摘要
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48 h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。
Objective To investigate the effects of genistein on ERK1/2 MAPK signaling transduction pathway of human breastcancer cell 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 dif- ferent concentrations of genistein and MEK1/2 inhibitor, the cell survival ratios decreased. Western blot showed that the protein expressions of ERK1/2, c-Junand c-Fos 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.
出处
《中国公共卫生》
CAS
CSCD
北大核心
2006年第5期546-547,共2页
Chinese Journal of Public Health
基金
国家自然科学基金(30271122)
江苏省科学技术厅项目(BK2002027)
