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

  1. Author:
    Pennie, W. D.
    Hegamyer, G. A.
    Young, M. R.
    Colburn, N. H.

  2. Author Address

    Colburn NH NCI, Gene Regulat Sect, Lab Biochem Physiol, Frederick Canc Res & Dev Ctr POB B,Bldg 560 Frederick, MD 21702 USA NCI, Gene Regulat Sect, Lab Biochem Physiol, Frederick Canc Res & Dev Ctr Frederick, MD 21702 USA
    1. Year: 1999
  2. Journal: Cell Growth and Differentiation
    1. 10
    2. 4
    3. Pages: 279-286
  4. Type of Article: Article
  1. 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 HpaII 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 HpaII sites. Thus, hypermethylation at specific sequences in the TIMP-3 promoter appears to contribute to the silencing of the gene in neoplastic cells. [References: 42]

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