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首页> 外文期刊>Cell biology international. >Caveolin-1 upregulates Fut8 expression by activating the Wnt/beta-catenin pathway to enhance HCC cell proliferative and invasive ability
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Caveolin-1 upregulates Fut8 expression by activating the Wnt/beta-catenin pathway to enhance HCC cell proliferative and invasive ability

机译：Caveolin-1通过激活WNT /β-Catenin途径来提高WNT /β-连环蛋白途径来提高HCC细胞增殖和侵入能力

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摘要

Caveolin-1 (Cav-1), a critical structural protein of caveolae, plays an oncogenic role by participating in abnormal protein glycosylation in hepatocellular carcinoma (HCC). However, the mechanism by which Cav-1 regulates glycosylation and glycosyltransferase expression has yet to be fully defined. Here, we show that Cav-1 promotes the expression of alpha-1,6-fucosyltransferase (Fut8), which catalyzes the transfer of GDP-fucose to the core structure of the N-sugar chain. In this study, we show that the mouse HCC cell line, Hepa1-6, which has low Fut8 transcriptional and protein levels, also lacks Cav-1 expression, whereas the mouse HCC cell line, Hca-F, has strong Fut8 expression and high transcriptional and protein levels of Cav-1. Subsequently, Cav-1 overexpression in Hepa1-6 was found to activate Wnt/beta-catenin signaling, which leads to downstream binding of the T cell factor/lymphoid enhancer factor to theFut8promoter region for activation of its transcription. In contrast, knockdown of Cav-1 expression in Hca-F caused the Wnt/beta-catenin pathway to be significantly inhibited, which attenuates the expression of Fut8. We further show that Cav-1-induced upregulation of Fut8 expression enhanced proliferation and invasion by mouse HCC cells in vitro. Our current findings provide molecular evidence that Cav-1 plays an important role in regulating glycosyltransferase expression and may participate in abnormal glycosylation, which mediates the proliferation and invasion of HCC.
机译：Caveolin-1（Cav-1）是caveolae的关键结构蛋白，通过参与肝细胞癌（HCC）的异常蛋白糖基化而发挥致癌作用。然而，Cav-1调节糖基化和糖基转移酶表达的机制尚未完全确定。在这里，我们发现Cav-1促进α-1,6-岩藻糖基转移酶（Fut8）的表达，后者催化GDP-岩藻糖转移到N-糖链的核心结构。在这项研究中，我们发现具有较低Fut8转录和蛋白质水平的小鼠肝癌细胞系Hepa1-6也缺乏Cav-1表达，而小鼠肝癌细胞系Hca-F具有较强的Fut8表达和较高的Cav-1转录和蛋白质水平。随后，在Hepa1-6中发现Cav-1过表达激活Wnt/β-连环蛋白信号，从而导致T细胞因子/淋巴增强子因子下游结合到UT8启动子区域以激活其转录。相反，Hca-F中Cav-1表达的下调导致Wnt/β-连环蛋白途径被显著抑制，从而减弱Fut8的表达。我们进一步表明，Cav-1诱导的Fut8表达上调在体外增强了小鼠肝癌细胞的增殖和侵袭。我们目前的研究结果提供了分子证据，表明Cav-1在调节糖基转移酶表达中起重要作用，并可能参与异常糖基化，从而介导HCC的增殖和侵袭。

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