+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: not found

      Silencing of the E-cadherin invasion-suppressor gene by CpG methylation in human carcinomas.

      Proceedings of the National Academy of Sciences of the United States of America

      Azacitidine, pharmacology, Base Sequence, Cadherins, genetics, Carcinoma, pathology, DNA Primers, DNA, Neoplasm, chemistry, Gene Expression, drug effects, Genes, Regulator, Genes, Tumor Suppressor, Humans, Methylation, Molecular Sequence Data, Neoplasm Invasiveness, Oligodeoxyribonucleotides, Promoter Regions, Genetic, RNA, Messenger, RNA, Neoplasm, Tumor Cells, Cultured

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          E-Cadherin, a cell adhesion molecule, which plays a key role in maintaining the epithelial phenotype, is regarded as an invasion-suppressor gene in light of accumulating evidence from in vitro experiments and clinical observations. In an attempt to clarify the mechanism responsible for inactivation of this gene in carcinomas, we investigated the methylation state around the promoter region by digestion of DNA with the methylation-sensitive restriction enzyme Hpa II, as CpG methylation of the promoter has been postulated to be a mechanism of transcriptional inactivation of some genes. We found that E-cadherin expression-negative carcinoma cell lines were accompanied by the hypermethylation state, whereas E-cadherin-positive cell lines were not. Furthermore, treatment of E-cadherin-negative carcinoma cells with the demethylating agent 5-azacytidine resulted in reexpression of the gene and reversion of scattered spindle-shaped cells to cells with epithelial morphology. These results suggest that hypermethylation around the promoter may be a mechanism of E-cadherin inactivation in human carcinomas and that treatment of E-cadherin-inactivated cells with a demethylating agent may cause gene expression reversion leading to epithelial morphogenesis with acquisition of the homophilic cell-cell adhesive property.

          Related collections

          Author and article information



          Comment on this article