三羟异黄酮对人乳腺癌细胞外调节激酶影响

目的探讨三羟异黄酮（genistein）对人乳腺癌细胞株MDA-MB-231细胞外调节激酶1/2（ERK1/2）MAPK信号转导通路的影响.方法采用四甲基偶氮噻唑蓝（MTT）比色法分别检测三羟异黄酮以及与ERK1/2上游激酶MEK1/2抑制剂联合作用时对MDA-MB-231增殖的抑制作用;应用Western blot蛋白免疫印记法分别检测ERK1/2总蛋白、c-Jun、c-Fos蛋白的表达.结果 MTT结果显示,与对照组相比,三羟异黄酮作用48h后,细胞存活度随浓度增加而降低,合用MEK1/2抑制剂细胞存活度最低;Western blot分析提示,随三羟异黄酮剂量的增加,ERK1/2、c-Jun、c-Fos蛋白表达增加,但合用抑制剂后蛋白表达降低.结论三羟异黄酮可以抑制MDA-MB-231细胞增殖,并激活了ERK1/2 MAPK信号转导通路;MEK1/2抑制剂可以抑制三羟异黄酮介导的ERK1/2活化,同时提高三羟异黄酮的肿瘤抑制作用.

Effects of genistein on ERK1/2 MAPK signaling transduction pathway of human breast cancer cell MDA-MB-231

Objective To investigate the effects of genistein on ERK1/2 MAPK signaling transduction pathway of human breastcancer celI MDA-MB-231.Methods The inhibitive effects of genistein and MEK1/2 inhibitor on MDA-MB-231 cells were observed with the methyl thiazolyl tetrazolium(MTT)assay.The ERK1/2 MAPK,c-Jun and c-Fos protein expressions were detected by Western blot.Results MTT assay showed that compared to control cells,after 48?h treatment of different concentrations of genistein and MEK1/2 inhibitor,the cell survival ratios decreased.Western blot showed that the protein expressions of ERK1/2,c-Junand cFos increased with the dose of genistein,while that of the combination of genistein and the MEK/2 inhibition decreased.Conclusion Genistein could inhibit the cell proliferation of MDA-MB-231 and activate the ERK1/2 MAPK signaling transduction pathway.The inhibitor of MEK1/2 can block ERK1/2 activation and enhance the cancer inhibition effect of genistein.