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Cell Growth & Differentiation Vol. 10, 279-286, April 1999
© 1999 American Association for Cancer Research

Specific Methylation Events Contribute to the Transcriptional Repression of the Mouse Tissue Inhibitor of Metalloproteinases-3 Gene in Neoplastic Cells

William D. Pennie1, Glenn A. Hegamyer, Matthew R. Young and Nancy H. Colburn2

Gene Regulation Section, Laboratory of Biochemical Physiology, Building 560, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, Maryland 21702

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.




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Cancer Research Clinical Cancer Research
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Molecular Cancer Research Cell Growth & Differentiation
Copyright © 1999 by the American Association of Cancer Research.