Methylation-independent silencing of the p73 gene in neuroblastoma

Oncogene. 2000 Sep 14;19(39):4553-6. doi: 10.1038/sj.onc.1203807.

Abstract

p73 is a p53 homolog that, in vitro, inhibits cell growth and induce apoptosis. In some tumors p73 is monoallelically expressed and this raised the possibility that this gene is subjected to imprinting. Silencing of p73 in acute leukemia and in Burkitt's lymphoma occurs in association with the aberrant methylation of the first exon of the gene. We have analysed the methylation pattern of the p73 promoter and of upstream and downstream sequences in neuroblastoma. Our results demonstrate that p73 expression in this tumor is not regulated by methylation. We concluded that it is unlikely that p73 is imprinted in neuroblastoma and that the methylation-dependent silencing of this gene, thus far, is a characteristic of hematologic malignancies. Oncogene (2000) 19, 4553 - 4556.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Base Sequence
  • CpG Islands
  • DNA Methylation*
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • Gene Expression Regulation, Neoplastic
  • Gene Silencing
  • Genes, Tumor Suppressor*
  • HL-60 Cells
  • Humans
  • Molecular Sequence Data
  • Neuroblastoma / genetics*
  • Nuclear Proteins / genetics*
  • Nuclear Proteins / metabolism
  • Polymerase Chain Reaction / methods
  • Promoter Regions, Genetic
  • Tumor Protein p73
  • Tumor Suppressor Proteins

Substances

  • DNA-Binding Proteins
  • Nuclear Proteins
  • TP73 protein, human
  • Tumor Protein p73
  • Tumor Suppressor Proteins