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Knockdown of FUT3 disrupts the proliferation, migration, tumorigenesis and TGF-β induced EMT in pancreatic cancer cells

Fucosyltransferases (FUTs) are critical for glycoproteins and glycolipid chains and serve an important role in the adhesive interaction between selectins and their ligands, which contribute to tumor cell spread and metastasis. While multiple cancer cell lines heavily express FUT3, the present study...

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Detalles Bibliográficos
Autores principales: Zhan, Ling, Chen, Lianyu, Chen, Zhen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6019892/
https://www.ncbi.nlm.nih.gov/pubmed/29963165
http://dx.doi.org/10.3892/ol.2018.8738
Descripción
Sumario:Fucosyltransferases (FUTs) are critical for glycoproteins and glycolipid chains and serve an important role in the adhesive interaction between selectins and their ligands, which contribute to tumor cell spread and metastasis. While multiple cancer cell lines heavily express FUT3, the present study investigated the expression level of FUT3 in different human pancreatic cancer cell lines. Forced expression and knockdown of FUT3 in different pancreatic cancer cell line demonstrated that FUT3 is important in cell proliferation. Using wound healing and transwell assays, it was observed that the migratory ability was decreased in FUT3 downregulated Capan-1 cell line, compared with the normal Capan-1 cell line. Furthermore, it was demonstrated that the knockdown of FUT3 impaired the adhesion of Capan-1 with E-selectin and inhibited transforming growth factor (TGF)-β-induced epithelial-mesenchymal transition. These data suggest that the knockdown of FUT3 inhibits the tumorigenesis in vivo and FUT3 may be a promising target aiming at reducing the metastatic virulence of pancreatic cancer cells.