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首页> 外文期刊>Oncology letters >Knockdown of FUT3 disrupts the proliferation, migration, tumorigenesis and TGF-beta induced EMT in pancreatic cancer cells
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Knockdown of FUT3 disrupts the proliferation, migration, tumorigenesis and TGF-beta induced EMT in pancreatic cancer cells

机译:Fut3的敲低扰乱了胰腺癌细胞中诱导EMT的增殖,迁移,肿瘤鉴定和TGF-β

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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.
机译:岩藻糖基转移酶(FUTS)对糖蛋白和糖脂链至关重要,并在选择汀及其配体之间的粘合剂相互作用中发挥重要作用,这有助于肿瘤细胞扩散和转移。虽然多种癌细胞系重高表达Fut3,但本研究研究了不同人类胰腺癌细胞系中FUT3的表达水平。 Fut3在不同胰腺癌细胞中的强迫表达和敲低证明Fut3在细胞增殖中是重要的。使用伤口愈合和Transwell测定,观察​​到Fut3下调的蜡皮-1细胞系中迁移能力下降,与正常的蜡皮-1细胞系相比。此外,证明Fut3的敲低损害了蜡的粘附性与e-SELETIN,抑制转化生长因子(TGF) - 诱导的上皮 - 间充质转变。这些数据表明Fut3的敲低抑制体内和Fut3中的肿瘤内酯可能是一个有前途的目标,旨在降低胰腺癌细胞的转移性毒力。

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