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首页> 外文期刊>Journal of Cellular Physiology >Galectin-1 Controls the Proliferation and Migration of Liver Sinusoidal Endothelial Cells and Their Interaction With Hepatocarcinoma Cells
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Galectin-1 Controls the Proliferation and Migration of Liver Sinusoidal Endothelial Cells and Their Interaction With Hepatocarcinoma Cells

机译：Galectin-1控制核扩散和肝正弦内皮细胞迁移与肝癌细胞和他们的相互作用

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摘要

Galectin-1 (Gal1), a -galactoside-binding protein elevated in hepatocellular carcinoma (HCC), promotes epithelial-mesenchymal transition (EMT) and its expression correlates with HCC growth, invasiveness, and metastasis. During the early stages of HCC, transforming growth factor (1) (TGF-(1)) acts as a tumor suppressor; however in advanced stages, HCC cells lose their cytostatic response to TGF-(1) and undergo EMT. Here, we investigated the role of Gal1 on liver endothelial cell biology, and the interplay between Gal1 and TGF-(1) in HCC progression. By Western blot and immunofluorescence, we analyzed Gal1 expression, secretion and localization in HepG2 and HuH-7 human HCC cells, and in SK-HEP-1 human liver sinusoidal endothelial cells (SECs). We used loss-of-function and gain-of-function experiments to down- or up-regulate Gal1 expression, respectively, in HepG2 cells. We cultured SK-HEP-1 cells with conditioned media from HCC cells secreting different levels of Gal1, and demonstrated that Gal1 derived from tumor hepatocytes induced its own expression in SECs. Colorimetric and scratch-wound assays revealed that secretion of Gal1 by HCC cells induced SEC proliferation and migration. Moreover, by fluorescence microscopy we demonstrated that Gal1 promoted glycan-dependent heterotypic adhesion of HepG2 cells to SK-HEP-1 SECs. Furthermore, TGF-(1) induced Gal1 expression and secretion by HCC cells, and promoted HepG2 cell adhesion to SK-HEP-1 SECs through a Gal1-dependent mechanism. Finally, Gal1 modulated HepG2 cell proliferation and sensitivity to TGF-(1)-induced growth inhibition. Our results suggest that Gal1 and TGF-(1) might function coordinately within the HCC microenvironment to regulate tumor growth, invasion, metastasis, and angiogenesis. J. Cell. Physiol. 231: 1522-1533, 2016. (c) 2015 Wiley Periodicals, Inc.
机译：Galectin-1 (Gal1) -galactoside-binding蛋白质在肝细胞癌(HCC)升高,促进epithelial-mesenchymal过渡(EMT)和它的表达与肝细胞癌增长、侵袭性和转移。肝细胞阶段,转化生长因子(1)(TGF -(1))作为一个肿瘤抑制;晚期肝癌细胞失去细胞抑制剂应对TGF -(1)并接受EMT。调查Gal1在肝脏的作用内皮细胞生物学,和相互作用Gal1和TGF -(1)在肝细胞癌的进展。免疫印迹和免疫荧光,我们分析Gal1表达,分泌和本地化HepG2 HuH-7人类肝癌细胞,在SK-HEP-1人类的肝脏正弦内皮细胞(秒)。我们使用功能丧失和功能实验,或调控Gal1表达式,分别在HepG2细胞。培养条件媒体SK-HEP-1细胞肝癌细胞分泌不同级别的Gal1,证明Gal1来自肿瘤肝细胞诱导自己的表达秒。透露,分泌的Gal1肝癌细胞诱导交会扩散和迁移。此外,通过荧光显微镜证明Gal1提升glycan-dependent异形的SK-HEP-1 HepG2细胞的粘附秒。由肝细胞表达和分泌提升HepG2细胞粘附SK-HEP-1秒通过Gal1-dependent机制。调制HepG2细胞增殖全身的敏感TGF -(1)抑制增长。我们的研究结果表明,Gal1和TGF - (1)在肝细胞癌功能协调微环境调节肿瘤的生长,入侵、转移和血管生成。杂志。231:1522 - 1533年,2016年。期刊、公司。

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