中国药理学通报2018，Vol.34Issue(5)：690-694,5.DOI:10.3969/j.issn.1001-1978.2018.05.020
NF-κB和MAPK信号通路参与金雀异黄酮诱导乳腺癌MDA-MB-231细胞凋亡的体外研究
In vitro study of genistein inducing apoptosis in MDA-MB-231 breast cancer cells via NF-κB and MAPK signaling pathways
摘要
Abstract
Aim To study the effect of genistein on apoptosis in human breast cancer MDA-MB-231 cells and the underlying mechanisms. Methods MTT as-say was used to observe the inhibitory rate on human breast cancer MDA-MB-231 cells treated with genistein. Colony assay was used to determine the cell colony formation rate on human breast cancer MDA-MB-231 cells treated with genistein. Western blot was used to detect the expression of Bcl-2, Bax, caspase-3,NF-κB, ERK, p-ERK, JNK and p-JNK in human breast cancer MDA-MB-231 cells treated with genistein. Results The results of MTT assay showed that genistein inhibited the viability of breast cancer MDA-MB-231 cells in a time- and concentration-de-pendent manner. Colony assay suggested that genistein had an antiproliferative effect on MDA-MB-231 cells. The expression levels of Bcl-2, NF-κB and p-ERK were significantly down-regulated compared with con-trol(P < 0.01). However, the expression of Bax, caspase-3 and p-JNK was significantly up-regulated(P<0.01). Conclusions Genistein could inhibit the growth of human breast cancer MDA-MB-231 cells and induce apoptosis,and the mechanism may be related to the inhibition of NF-κB, ERK/MAPK signaling path-ways and the activation of JNK/MAPK signaling path-way.关键词
金雀异黄酮/乳腺癌/MDA-MB-231细胞/凋亡/NF-κB/ERK/JNKKey words
genistein/breast cancer/MDA-MB-231 cells/apoptosis/NF-κB/ERK/JNK分类
医药卫生引用本文复制引用
韦立群,徐成飞,李婉婷,潘晓杭,黄道航,甘嘉亮,唐双意..NF-κB和MAPK信号通路参与金雀异黄酮诱导乳腺癌MDA-MB-231细胞凋亡的体外研究[J].中国药理学通报,2018,34(5):690-694,5.基金项目
广西研究生教育创新计划项目(No YCSW2017110) （No YCSW2017110）
广西高校科学技术研究项目(No 2013ZD015) （No 2013ZD015）
广西卫生计生委自筹课题(No Z2016290) （No Z2016290）
