AIM: To investigate the effect of Genistein on epithelial-mesenchymal transdifferentiation (EMT) induced by transforming growth factor-β1 (TGF-βl) in human pancreatic cancer cell line Panc-1, and to explore the mechanism of Genistein inhibiting invasion of Panc-1 cells. METHODS: Panc-1 cells were treated with TGF-β1 and Genistein (0, 1, 25, 50 μmol/L), and those treated with PSB served as controls. Tran- swell chamber assay was performed to deter- mine the invasion ability change of Panc-1 cells. Reverse transcription-polymerase chain reaction (RT-PCR)was used to estimate the mRNA expression of vimentin and E-cadherin.Western bloting assay was used to measure the protein expression of E-cadherin.Cell structure was observed by microscopy. RESULTS:TGF-βl obviously promoted EMT and invasion abilibty of Panc-1 cells.Not only the invasion ability but also EMT induced by TGF-βl were significantly inhibited by Genistein in a dose-dependent manner.The number of Panc-1 cells was larger in 0μmol/L Genistein group than that in the control group(99.16±11.30 vs 65.46±8.99,P<0.05).Genistein at concentraion of 50μmol/L down-regulated the mRNA expression of vimentin and up-regulated the mRNA and protein expression of E-cadherin.The characteristic morphology of EMT was reversed. CONCLUSION:Genistein can inhibit TGF-β1-induced invasion of Panc-1 cells remarkably, which may be one of its anti-invasion mechanisms.

目的:研究金雀异黄素对人胰腺癌细胞系Panc-1诱导细胞上皮-间质样转化的作用,以探讨金雀异黄素抑制胰腺癌侵袭作用的机制.
方法:用TGF-β1和不同浓度金雀异黄素(0、1、25、50微摩尔/升)处理Panc-1细胞,对照组加入等量PSB.采用Transwell小室法检测金雀异黄素作用于TGF-β1诱导Panc-1细胞后侵袭力的变化;RT-PCR技术检测波形蛋白(Vimentin)、E-钙依赖黏附素(E-Cadherin)的mRNA表达;Western blot蛋白印迹法检测E-Cadherin蛋白的表达;应用显微镜观察分析细胞结构的改变.
结果:TGF-β1对Panc-1细胞有显著诱导上皮-间质转化的作用,并增加细胞侵袭力, 金雀异黄素不但对诱导后Panc-1细胞侵袭力有抑制,对细胞上皮-间质样转化也有抑制,且这种作用呈剂量依赖性。0微摩尔/升金雀异黄素组细胞计数明显比对照组高(99.16±11.30vs65.46±8.99,P<0.05),50微摩尔/升金雀异黄素处理诱导后细胞48h,细胞侵袭力下降,Vimentin mRNA表达水平降低, 而E-Cadherin mRNA和蛋白表达水平升高,细胞形态学间质样特性被逆转.
结论: 金雀异黄素具有明显抑制TGF-β1诱导的人胰腺癌细胞Panc-1侵袭力的作用,这可能是其抗侵袭作用的机制之一.