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Promoter hypermethylation of DLC-1, a candidate tumor suppressor gene, in several common human cancers.

Authors
Yuan-BZ; Durkin-ME; Popescu-NC
Source
Cancer Genet Cytogenet 2003 Jan; 140(2):113-117
NIOSHTIC No.
20023526
Abstract
Aberrant methylation of CpG islands within the promoter regions of tumor suppressor or cancer-related genes is a common mechanism leading to the silencing of gene expression. To determine whether aberrant methylation is a contributing factor to transcriptional inactivation of DLC-1 (deleted in liver cancer-1), a candidate tumor suppressor gene, we examined its methylation status in twelve hepatocellular carcinoma, breast, colon, and prostate tumor cell lines with low or undetectable expression of DLC-1. By Southern blot analysis of DNA digested with the methylation sensitive enzyme HpaII, we found a different degree of promoter hypermethylation in all cell lines with aberrant DLC-1 expression. The hypermethylation status was reversed by the addition of 5-aza-2'-deoxycytidine, a demethylating agent, in one human hepatocellular carcinoma line. These observations suggest that hypermethylation is responsible for abrogating the function of the DLC-1 gene in a subset of liver, breast, colon, and prostate cancers.
Keywords
Cancer; Genetics; Tumor-inhibition; Tumors; Liver-tumors; Genes; Chromosome-damage; Cell-alteration; Cell-morphology; Proteins; Enzymes
Contact
Laboratory of Experimental Carcinogenesis, Building 37 Room 3C05, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
CODEN
CGCYDF
Publication Date
20030115
Document Type
Journal Article
Email Address
popsecun@mail.nih.gov
Fiscal Year
2003
NTIS Accession No.
NTIS Price
Issue of Publication
2
ISSN
0165-4608
NIOSH Division
HELD
Source Name
Cancer Genetics and Cytogenetics
State
MD; WV
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