雌马酚抑制人乳腺癌MCF-7细胞增殖及机制研究  被引量:2

Study on the inhibiting effects of equol on MCF-7 cells proliferation and its molecular mechanisms

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作  者:王萌[1] 任国峰[1] 

机构地区:[1]中南大学公共卫生学院营养与食品卫生学系,长沙410078

出  处:《卫生研究》2014年第1期11-15,共5页Journal of Hygiene Research

基  金:国家自然科学基金(No.30500407)

摘  要:目的研究雌马酚对人乳腺癌细胞MCF-7增殖的抑制作用并初步探讨其分子机制。方法利用MTT法测定不同浓度(0.1、0.5、1、5和10μmol/L)雌马酚对MCF-7细胞增殖率的影响,流式细胞仪测定雌马酚对细胞凋亡率和细胞周期的影响,Western blot测定bag-1、bcl-2、VEGF、ERK1/2、p-ERK1/2、p38以及p-p38蛋白表达。结果随着雌马酚浓度升高,人乳腺癌细胞MCF-7的增殖率下降(P<0.05),细胞凋亡率升高,细胞周期被阻滞于G0/G1期,雌马酚可以下调bag-1、bcl-2、VEGF、p-ERK1/2以及p-p38蛋白表达,并具有一定剂量-效应关系。结论雌马酚可以通过促进细胞凋亡并阻滞细胞周期于G0/G1期,以及下调bag-1、bcl-2、VEGF蛋白、抑制ERK1/2和p38蛋白磷酸化的方式实现对人乳腺癌细胞MCF-7增殖的抑制。Objective To investigate the proliferation inhibition effects of equol on human breast cancer cell line MCF-7 and explore its molecular mechanisms. Methods MCF-7 cells were treated with different concentration of equol, including 0. 1, 0.5, 1, 5 and 10 Ixmol/L. After the treatment, the proliferation rate of cells was examined by MTT method and the cell apoptosis percentage and cell cycle phase were determined by flow cytometry. The bag-l, bcl-2, VEGF, ERK1/2, p-ERK1/2, p38 and p-p38 protein were determined using Western blotting. Results A dose and time effect of proliferation inhibition of equol was proved in MCF-7. The MCF-7 cell apoptosis percentage increased significantly in the groups of equol, and the cell cycle arrest in G0/Ca phase. The expression of bag-l, bel-2, VEGF, p-ERK1/2 and p-p38 protein were decreased gradually with the increase concentration of equol. Conclusion The equol could inhibit the proliferation of the breast cancer cell lines MCF-7 and its inhibitory effect may be due to inducing apoptosis, arresting the cell cycle in G0/G1 phase, down-regulating the expression of bag-l, bcl-2, VEGF, p-ERK1/2 and p-p38 protein.

关 键 词:雌马酚 凋亡 乳腺癌 P38 

分 类 号:R737.9[医药卫生—肿瘤] Q946.885[医药卫生—临床医学]

 

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