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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 study the inhibitory effect of equol on the proliferation of human breast cancer cell line MCF-7 and to explore its molecular mechanism. Methods MTT assay was used to determine the effect of different concentrations (0.1, 0.5, 1, 5 and 10 μmol / L) of equol on the proliferation of MCF-7 cells. The effect of equol on the apoptosis rate and cell cycle The expression of bag-1, bcl-2, VEGF, ERK1 / 2, p-ERK1 / 2, p38 and p-p38 protein were detected by Western blot. Results With the increase of equol concentration, the proliferation rate of human breast cancer cell line MCF-7 was decreased (P <0.05), the apoptosis rate was increased, cell cycle was arrested in G0 / G1 phase, and equol was down-regulated bag-1, bcl-2, VEGF, p-ERK1 / 2 and p-p38 protein expression, and have a dose-effect relationship. Conclusion Equol can promote human breast cancer by promoting apoptosis and arresting the cell cycle at G0 / G1 phase, as well as down-regulating bag-1, bcl-2 and VEGF proteins and inhibiting the phosphorylation of ERK1 / 2 and p38 proteins Inhibition of cell proliferation of MCF-7.