摘要
目的探讨滇重楼皂苷对前列腺癌细胞增殖、周期和促凋亡的作用,以及对磷酸化CDK2表达的影响。方法使用不同浓度(0.1、0.3、1.0、3.0、10.0μmol/L)的滇重楼皂苷处理前列腺癌细胞株PC-3和Du145,应用MTT和流式细胞技术检测细胞增殖、周期分布和凋亡的改变,进一步运用免疫印迹法检测细胞周期及凋亡相关蛋白表达的改变。结果滇重楼皂苷明显抑制前列腺癌细胞株(PC-3及Du145)的增殖,使细胞在G0/G1期发生阻滞,并诱导细胞显著凋亡,抑制效果呈时间剂量梯度依赖关系;p21蛋白与Cleaved-Caspase-3表达水平明显上调,磷酸化CDK2、磷酸化RB蛋白下调。结论滇重楼皂苷增加p21蛋白水平,抑制细胞周期关键调控因子CDK2及RB的磷酸化,并且激活Caspase-3参与的细胞凋亡信号通路,从而抑制前列腺癌细胞增殖、阻断细胞周期,并诱导细胞凋亡,具有抗肿瘤活性。
Objective To investigate the effects of polyphyllinⅠon the proliferation,cell cycle and apoptosis of prostate cancer cells,and to explore its effect on the expression of phosphorylated CDK2.Methods PC-3 and Du145 cells were treated with different concentrations of polyphyllinⅠ(0.1,0.3,1.0,3.0,10.0μmol/L).The changes of cell proliferation,cell cycle and apoptosis were detected with MTT and flow cytometry.The effects of polyphyllinⅠon cell cycle and apoptosis-related proteins were further detected with Western blotting.Results PolyphyllinⅠsignificantly inhibited the proliferation of PC-3 and Du145 cells,especially in G0/G1 phase,and induced apoptosis in a time-and dose-dependent manner.The expressions of P21 and Cleaved caspase-3 were significantly up-regulated,while the expressions of phosphorylated CDK2 and RB were down-regulated.Conclusion PolyphyllinⅠcan inhibit the phosphorylation of CDK2 and RB by upregulating the protein expression of P21 and activating Caspase-3-mediated apoptosis signaling pathway.It has anti-tumor effect by inhibiting the proliferation of prostate cancer cells,arresting the cell cycle,and inducing cell apoptosis.
作者
申正超
申吉泓
谢星星
宋娜
李旭华
石西南
柯坤彬
SHEN Zhengchao;SHEN Jihong;XIE Xingxing;SONG Na;LI Xuhua;SHI Xinan;KE Kunbin(Department of Urology,The First Affiliated Hospital of Kunming Medical University,Kunming 650032;Yunnan University of Chinese Medicine,Kunming 650500,China)
出处
《现代泌尿外科杂志》
CAS
2021年第10期867-872,共6页
Journal of Modern Urology
基金
国家自然科学基金资助项目(No.81802548,81860451,82060862)
云南省科技厅-昆明医科大学应用基础研究联合专项[No.2019FE001(-064)]
云南省教育厅科学研究基金项目(No.2019Y0356)
昆明医科大学研究生创新基金(No.2020S132)
云南省科技厅-中医联合基础面上基金[No.2019FF002(-050)]。
