Epigallocatech in-3-gallate inhibits the invasion of human oral cancer cells and decreases the productions of matrix metalloproteinases and urokinase-plasminogen activator
Epigallocatech in-3-gallate inhibits the invasion of human oral cancer cells and decreases the productions of matrix metalloproteinases and urokinase-plasminogen activator
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DOI：
10.1111/j.1600-0714.2007.00588.x
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发表时间：
2007-11-01
影响因子：
3.3
通讯作者：
Chang, Yu-Chao
中科院分区：
文献类型：
--
作者：
Ho, Yung-Chuan;Yang, Shun-Fa;Chang, Yu-Chao
背景：绿茶多酚被认为对人体健康有益，尤其是近年来作为癌症化学预防剂。表没食子儿茶素没食子酸酯（EGCG）是绿茶中含量最丰富的多酚，在动物和流行病学研究中已被证明可抑制结肠肿瘤发生，然而其在口腔癌变中的作用仍有待阐明。
方法：采用细胞毒性、侵袭和迁移实验来研究人舌癌细胞系OC2细胞暴露于EGCG后的影响。为了明确EGCG在癌症转移中的具体作用，进行明胶酶谱和酪蛋白酶谱分析以评估EGCG对OC2细胞中基质金属蛋白酶（MMP）-2、MMP - 9和尿激酶型纤溶酶原激活剂（uPA）分泌的影响。
结果：在无细胞毒性的情况下，EGCG对OC2细胞的侵袭和迁移表现出剂量依赖性抑制作用（P < 0.05）。还发现EGCG以浓度依赖的方式降低MMP - 2、MMP - 9和uPA的表达（P < 0.05）。
结论：综上所述，这些结果表明EGCG能够抑制人口腔癌细胞的侵袭和迁移，其作用可能部分归因于MMP - 2、MMP - 9和uPA产生的减少。
BACKGROUND: Green tea polyphenols are considered beneficial to human health, especially as cancer chemopreventive agents in recent years. Epigallocatechin3-gallate (EGCG), the most abundant polyphenol in green tea, has been proven to suppress colonic tumorigenesis in animal and epidemiological studies, whereas its role in the oral carcinogenesis remains to be elucidated.METHODS: Cytotoxicity, invasion, and migration assays were used to investigate the effects of human oral cancer cell line OC2 cells exposed to EGCG. To look at the precise involvement of EGCG in cancer metastasis, gelatin zymography and casein zymography were performed to evaluate the impacts of EGCG on matrix metalloproteinase (MMP)-2, MMP-9, and urokinase plasminogen activator (uPA) secretion in OC2 cells.RESULTS: EGCG exhibited a dose-dependent inhibitory effect on the invasion and migration of OC2 cells in the absence of cytotoxicity (P < 0.05). EGCG was also found to decrease the expressions of MMP-2, MMP-9, and uPA in a concentration-dependent manner (P < 0.05).CONCLUSION: Taken together, these results suggest that EGCG could inhibit the invasion and migration of human oral cancer cells and that the effects may partially because of the decreased productions of MMP-2, MMP-9, and uPA.