It is generally accepted that esophageal adenocarcinoma arises from a Barrett's 
metaplastic lesion. Altered glycoprotein expression has been demonstrated in 
tissue from patients with Barrett's esophagus and esophageal cancer but the 
mechanisms regarding such changes are unknown. The bile acid deoxycholic acid 
(DCA) alters many cell signaling pathways and is implicated in esophageal cancer 
progression. We have demonstrated that DCA disrupts Golgi structure and affects 
protein secretion and glycosylation processes in cell lines derived from normal 
squamous epithelium (HET-1A) and Barrett's metaplastic epithelium (QH). Cell 
surface expression of glycans was identified using carbohydrate-specific probes 
(wheat germ agglutinate, conconavalin A, peanut agglutinin, lithocholic acid and 
Ulex europaeus agglutinin) that monitored N-glycosylation, O-glycosylation and 
core fucosylation in resting and DCA-treated cells. DCA altered intracellular 
localization and reduced cell surface expression of N-acetyl-D-glucosamine, 
α-methyl-mannopyranoside (Man/Glc) and fucose in both cell lines. Furthermore, 
DCA reduced the expression of epithelial growth factor receptor and E-cadherin 
in a manner analogous to treatment of cells with the N-glycan biosynthesis 
inhibitor tunicamycin. This is the first study to identify an altered Golgi 
structure and glycomic profile in response to DCA in esophageal epithelial 
cells, a process which could potentially contribute to metaplasia, dysplasia and 
cancer of the esophagus.