AIM:To evaluate the significance of KL-6/MUC1(a type of MUC1)glycosylation in pancreatic cancer progression.METHODS:KL-6/MUC1 expression was detected by immunohistochemistry in 48 patients with pancreatic duct cell carcinoma.The N-/O-glycosylation inhibitors(tunicamycin and benzyl-N-acetyl-α-galactosaminide)were then used to interfere with KL-6/MUC1 glycosylation in two pancreatic carcinoma cell lines,and the effects on KL-6/MUC1 expression,and cell adhesion and invasion were determined.In addition,protein expression of epithelial-mesenchymal transition markers,E-cadherin and vimentin,were evaluated in cells after treatment with glycosylation inhibitors.RESULTS:Overexpression of KL-6/MUC1 was found in all pancreatic cancer tissues,but not in the surrounding normal pancreatic tissues.The expression profile of KL-6/MUC1 was significantly decreased after treatment with the inhibitors.The adhesion and invasive ability of cancer cells were significantly decreased after drug treatment,and increased E-cadherin and decreased vimentin expression were found.CONCLUSION:KL-6/MUC1 glycosylation is involved in pancreatic cancer metastasis and invasion.Therapeutic strategies which target this may help control the aggressive behavior of pancreatic cancer cells. AIM: To evaluate the significance of KL-6 / MUC1 (a type of MUC1) glycosylation in pancreatic cancer progression. METHODS: KL-6 / MUC1 expression was detected by immunohistochemistry in 48 patients with pancreatic duct cell carcinoma. N- -glycosylation inhibitors (tunicamycin and benzyl-N-acetyl-α-galactosaminide were then used to interfere with KL-6 / MUC1 glycosylation in two pancreatic carcinoma cell lines, and the effects on KL-6 / MUC1 expression, and cell adhesion and invasion were determined. In addition, protein expression of epithelial-mesenchymal transition markers, E-cadherin and vimentin, were evaluated in cells after treatment with glycosylation inhibitors .RESULTS: Overexpression of KL-6 / MUC1 was found in all pancreatic cancer tissues, but not in the surrounding normal pancreatic tissues. The expression profile of KL-6 / MUC1 was significantly decreased after treatment with the inhibitors. adhesion and invasive ability of cancer cells were significantly decreased after drug treatment, and i ncreased E-cadherin and decreased vimentin expression were found. CONCLUSION: KL-6 / MUC1 glycosylation is involved in pancreatic cancer metastasis and invasion. Therapeutic strategies which target this may help control the aggressive behavior of pancreatic cancer cells.