ArticleWorld journal of gastroenterology2014
Inhibition of KL-6/MUC1 glycosylation limits aggressive progression of pancreatic cancer.
Article in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Hypoxia‑mediated Krebs von den Lungen‑6 expression in breast cancer: Implications for tumor invasion and metastasis.Oncology reports · 2026Article
- Bulky glycocalyx drives cancer invasiveness by modulating substrate-specific adhesion.PNAS nexus · 2024Article
- Glycosylated modification of MUC1 maybe a new target to promote drug sensitivity and efficacy for breast cancer chemotherapy.Cell death & disease · 2022Article
- Update on the role of C1GALT1 in cancer.Oncology letters · 2022Review
- MUC1: Structure, Function, and Clinic Application in Epithelial Cancers.International journal of molecular sciences · 2021Review
- The glycosylation landscape of pancreatic cancer.Oncology letters · 2019Review
- Serum carbohydrate antigen 153 and renal function in patients with type 2 diabetes mellitus.Journal of clinical laboratory analysis · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo evaluate the significance of KL-6/MUC1 (a type of MUC1) glycosylation in pancreatic cancer progression.
methodsKL-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.
resultsOverexpression 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.
conclusionKL-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.
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