三羟异黄酮对人乳腺癌细胞外调节激酶影响

李晶; 李忠; 莫宝庆

doi:10.11847/zgggws2006-22-05-23

三羟异黄酮对人乳腺癌细胞外调节激酶影响

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

摘要

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。

Abstract:
Objective To investigate the effects of genistein on ERK1/2 MAPK signaling transduct ion 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, e-Jun and e-Fos protein expressions were detected by Western blot.
Results MTT assay showed that compared to control cells, after 48 h treatment of different concentr ations of genistein and MEK1/2 inhibitor, the cell survival ratios decreased.Western blot showed that the protein expressions of ERK 1/2, c-Junand c-Fos increased with the dose of genistein, while that of the combination of genistein and the MEK/2 inhibitio n 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.

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