花姜酮纳米颗粒通过p53通路诱导细胞周期阻滞发挥对肝细胞癌细胞的抗肿瘤作用  

Zerumbone nanoparticles induce cell cycle arrest through the p53 pathway and exert antitumor effects on hepatocellular carcinoma cells

作　　者：刘海石[1] 张文林 王鹏 郭佐铭 张玉宝[1] 张松岩[1] Liu Haishi;Zhang Wenlin;Wang Peng;Guo Zuoming;Zhang Yubao;Zhang Songyan(Department of Hepatobiliary and Pancreatic Surgery,Harbin Medical University Cancer Hospital,Harbin 150040,Heilongjiang,China;Yichun Forestry Administration Central Hospital,Yichun 153000,Heilongjiang,China)

机构地区：[1]哈尔滨医科大学附属肿瘤医院肝胆胰外科,黑龙江哈尔滨150040 [2]伊春林业管理局中心医院,黑龙江伊春153000

出　　处：《肝癌电子杂志》2020年第2期44-47,共4页Electronic Journal of Liver Tumor

基　　金：黑龙江省卫生计生委科研课题(2018-239)。

摘　　要：目的:本研究旨在探索花姜酮纳米颗粒对人肝细胞癌细胞抗肿瘤作用及其机制。方法:检测花姜酮纳米颗粒对人肝细胞癌HepG-2细胞的细胞增殖、集落形成、侵袭、p16、p21、p53、CyclinD1及CDK4蛋白在Western-Blot上的表达水平及细胞周期分布的影响。结果:花姜酮纳米颗粒可以上调人肝细胞癌HepG-2细胞p16、p21及p53蛋白的表达,下调CyclinD1和CDK4蛋白的表达,引起细胞周期G1-S期阻滞,使人肝细胞癌HepG-2细胞的增殖,集落形成及侵袭能力下降。结论:花姜酮纳米颗粒通过p53通路引起人肝细胞癌HepG-2细胞周期G1-S期阻滞,抑制其恶性生物学行为。Objective:The purpose of this study was to explore the anti-tumor effect of HJT1-NP on human hepatocellular carcinoma cells and its mechanism.Methods:To investigate HJT1-NP effects on cell proliferation,colony formation,invasion,proteins expression levels of p16,p21,p53,CyclinDl and CDK4 in human hepatocellular carcinoma HepG-2 cells by western-blot analysis and cell cycle distribution.Results:The HJT1-NP could up-regulate the proteins expression of p16,p21 and p53 in human hepatocellular carcinoma HepG-2 cells,down-regulate the proteins expression of CyclinDl and CDK4,induce G1-S phase arrest of cell cycle,and decrease the proliferation,colony formation and invasion ability of human hepatocellular carcinoma HepG-2 cells.Conclusion:HJT1-NP could induce G1-S phase arrest of human hepatocellular carcinoma HepG-2 cells and inhibit its malignant biological behavior through P53 pathway.

关 键 词：花姜酮 纳米 细胞周期 P53蛋白 

分 类 号：R735.7[医药卫生—肿瘤]