Inhibition of KL-6/MUC1 glycosylation limits aggressive progression of pancreatic cancer

Autor: Norihiro Kokudo, Ke-Ming Zhang, Xin Zhao, Wei Tang, Huanli Xu
Rok vydání: 2014
Předmět:
Research Report
Male
Acetylgalactosamine
Glycosylation
Time Factors
Metastasis
chemistry.chemical_compound
Cell Movement
Enzyme Inhibitors
skin and connective tissue diseases
MUC1
Aged
80 and over
Tunicamycin
Gastroenterology
General Medicine
Middle Aged
Cadherins
Adenocarcinoma
Papillary
Disease Progression
Female
CA19-9
Carcinoma
Pancreatic Ductal
Adult
Epithelial-Mesenchymal Transition
Antineoplastic Agents
Biology
digestive system
Antigens
CD
Cell Line
Tumor
Pancreatic cancer
Benzyl Compounds
Biomarkers
Tumor
Cell Adhesion
medicine
Humans
Vimentin
Neoplasm Invasiveness
Epithelial–mesenchymal transition
Cell adhesion
neoplasms
Aged
Cell Proliferation
Dose-Response Relationship
Drug
Mucin-1
medicine.disease
biological factors
digestive system diseases
Pancreatic Neoplasms
chemistry
Immunology
Cancer research
Neoplasms
Cystic
Mucinous
and Serous
Zdroj: World Journal of Gastroenterology. 20:12171
ISSN: 1007-9327
Popis: To evaluate the significance of KL-6/MUC1 (a type of MUC1) glycosylation in pancreatic cancer progression.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.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.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.
Databáze: OpenAIRE
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