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绿茶儿茶素通过靶向 COX-2、PGE2 受体和上皮-间充质转化来降低人黑色素瘤细胞的侵袭潜力。

Green tea catechins reduce invasive potential of human melanoma cells by targeting COX-2, PGE2 receptors and epithelial-to-mesenchymal transition.

机构信息

Department of Dermatology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.

出版信息

PLoS One. 2011;6(10):e25224. doi: 10.1371/journal.pone.0025224. Epub 2011 Oct 13.

Abstract

Melanoma is the most serious type of skin disease and a leading cause of death from skin disease due to its highly metastatic ability. To develop more effective chemopreventive agents for the prevention of melanoma, we have determined the effect of green tea catechins on the invasive potential of human melanoma cells and the molecular mechanisms underlying these effects using A375 (BRAF-mutated) and Hs294t (Non-BRAF-mutated) melanoma cell lines as an in vitro model. Employing cell invasion assays, we found that the inhibitory effects of green tea catechins on the cell migration were in the order of (-)-epigallocatechin-3-gallate (EGCG)>(-)-epigallocatechin>(-)-epicatechin-3-gallate>(-)-gallocatechin>(-)-epicatechin. Treatment of A375 and Hs294t cells with EGCG resulted in a dose-dependent inhibition of cell migration or invasion of these cells, which was associated with a reduction in the levels of cyclooxygenase (COX)-2, prostaglandin (PG) E(2) and PGE(2) receptors (EP2 and EP4). Treatment of cells with celecoxib, a COX-2 inhibitor, also inhibited melanoma cell migration. EGCG inhibits 12-O-tetradecanoylphorbol-13-acetate-, an inducer of COX-2, and PGE(2)-induced cell migration of cells. EGCG decreased EP2 agonist (butaprost)- and EP4 agonist (Cay10580)-induced cell migration ability. Moreover, EGCG inhibited the activation of NF-κB/p65, an upstream regulator of COX-2, in A375 melanoma cells, and treatment of cells with caffeic acid phenethyl ester, an inhibitor of NF-κB, also inhibited cell migration. Inhibition of melanoma cell migration by EGCG was associated with transition of mesenchymal stage to epithelial stage, which resulted in an increase in the levels of epithelial biomarkers (E-cadherin, cytokeratin and desmoglein 2) and a reduction in the levels of mesenchymal biomarkers (vimentin, fibronectin and N-cadherin) in A375 melanoma cells. Together, these results indicate that EGCG, a major green tea catechin, has the ability to inhibit melanoma cell invasion/migration, an essential step of metastasis, by targeting the endogenous expression of COX-2, PGE(2) receptors and epithelial-to-mesenchymal transition.

摘要

黑色素瘤是最严重的皮肤疾病类型,也是皮肤疾病导致死亡的主要原因,因为它具有高度转移性。为了开发更有效的化学预防剂来预防黑色素瘤,我们使用 A375(BRAF 突变)和 Hs294t(非 BRAF 突变)黑色素瘤细胞系作为体外模型,确定了绿茶儿茶素对人黑色素瘤细胞侵袭潜力的影响及其潜在机制。采用细胞侵袭实验,我们发现绿茶儿茶素对细胞迁移的抑制作用按以下顺序排列:(-)-表没食子儿茶素-3-没食子酸酯(EGCG)>(-)-表没食子儿茶素>(-)-表儿茶素-3-没食子酸酯>(-)-没食子儿茶素>(-)-表儿茶素。用 EGCG 处理 A375 和 Hs294t 细胞,可剂量依赖性地抑制这些细胞的迁移或侵袭,同时 COX-2、前列腺素(PG)E2 和 PGE2 受体(EP2 和 EP4)的水平降低。用 COX-2 抑制剂塞来昔布处理细胞也抑制黑色素瘤细胞迁移。EGCG 抑制 12-O-十四烷酰佛波醇-13-乙酸酯(COX-2 的诱导剂)和 PGE2 诱导的细胞迁移。EGCG 降低 EP2 激动剂(butaprost)和 EP4 激动剂(Cay10580)诱导的细胞迁移能力。此外,EGCG 抑制 A375 黑色素瘤细胞中 COX-2 的上游调节因子 NF-κB/p65 的激活,用 NF-κB 抑制剂咖啡酸苯乙酯处理细胞也抑制细胞迁移。EGCG 抑制黑色素瘤细胞迁移与间充质阶段向上皮阶段的转变有关,导致上皮生物标志物(E-钙粘蛋白、细胞角蛋白和桥粒蛋白 2)水平升高,间充质生物标志物(波形蛋白、纤连蛋白和 N-钙粘蛋白)水平降低。总之,这些结果表明,绿茶儿茶素 EGCG 通过靶向 COX-2、PGE2 受体和上皮-间充质转化的内源性表达,具有抑制黑色素瘤细胞侵袭/迁移的能力,这是转移的一个重要步骤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6854/3192733/1caaaf86da81/pone.0025224.g001.jpg

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