实用肿瘤学杂志 ›› 2024, Vol. 38 ›› Issue (4): 254-261.doi: 10.11904/j.issn.1002-3070.2024.04.007

• 基础研究 • 上一篇    下一篇

β-紫罗兰酮通过NF-κB途径抑制乳腺癌细胞增殖

高光强1, 王发琳1, 李娟2, 田虹1, 果思伽3, 于晓兰4, 杨婷婷1, 刘家仁1   

  1. 1.哈尔滨医科大学附属第四医院检验科(哈尔滨 150001);
    2.云南省阜外心血管病医院检验科;
    3.深圳市妇幼保健医院检验科;
    4.哈尔滨医科大学附属第六医院检验科
  • 收稿日期:2023-12-13 修回日期:2024-08-08 出版日期:2024-08-28 发布日期:2024-09-25
  • 通讯作者: 刘家仁,E-mail:jiarenliu@hrbmu.edu.cn
  • 作者简介:高光强,男,(1970-),硕士,副主任技师,从事临床检验相关的工作。
  • 基金资助:
    国家自然科学基金(编号:82172580)

β-Ionone suppresses breast cancer cell proliferation through the NF-κB pathway

GAO Guangqiang1, WANG Falin1, LI Juan2, TIAN Hong1, GUO Sijia3, YU Xiaolan4, YANG Tingting1, LIU Jiaren1   

  1. 1. Department of Clinical Laboratory,The 4th Affiliated Hospital of Harbin Medical University,Harbin 150001,China;
    2. Department of Clinical Laboratory,Fuwai Yunnan Cardiovascular Hospital;
    3. Department of Clinical Laboratory,Shenzhen Maternity and Child Health Hospital;
    4. Department of Clinical Laboratory,The 6th Affiliated Hospital of Harbin Medical University
  • Received:2023-12-13 Revised:2024-08-08 Online:2024-08-28 Published:2024-09-25

摘要: 目的 探讨β-紫罗兰酮(β-Ionone,BI)通过调节核因子-κB(Nuclear factor kappa-B,NF-κB)对乳腺癌细胞增殖过程的抑制作用及其可能的机制。方法 采用亚甲基蓝(Methylene blue,MB)法和MTT法测定人乳腺癌BT549细胞和MCF-7细胞活性,孔雀石绿磷酸盐法检测蛋白磷酸酶2A(Protein phosphatase 2A,PP2A)活性、免疫印迹法检测磷酸化P65(p-P65)(s536和s311)、PP2A(A、B和C)和磷酸化共济失调毛细血管扩张突变基因(Phosphorylation-ataxia telangiectasia-mutated gene,p-ATM)(s1981)蛋白水平。结果 BI可明显抑制人乳腺癌BT549细胞和MCF-7细胞的增殖,且呈时间和剂量依赖性,差异具有统计学意义(P<0.01)。MCF-7细胞经BI处理后,NF-κB活性被显著抑制,表现为磷酸化P65(s536和s311)的蛋白水平显著降低,PP2A的蛋白水平升高,差异具有统计学意义(P<0.05)。此外,BI还显著地降低PP2A抑制剂冈田酸(Okadaic acid,OA)对MCF-7细胞中P65蛋白和ATM蛋白的磷酸化作用。结论 该研究表明BI通过抑制NF-κB活性来抑制乳腺癌细胞的增殖,其机制可能是BI通过增加PP2A活性调节NF-κB通路。

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

Abstract: Objective This article aimed to explore the inhibitory effect of β-ionone(BI)on the proliferation of breast cancer 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 activity 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 significantly 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 protein,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.

Key words: Breast cancer, β-Ionone, Protein phosphatase 2A, Nuclear factor kappa-B, Ataxia telangiectasia-mutated gene

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