E-cadherin expression in gastroesophageal reflux disease, Barrett's esophagus, and esophageal adenocarcinoma: an immunohistochemical and immunoblot study.

Abstract

Cadherins are cell adhesion molecules that are thought to play a vital role in cell-cell adhesion; loss or down-regulation of their expression has been implicated in neoplasia. Barrett's esophageal columnar metaplasia (BE) is a premalignant lesion for esophageal adenocarcinoma with clinical symptoms similar to those of gastroesophageal reflux disease and esophagitis. In this study, we investigated the potential relationship between E-cadherin expression and inflammation, metaplasia, and carcinogenesis in esophagitis, BE, and esophageal adenocarcinoma. Endoscopically obtained mucosal biopsy specimens of esophagitis (n = 6), BE with or without dysplasia (n = 16), and esophageal adenocarcinoma (n = 6) were analyzed for the expression of E-cadherin by both Western analysis and immunoperoxidase staining. Densitometric analysis of Western blots revealed the expression of E-cadherin to be significantly lower in patients with BE compared with normal esophageal epithelium, regardless of the presence or absence of dysplasia (p < 0.03). No significant differences were noticed between the normal esophagus and the esophagitis groups. In the adenocarcinoma group, one patient showed complete loss of E-cadherin expression, and the other five patients showed significantly reduced expression that was even lower than that in BE (p < 0.01). Immunoperoxidase staining matched the Western analysis results. We conclude that loss of or reduced E-cadherin expression may play a role in the progression of BE to adenocarcinoma.