圣草酚通过调控c-Myc/AR轴对三阴性乳腺癌MDA-MB-231细胞增殖和凋亡的影响  

Effects of eriodictyol on the proliferation and apoptosis of triple-negative breast cancer MDA-MB-231 cells via c-Myc/AR axis

作　　者：刘汉成[1] 李慧明[1] 张杰[1] 孟庆来[1] 丁实[2] 马立辉[1] Liu Hancheng;Li Huiming;Zhang Jie;Meng Qinglai;Ding Shi;Ma Lihui(Dept of Breast Surgery,Affiliated Hospital of Chengde Medical College,Chengde 067020;Dept of Pharmacology,Chengde Medical College,Chengde 067000)

机构地区：[1]承德医学院附属医院乳腺外科,承德067020 [2]承德医学院药理学教研室,承德067000

出　　处：《安徽医科大学学报》2022年第6期891-896,共6页Acta Universitatis Medicinalis Anhui

基　　金：河北省卫生健康委医学科学研究课题计划(编号:20211331)。

摘　　要：目的 探究圣草酚(Eri)对三阴性乳腺癌MDA-MB-231细胞增殖和凋亡的影响及其可能作用机制。方法 采用不同浓度Eri干预MDA-MB-231细胞后,MTT法检测细胞增殖水平;平板克隆实验检测细胞克隆形成能力;流式细胞术检测细胞凋亡水平;Western blot检测细胞中活性半胱天冬酶-3(Cleaved-caspase-3)、B淋巴细胞瘤-2相关X(Bax)、B淋巴细胞瘤-2(Bcl-2)、细胞髓细胞瘤(c-Myc)、雄激素受体(AR)蛋白表达水平;MDA-MB-231细胞转染si-c-Myc,再联合50μmol/L Eri处理,MTT法检测细胞增殖水平;流式细胞术检测细胞凋亡水平;qRT-PCR检测细胞中c-Myc mRNA表达水平;Western blot检测细胞中c-Myc和AR蛋白表达水平。结果 Eri可抑制MDA-MB-231细胞增殖活性,并呈现浓度和时间依赖性。不同浓度Eri处理可降低MDA-MB-231细胞克隆形成能力,促进细胞凋亡,上调Cleaved-caspase-3、Bax蛋白表达水平,下调Bcl-2、c-Myc、AR蛋白表达水平。c-Myc基因沉默可抑制MDA-MB-231细胞增殖活性,促进细胞凋亡,下调c-Myc和AR蛋白表达水平。50μmol/L Eri联合处理不能增强c-Myc基因沉默对MDA-MB-231细胞增殖的抑制作用和凋亡的促进作用。结论 Eri可抑制三阴性乳腺癌MDA-MB-231细胞增殖,并诱导其凋亡,其作用机制可能与调控c-Myc/AR轴有关。Objective To explore the effect of eriodictyol(Eri)on the proliferation and apoptosis of triple-negative breast cancer MDA-MB-231 cells and its possible mechanism.Methods MDA-MB-231 cells were treated with different concentrations of Eri.MTT method was used to detect the level of cell proliferation.Plate clone method was used to detect the the level of cell clonality.The apoptosis level was detected by flow cytometry.Western blot was used to detect protein expression levels of Cleaved-caspase-3,Bax,Bcl-2,c-Myc and AR.MDA-MB-231 cells were transfected with si-c-Myc and then combined treatment with 50μmol/L Eri.MTT method was used to detect the level of cell proliferation.The apoptosis level was detected by flow cytometry.Western blot was used to detect protein expression levels of c-Myc and AR.Results Eri inhibited the proliferation activity of MDA-MB-231 cells in a dose and time-dependent manner.Treatment with different concentrations of Eri reduced cloning ability of MDA-MB-231 cells,promoted cell apoptosis,up-regulated the protein expression levels of Cleaved-caspase-3 and Bax,and down-regulated the protein expression level of Bcl-2,c-Myc and AR.Knockdown of c-Myc expression inhibited MDA-MB-231 cells growth,promoted cell apoptosis,and down-regulated the protein expression level of c-Myc and AR,while combined treatment with 50μmol/L Eri could not enhance the situation.Conclusion Er inhibits proliferation and induces apoptosis in triple-negative breast cancer MDA-MB-231 cells,which may be achieved by inhibiting c-Myc/AR axis.

关 键 词：圣草酚 三阴性乳腺癌 增殖 凋亡 C-MYC 雄激素受体 

分 类 号：R285[医药卫生—中药学]