Network modeling of the transcriptional effects of copy number aberrations in glioblastoma

Mol Syst Biol. 2011 Apr 26:7:486. doi: 10.1038/msb.2011.17.

Abstract

DNA copy number aberrations (CNAs) are a hallmark of cancer genomes. However, little is known about how such changes affect global gene expression. We develop a modeling framework, EPoC (Endogenous Perturbation analysis of Cancer), to (1) detect disease-driving CNAs and their effect on target mRNA expression, and to (2) stratify cancer patients into long- and short-term survivors. Our method constructs causal network models of gene expression by combining genome-wide DNA- and RNA-level data. Prognostic scores are obtained from a singular value decomposition of the networks. By applying EPoC to glioblastoma data from The Cancer Genome Atlas consortium, we demonstrate that the resulting network models contain known disease-relevant hub genes, reveal interesting candidate hubs, and uncover predictors of patient survival. Targeted validations in four glioblastoma cell lines support selected predictions, and implicate the p53-interacting protein Necdin in suppressing glioblastoma cell growth. We conclude that large-scale network modeling of the effects of CNAs on gene expression may provide insights into the biology of human cancer. Free software in MATLAB and R is provided.

MeSH terms

  • Cell Line, Tumor
  • Chromosome Aberrations
  • Databases, Factual
  • Gene Dosage*
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic
  • Gene Regulatory Networks
  • Genome, Human
  • Genome-Wide Association Study
  • Glioblastoma / genetics*
  • Glioblastoma / metabolism
  • Glioblastoma / mortality
  • Glioblastoma / pathology
  • Humans
  • Models, Genetic
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism*
  • Nervous System Neoplasms / genetics*
  • Nervous System Neoplasms / metabolism
  • Nervous System Neoplasms / mortality
  • Nervous System Neoplasms / pathology
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Prognosis
  • Software
  • Transcriptional Activation / genetics*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Nerve Tissue Proteins
  • Nuclear Proteins
  • Tumor Suppressor Protein p53
  • necdin