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

被引:31
作者
Zhan, Ling [1 ,2 ]
Chen, Lianyu [1 ,2 ]
Chen, Zhen [1 ,2 ]
机构
[1] Fudan Univ, Shanghai Canc Ctr, Dept Integrat Oncol, 270 Dong An Rd, Shanghai 200032, Peoples R China
[2] Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai 200032, Peoples R China
基金
美国国家科学基金会;
关键词
fucosyltransferase; metastasis; E-selectin; epithelial-to-mesenchymal transition; pancreatic cancer; EPITHELIAL-MESENCHYMAL TRANSITION; SIALYL LEWIS(A); E-SELECTIN; CARCINOMA CELLS; METASTATIC PROPERTIES; PROGNOSTIC VALUE; STEM-CELLS; EXPRESSION; ADHESION; ANTIGEN;
D O I
10.3892/ol.2018.8738
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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)-beta-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.
引用
收藏
页码:924 / 930
页数:7
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