Published online Sep 14, 2014. doi: 10.3748/wjg.v20.i34.12171
Revised: May 23, 2014
Accepted: June 21, 2014
Published online: September 14, 2014
Processing time: 178 Days and 6.4 Hours
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.
Core tip: Aberrant glycosylation of MUC1 is associated with aggressive tumor behavior in many carcinomas. This study evaluated the significance of KL-6/MUC1 glycosylation in pancreatic cancer progression. The results indicate the important involvement of KL-6/MUC1 glycosylation in pancreatic cancer metastasis and invasion, which may be related to the epithelial-mesenchymal transition process. Therapeutic strategies which target glycosylation of KL-6/MUC1 may be useful for controlling the aggressive behavior of pancreatic cancer cells.