Overexpressed N-fucosylation on the cell surface driven by FUT3, 5, and 6 promotes cell motilities in metastatic pancreatic cancer cell lines.

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  • Additional Information
    • Source:
      Publisher: Elsevier Country of Publication: United States NLM ID: 0372516 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1090-2104 (Electronic) Linking ISSN: 0006291X NLM ISO Abbreviation: Biochem Biophys Res Commun Subsets: MEDLINE
    • Publication Information:
      Publication: <2002- >: San Diego, CA : Elsevier
      Original Publication: New York, Academic Press.
    • Subject Terms:
      Fucosyltransferases/*genetics ; Pancreatic Neoplasms/*genetics; Cell Line, Tumor ; Cell Movement ; Fucose/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Neoplasm Invasiveness/genetics ; Neoplasm Metastasis/genetics ; Up-Regulation
    • Abstract:
      Pancreatic cancer is a highly malignant tumor of the digestive system. Previous studies have shown that abnormal cell surface glycosylation is associated with cancer metastasis, which suggests that glycosylation changes may open a new window for discovering metastasis-related pathways. In this study, we used a microarray with 55 lectins to screen for altered glycosylation between two metastatic pancreatic cancer lines (Capan-1 and Su.86.86) and two nonmetastatic pancreatic cancer lines (Panc-1 and MIA PaCa-2), and we further analyzed three lectins with high-binding activities (AAL, UEA-I, and PHA-E) in cell motility assays using these pancreatic cancer cells to detect whether blocking certain forms of cell surface glycosylation affects any processes associated with metastasis. As a result, we found that AAL, a fucose-specific lectin, has different binding patterns between metastatic pancreatic cancer and nonmetastatic pancreatic cancer lines and inhibits cell motility in metastatic pancreatic cancer cells. Furthermore, the N-fucosylation-related genes FUT3, 5, and 6 were found to be responsible for the elevated fucosylation in metastatic pancreatic cells through real-time PCR screening. In summary, our findings that the specific bindings of AAL on cell surfaces and highly expressed FUT3, 5, and 6 in metastatic pancreatic cancer cells, although preliminary, are encouraging, and our established combined method is also suitable for discovering metastasis-related mechanisms in other cancers.
      (Copyright © 2019. Published by Elsevier Inc.)
    • Contributed Indexing:
      Keywords: Lectin microarray; Metastasis; N -fucosylation; Pancreatic cancer cells
    • Accession Number:
      28RYY2IV3F (Fucose)
      EC 2.4.1.- (FUT5 protein, human)
      EC 2.4.1.- (Fucosyltransferases)
      EC 2.4.1.65 (3-galactosyl-N-acetylglucosaminide 4-alpha-L-fucosyltransferase)
      EC 2.4.1.65 (FUT6 protein, human)
    • Publication Date:
      Date Created: 20190228 Date Completed: 20191216 Latest Revision: 20210830
    • Publication Date:
      20231215
    • Accession Number:
      10.1016/j.bbrc.2019.02.092
    • Accession Number:
      30808544