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
Cancer Genetics and Cytogenetics