World journal of gastroenterology · 2014
Inhibition of KL-6/MUC1 glycosylation limits aggressive progression of pancreatic cancer.
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Xu Huan-Li, Zhao Xin, Zhang Ke-Ming, Tang Wei, Kokudo Norihiro
Аннотация
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.
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.
Предметные рубрики MeSH
AcetylgalactosamineAdenocarcinoma, PapillaryAdultAgedAged, 80 and overAntigens, CDAntineoplastic AgentsBenzyl CompoundsBiomarkers, TumorCadherinsCarcinoma, Pancreatic DuctalCell AdhesionCell Line, TumorCell MovementCell ProliferationDisease ProgressionDose-Response Relationship, DrugEnzyme InhibitorsEpithelial-Mesenchymal TransitionFemaleGlycosylationHumansMaleMiddle AgedMucin-1Neoplasm InvasivenessNeoplasms, Cystic, Mucinous, and SerousPancreatic NeoplasmsTime FactorsTunicamycinVimentin