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目的:研究金雀异黄素对乳腺癌细胞(MDA-MB-231)浸润能力的影响及其可能机制。方法:不同浓度的金雀异黄素(25～100μmol/L)孵育MDA-MB-231细胞24 h,用Transwell assay检测细胞浸润能力;用免疫印迹法比较细胞内磷酸化和总细胞外信号调节激酶(ERK)蛋白含量的改变;用免疫荧光实验检测细胞内磷酸化ERK的分布;用DHE染色及荧光显微镜检测细胞内超氧阴离子水平。结果:金雀异黄素处理使细胞浸润能力降低;同时,金雀异黄素的处理引起细胞内磷酸化ERK量明显降低,且磷酸化ERK在核内含量明显下降;ERK抑制剂U0126作用于细胞亦能明显降低细胞的浸润能力;金雀异黄素处理还能使细胞内超氧阴离子含量明显下降,超氧阴离子清除剂TEMPOL不仅明显抑制磷酸化ERK含量,同时细胞浸润能力也明显降低。结论:金雀异黄素可能通过抑制乳腺癌细胞的超氧阴离子水平和ERK活性,进而抑制MDA-MB-231乳腺癌细胞的浸润能力。
Objective: To investigate the effect of genistein on the infiltration of breast cancer cells (MDA-MB-231) and its possible mechanism. Methods: MDA-MB-231 cells were incubated with different concentrations of genistein (25-100 μmol / L) for 24 h. The cell infiltration was detected by Transwell assay. The phosphorylation and total extracellular signal (ERK). The distribution of intracellular phosphorylated ERK was detected by immunofluorescence assay. The intracellular superoxide anion level was detected by DHE staining and fluorescence microscopy. Results: Genistein treatment decreased the cell infiltration capacity. At the same time, genistein treatment resulted in a significant decrease of intracellular phosphorylated ERK levels and a marked decrease of phosphorylated ERK in the nucleus; ERK inhibitor U0126 Cells also significantly reduce the infiltration capacity of cells; genistein treatment can make the content of superoxide anion cells decreased significantly, superoxide anion scavenger TEMPOL not only significantly inhibited the phosphorylation of ERK content, while the cell infiltration capacity was significantly reduced. CONCLUSION: Genistein may inhibit the infiltration of MDA-MB-231 breast cancer cells by inhibiting the superoxide anion level and ERK activity of breast cancer cells.