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Promoter hypermethylation of DLC-1, a candidate tumor suppressor gene, in several common human cancers.
Yuan-BZ; Durkin-ME; Popescu-NC
Cancer Genet Cytogenet 2003 Jan; 140(2):113-117
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.
Cancer; Genetics; Tumor-inhibition; Tumors; Liver-tumors; Genes; Chromosome-damage; Cell-alteration; Cell-morphology; Proteins; Enzymes
Laboratory of Experimental Carcinogenesis, Building 37 Room 3C05, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Issue of Publication
Cancer Genetics and Cytogenetics
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