中文摘要：

目的探讨表没食子儿茶素没食子酸酯（epigallocaechin-3-gallate，EGCG）对重组人转化生成因子p1（transforming growth factor—β1，TGF-β1）蛋白诱导的头颈鳞癌细胞上皮一问质转化的影响及其分子机制。方法5ng／mlTGF—β1作用于头颈鳞癌Tu686细胞24h后，再加入浓度为20μmo／L的EGCG处理24h，观察其上皮一间质转化的形态学改变；5ng／mlTGF-β1作用24h后，加入不同浓度（0、10、20、30μmol／L）EGCG作用24h，反转录聚合酶链反应（RT—PCR）和Westernblot检测上皮细胞标志物钙黏蛋白（E—cadhefin）、间质细胞标志物波形蛋白（Vimentin）及TGF-β1信号通路抑制性蛋白Smad7的表达；20μmol／LEGCG作用于5ng／mlTGF—β1处理过的Tu686细胞，于不同的时间点（6、12、24h）收集细胞，检测E—cadherin及Vimentin的表达。结果TGF-β1能诱导头颈鳞癌Tu686细胞发生上皮一间质转化形态学及分子水平改变，E—cadherin表达下调、Vimentin的表达增强，TGF-β1信号通路抑制性蛋白Smad7表达下调；EGCG能有效抑制TGF-β1诱导的上皮一问质转化过程，能促进E-cadherin表达上调、Vimentin表达下降及Smad7表达升高。结论EGCG能有效抑制TGF-β1诱导的头颈鳞癌Tu686细胞发生的上皮一间质转化过程，且该抑制作用可能与TGF-β1信号通路中抑制性因子Smad7的表达升高有关。

英文摘要：

Objective To study the effect and molecular mechanism of epigallocaechin-3-gallate （EGCG） on epithelial-mesenchymal transition （EMT） in vitro induced by human recombinant TGF-β1 protein in squamous cell carcinoma of the head and neck. Methods EMT morphological changes of Tu686 cells were observed after sequential treatment of 5 ng/ml TGF-β1 and 20 p, mol/L EGCG. Tu686 cells were collected after the treatment of 5 ng/ml TGF-β1 for 24 h and EGCG with different concentrations （ 0, 10, 20, 30 μmol/L） for another 24 h or 20 Ixmol/L EGCG treatment for different time phase（6, 12, 24 h）. Then RT-PCR and Western-blot were applied to detect mRNA and protien expression level of epithelial cell marker E-cadherin, mesenchymal cell marker Vimentin and Smad7, an inhibit molecule of TGF-β1 mediated pathway in Tu686 cells. Results TGF-β1 successfully induced characterized EMT morphological and molecular changes in Tu686 cells, in which expression of E-cadherin decreased, Vimentin increased and Smad7 declined. However, EGCG could reverse the TGF-β1 mediated process of EMT by downregulating the expression of Vimentin and upregulating the expression of E-cadherin and Smad7. Conclusion EGCG significantly inhibits TGF-β1-mediated EMT inTu686 cell lines of SCCHN, which maybe associated with the upregulated-expression of Smad7, an inhibitor in TGF-β1 signaling pathway.