Genome-wide identification of PAX3-FKHR binding sites in rhabdomyosarcoma reveals candidate target genes important for development and cancer

Cancer Res. 2010 Aug 15;70(16):6497-508. doi: 10.1158/0008-5472.CAN-10-0582. Epub 2010 Jul 27.

Abstract

The PAX3-FKHR fusion protein is present in a majority of alveolar rhabdomyosarcomas associated with increased aggressiveness and poor prognosis. To better understand the molecular pathogenesis of PAX3-FKHR, we carried out the first, unbiased genome-wide identification of PAX3-FKHR binding sites and associated target genes in alveolar rhabdomyosarcoma. The data shows that PAX3-FKHR binds to the same sites as PAX3 at both MYF5 and MYOD enhancers. The genome-wide analysis reveals that the PAX3-FKHR sites are (a) mostly distal to transcription start sites, (b) conserved, (c) enriched for PAX3 motifs, and (d) strongly associated with genes overexpressed in PAX3-FKHR-positive rhabdomyosarcoma cells and tumors. There is little evidence in our data set for PAX3-FKHR binding at the promoter sequences. The genome-wide analysis further illustrates a strong association between PAX3 and E-box motifs in these binding sites, suggestive of a common coregulation for many target genes. We also provide the first direct evidence that FGFR4 and IGF1R are the targets for PAX3-FKHR. The map of PAX3-FKHR binding sites provides a framework for understanding the pathogenic roles of PAX3-FKHR, as well as its molecular targets to allow a systematic evaluation of agents against this aggressive rhabdomyosarcoma.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Anaplastic Lymphoma Kinase
  • Binding Sites
  • Cell Line, Tumor
  • E-Box Elements
  • Genome, Human
  • Genome-Wide Association Study
  • Humans
  • MyoD Protein / genetics
  • MyoD Protein / metabolism
  • N-Myc Proto-Oncogene Protein
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism
  • Oncogene Proteins / genetics
  • Oncogene Proteins / metabolism
  • Oncogene Proteins, Fusion / genetics*
  • Oncogene Proteins, Fusion / metabolism
  • Protein-Tyrosine Kinases / genetics
  • Protein-Tyrosine Kinases / metabolism
  • Receptor Protein-Tyrosine Kinases
  • Receptor, Fibroblast Growth Factor, Type 4 / genetics
  • Receptor, IGF Type 1 / antagonists & inhibitors
  • Receptor, IGF Type 1 / biosynthesis
  • Receptor, IGF Type 1 / genetics
  • Regulatory Elements, Transcriptional
  • Rhabdomyosarcoma, Alveolar / genetics*
  • Rhabdomyosarcoma, Alveolar / metabolism
  • Sarcoma, Ewing / genetics
  • Sarcoma, Ewing / metabolism
  • Transcription Initiation Site
  • Up-Regulation

Substances

  • MYCN protein, human
  • MyoD Protein
  • MyoD1 myogenic differentiation protein
  • N-Myc Proto-Oncogene Protein
  • Nuclear Proteins
  • Oncogene Proteins
  • Oncogene Proteins, Fusion
  • PAX3-FKHR fusion protein, human
  • Anaplastic Lymphoma Kinase
  • FGFR4 protein, human
  • Protein-Tyrosine Kinases
  • Receptor Protein-Tyrosine Kinases
  • Receptor, Fibroblast Growth Factor, Type 4
  • Receptor, IGF Type 1