Objective This article aimed to explore the inhibitory effect of β-ionone(BI)on the proliferation of breast canc-er cells through the nuclear factor kappa-B(NF-κB)pathway and its possible mechanism.Methods The methylene blue assay and MTT assay were used to determine the viability of breast cancer cells.The malachite green phosphate assay was used to detect the ac-tivity of protein phosphatase 2A(PP2A).Western blot was used to detect the levels of phosphorylated P65(s534 and s311)(p-P65),PP2A(A,B and C),and phosphorylated ataxia telangiectasia mutant(p-ATM)(s1981)protein.Results BI could significant-ly inhibit the proliferation of human breast cancer BT549 cells and MCF-7 cells in a time-and dose-dependent manner,and the difference was statistically significant(P<0.01).After treated with BI,NF-κB activity was significantly inhibited in MCF-7 cells,as shown by a significant decrease in the level of phosphorylated P65(s311 and s534)protein and an increase in the level of PP2A pro-tein,and the difference was statistically significant(P<0.05).In addition,BI also significantly reduced the phosphorylation of P65 protein and ATM protein in MCF-7 cells by the PP2A inhibitor-okada acid(OA).Conclusion This study shows that BI inhibits the proliferation of breast cancer cells by inhibiting NF-κB activity,and its mechanism may be achieved by increasing PP2A activity to regulate the NF-κB pathway.
关键词
乳腺癌/β-紫罗兰酮/蛋白磷酸酶2A/核因子-κB/共济失调毛细血管扩张突变基因
Key words
Breast cancer/β-Ionone/Protein phosphatase 2A/Nuclear factor kappa-B/Ataxia telangiectasia-mutated gene
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