up-Regulation / drug effects
  • Up-Regulation / genetics

Substances

  • Biomarkers, Tumor
  • Insulin-Like Growth Factor Binding Protein 2
  • Nuclear Proteins
  • Receptor Protein-Tyrosine Kinases
  • DNA-Activated Protein Kinase
  • PRKDC protein, human