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[Cancer Research 61, 8094-8099, November 15, 2001]
© 2001 American Association for Cancer Research

Advances in Brief

Hypermethylation in Human Cancers of the RIZ1 Tumor Suppressor Gene, a Member of a Histone/Protein Methyltransferase Superfamily1

Yong Du, Tobias Carling, Wei Fang, Zhe Piao, Jin-Chuan Sheu and Shi Huang2

The Burnham Institute, La Jolla, California 92037 [Y. D., T. C., W. F., Z. P., S. H.]; Endocrine Surgery Unit, Department of Surgery, Uppsala University Hospital, S-751 85 Uppsala, Sweden [T. C.]; and Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan [J-C. S.]

The retinoblastoma protein-interacting zinc finger gene RIZ1 is a tumor suppressor gene and a member of a nuclear histone/protein methyltransferase superfamily. RIZ1 inactivation is commonly found in many types of human cancers and occurs through loss of mRNA expression, frameshift mutation, chromosomal deletion, and missense mutation. RIZ1 is also a tumor susceptibility gene in mice. We now show that loss of RIZ1 mRNA in human cancers is associated with DNA methylation of its promoter CpG island. Methylation of the RIZ1 promoter strongly correlated with lost or decreased RIZ1 mRNA expression in breast, liver, colon, and lung cancer cell lines as well as in liver cancer tissues. Treatment with the methylation inhibitor 5-aza-2'-deoxycytidine activated RIZ1 mRNA expression in cancer cells. Furthermore, methylation was found in 11 of 25 (44%) breast cancer specimens and 20 of 32 (62%) liver cancer specimens. Our results suggest that DNA methylation is a common mechanism in inactivating the RIZ1 tumor suppressor gene in human liver and breast cancers.




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Copyright © 2001 by the American Association for Cancer Research.