Specific methylation events contribute to the transcriptional repression of the mouse tissue inhibitor of metalloproteinases-3 gene in neoplastic cells

Cell Growth Differ. 1999 Apr;10(4):279-86.

Abstract

The tissue inhibitor of metalloproteinases-3 (TIMP-3) gene is specifically down-regulated in neoplastic cells of the mouse JB6 progression model, suggesting a role for TIMP-3 inactivation in neoplastic progression. On the basis of 5-azacytidine reversal, the mechanism for this down-regulation appears to involve changes in the methylation state of the TIMP-3 promoter. Although total genomic methylation levels are comparable, specific differences in the methylation of the TIMP-3 promoter were observed between preneoplastic and neoplastic JB6 cells at three Hpall sites, with preneoplastic cells being less methylated. Expression of antisense methyltransferase in a neoplastic JB6 variant known to be hypermethylated in TIMP-3 resulted in reactivation of the endogenous TIMP-3 gene and restoration of hypomethylated status to the three implicated Hpall sites. Thus, hypermethylation at specific sequences in the TIMP-3 promoter appears to contribute to the silencing of the gene in neoplastic cells.

MeSH terms

  • Animals
  • Blotting, Northern
  • Chromosome Mapping
  • Cytosine / metabolism
  • Deoxyribonuclease HpaII / pharmacology
  • Gene Expression Regulation, Neoplastic*
  • Genes, Regulator*
  • Luciferases / metabolism
  • Methylation
  • Mice
  • Models, Genetic
  • Oligonucleotides, Antisense
  • Promoter Regions, Genetic
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tissue Inhibitor of Metalloproteinase-3 / genetics*
  • Transfection
  • Tumor Cells, Cultured

Substances

  • Oligonucleotides, Antisense
  • Tissue Inhibitor of Metalloproteinase-3
  • Cytosine
  • Luciferases
  • Deoxyribonuclease HpaII