A supercritical-CO2 extract of Ganoderma lucidum spores inhibits cholangiocarcinoma cell migration by reversing the epithelial-mesenchymal transition
A supercritical-CO2 extract of Ganoderma lucidum spores inhibits cholangiocarcinoma cell migration by reversing the epithelial-mesenchymal transition
复制标题
灵芝孢子的超临界 CO2 提取物通过逆转上皮间质转化抑制胆管癌细胞迁移
DOI：
10.1016/j.phymed.2016.02.019
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发表时间：
2016-05-15
期刊：
影响因子：
7.9
通讯作者：
Liu, Xin
中科院分区：
文献类型：
--
作者：
Li, Lian;Guo, Hui-Jun;Liu, Xin
背景：Ganoderma Lucidum（G。lucidum）是一种东方医学蘑菇，数百年来在亚洲国家广泛使用，以预防和治疗不同的疾病，包括癌症。 G. lucidum孢子的超临界-CO2提取物在转化生长因子β1（TGF-beta 1）诱导的上皮 - 间质转变上（EMT）的胆管癌细胞。研究：这是一项对用不同浓度的G. lucidum.methods处理的人胆管癌TFK-1细胞的体外研究：从G. lucidum孢子（GLE）的超临界-CO2提取物（GLE）提取物（GLE）。超临界液二氧化碳完全孢子虫破裂的G. lucidum孢子（SCF-CO2）提取。 GLE在TGF-β1治疗（2 ng/ml）之前与人胆管癌TFK-1细胞预孵育48小时。通过蛋白质印迹和免疫荧光分析EMT标记的变化。通过用胶状素免疫染色评估F-肌动蛋白应激纤维的形成，并使用共聚焦显微镜检查。此外，通过Boyden室分析研究了GLE对TGF-BETA 1诱导的迁移的影响。分子：TGF-BETA 1诱导的E-钙粘蛋白表达的降低与上皮形态和细胞细胞接触的丧失有关。 N-钙粘着蛋白和纤连蛋白的同时增加在主要拉长成纤维细胞样细胞中显而易见。 GLE抑制了TGF-β1诱导的形态变化和钙粘蛋白表达的变化，并抑制了F-肌动蛋白应激纤维的形成，后者是EMT的标志。 GLE还抑制了TGF-BETA 1诱导的TFK-1细胞迁移。结论：我们的发现提供了新的证据，即通过抑制TGF-BETA 1-诱导的EMT，GLE抑制胆管癌在体外抑制胆管癌的迁移。 GLE可以在临床上用于预防和/或治疗癌症转移。 （C）2016年由Elsevier GmbH出版。
Background: Ganoderma lucidum (G. lucidum) is an oriental medical mushroom that has been widely used in Asian countries for centuries to prevent and treat different diseases, including cancer.Hypothesis/Purpose: The objective of this study was to investigate the effect of A supercritical-CO2 extract of G. lucidum spores on the transforming growth factor beta 1 (TGF-beta 1)-induced epithelial-mesenchymal transition (EMT) of cholangiocarcinoma cells.Study design: This was an in vitro study with human cholangiocarcinoma TFK-1 cells treated with varying concentrations of G. lucidum.Methods: A supercritical-CO2 extract of G. lucidum spores (GLE) was obtained from completely sporoderm-broken germinating G. lucidum spores by supercritical fluid carbon dioxide (SCF-CO2) extraction. GLE pre-incubated with human cholangiocarcinoma TFK-1 cells prior to TGF-beta 1 treatment (2 ng/ml) for 48 h. Changes in EMT markers were analyzed by western blotting and immunofluorescence. The formation of F-actin stress fibers was assessed via immunostaining with phalloidin and examined using confocal microscopy. Additionally, the effect of the GLE on TGF-beta 1-induced migration was investigated by a Boyden chamber assay.Results: TGF-beta 1-induced reduction in E-cadherin expression was associated with a loss of epithelial morphology and cell-cell contact. Concomitant increases in N-cadherin and Fibronectin were evident in predominantly elongated fibroblast-like cells. The GLE suppressed the TGF-beta 1-induced morphological changes and the changes in cadherin expression, and also inhibited the formation of F-actin stress fibers, which are a hallmark of EMT. The GLE also inhibited TGF-beta 1-induced migration of TFK-1 cells.Conclusion: Our findings provide new evidence that GLE suppress cholangiocarcinoma migration in vitro through inhibition of TGF-beta 1-induced EMT. The GLE may be clinically applied in the prevention and/or treatment of cancer metastasis. (C) 2016 Published by Elsevier GmbH.