In the current study, we find that bile acids increase MUC2 expression in SEG-1 esophageal adenocarcinoma cells, and the transcriptional activity of MUC2 promoter reporter construct transiently transfected into SEG-1 was increased by DCA and other bile acids in a dose-dependent fashion, indicating that bile acid-induced MUC2 up-regulation occurs at the transcriptional level. Here, MUC2 is linked to esophageal adenocarcinoma.