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[Cancer Research 59, 798-802, February 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 798-802, February 15, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

Methylation-associated Silencing of the Tissue Inhibitor of Metalloproteinase-3 Gene Suggests a Suppressor Role in Kidney, Brain, and Other Human Cancers1

Kurtis E. Bachman, James G. Herman2, Paul G. Corn, Adrian Merlo, Joseph F. Costello, Webster K. Cavenee, Stephen B. Baylin and Jeremy R. Graff3

The Johns Hopkins Oncology Center, Baltimore, Maryland 21231 [K. E. B., J. G. H., P. G. C., S. B. B., J. R. G.]; The Graduate Program in Cellular and Molecular Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21231 [K. E. B.]; Department of Research/Neurosurgery, University of Basel, CH-4031 Basel, Switzerland [A. M.]; and Ludwig Institute for Cancer Research, La Jolla, California 92093 [J. F. C., W. K. C.]

Tissue inhibitor of metalloproteinase-3 (TIMP-3) antagonizes matrix metalloproteinase activity and can suppress tumor growth, angiogenesis, invasion, and metastasis. Loss of TIMP-3 has been related to the acquisition of tumorigenesis. Herein, we show that TIMP-3 is silenced in association with aberrant promoter-region methylation in cell lines derived from human cancers. TIMP-3 expression was restored after 5-aza-2'deoxycytidine-mediated demethylation of the TIMP-3 proximal promoter region. Genomic bisulfite sequencing revealed that TIMP-3 silencing was related to the overall density of methylation and that discrete regions within the TIMP-3 CpG island may be important for the silencing of this gene. Aberrant methylation of TIMP-3 occurred in primary cancers of the kidney, brain, colon, breast, and lung, but not in any of 41 normal tissue samples. The most frequent TIMP-3 methylation was found in renal cancers, which originate in the tissue that normally expresses the highest TIMP-3 levels. This methylation correlated with a lack of detectable TIMP-3 protein in these tumors. Together, these data show that methylation-associated inactivation of TIMP-3 is frequent in many human tumors.




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