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Pathological changes in the epigenetic landscape of chromatin are hallmarks of cancer. The caudal-type homeobox gene  CDX2  is not expressed in normal gastric epithelia but rather in adult intestinal epithelia, and it is overexpressed in intestinal metaplasia (IM). However, it remains unclear how  CDX2  transcription is suppressed in normal gastric epithelial cells and overexpressed in IM. Here, we demonstrate that methylation of the  CDX2  promoter increases with age in  Helicobacter pylori -positive, noncancerous gastric tissue, whereas the promoter is demethylated in paired gastric tumors in which  CDX2  is upregulated. Moreover, we also found that the  CDX2  promoter is demethylated in IM as well as gastric tumor. Immunohistochemistry revealed that CDX2 is present in foci of parts of the gastric mucosae but highly expressed in IM as well as in gastric tumors, suggesting that the elevated level of CDX2 in IM and gastric tumors may be attributable to promoter demethylation. Our data suggest that  CDX2  repression may be associated with promoter methylation in noncancerous  H. pylori -positive mucosa but its upregulation might be attributable to increased promoter activity mediated by chromatin remodeling during gastric carcinogenesis.

carcinogenesis

Methylation of the  CDX2  promoter in  Helicobacter pylori -infected gastric mucosa increases with age and its rapid demethylation in gastric tumors is associated with upregulated gene expression