Piwil4基因敲除对HBV感染诱发肝癌细胞模型的抑制作用及相关机制  

Inhibitory effect of Piwil4knockdown on HBV infection-induced hepatoma carcinoma cell model and its related mechanisms

作　　者：刘卉蓉 周胤婵 潘德光 章琴音 余心琦 LIU Hui-rong;ZHOU Yin-chan;PAN De-guang;ZHANG Qin-yin;YU Xin-qi(The First People′s Hospital of Chun′an County,Hangzhou,Zhejiang 311700,China)

机构地区：[1]淳安县第一人民医院手术室,浙江杭州311700 [2]淳安县第一人民医院普外科,浙江杭州311700 [3]淳安县第一人民医院感染科,浙江杭州311700

出　　处：《中华医院感染学杂志》2021年第17期2566-2570,共5页Chinese Journal of Nosocomiology

基　　金：浙江杭州市科技局重点基金资助专病项目(20150733Q53)。

摘　　要：目的分析Piwil4基因敲除抑制乙型肝炎病毒(HBV)感染诱发肝癌细胞模型的相关机制。方法选取HBV全长的稳定肝癌细胞系HepG2.2.15作为HBV感染所诱发的肝癌细胞模型,做Piwil4基因敲除和过表达靶点选择、测序引物设计、质粒构建,转染至HepG2.2.15细胞,分为空白组(HepG2.2.15细胞未做任何处理)、敲除组(Piwil4基因敲除)、过表达组(Piwil4基因过表达)。测定细胞增殖、凋亡、迁移、侵袭及JNK/p38MAPK信号通路蛋白表达量。结果与空白组比较,过表达组Piwil4基因mRNA表达量升高,敲除组Piwil4基因mRNA表达量降低(P<0.05);与空白组比较,过表达组细胞增殖率升高,细胞凋亡率降低,敲除组细胞增殖率降低,细胞凋亡率升高,比较差异具有统计学意义(P<0.05);与空白组比较,过表达组细胞迁移、侵袭数升高,敲除组细胞迁移、侵袭数降低,比较差异具有统计学意义(P<0.05);与空白组比较,敲除组Caspase-3、Bax蛋白表达量升高,Survivin、Bcl-2、MMP-2、MMP-9蛋白表达量降低,JNK、p-JNK蛋白表达量升高,ERK、p-ERK、p38、p-p38蛋白表达量降低(P<0.05)。结论Piwil4基因敲除可抑制HBV感染所诱发的肝癌细胞增殖、迁移、侵袭,促进凋亡,发挥体外抗肿瘤作用,其机制可能与调控JNK/p38MAPK信号通路相关。OBJECTIVE To observe the inhibitory effect of Piwil4knockout on hepatitis B virus(HBV)infection-induced liver cancer cell model and analyze its related mechanisms.METHODS The HBV full-length stable hepatoma cell line HepG2.2.15was selected as the hepatoma cell model induced by HBV infection.Piwil4gene was knocked out,overexpression target was selected,sequencing primers were designed,plasmids were constructed and transfected into HepG2.2.15cells,which were divided into the blank group(unprocessed HepG2.2.15cells),the knockout group(knockout of Piwil4)and the overexpression group(overexpression of Piwil4).The proliferation,apoptosis,migration and invasion of cells as well as expression level of JNK/p38MAPK signaling pathway protein were determined.RESULTS The expression levels of mRNA of Piwil4of the overexpression group was significantly higher than that of the blank group,the expression levels of mRNA of Piwil4of the knockout group was significantly lower than that of the blank group(P<0.05).The proliferation rate of cells of the overexpression group was significantly higher than that of the blank group,the apoptosis rate of the overexpression group was significantly lower than that of the blank group;the proliferation rate of cells of the knockout group was significantly lower than that of the blank group,and the apoptosis rate of the knockout group was significantly higher than that of the blank group(P<0.05).The counts of cell migration and invasion of the overexpression group were significantly greater than those of the blank group,the counts of cell migration and invasion of the knockout group were significantly less than those of the blank group(P<0.05).The expression levels of Caspase-3,Bax proteins of the knockout group were significantly higher than those of the blank group,the expression levels of Survivin,Bcl-2,MMP-2and MMP-9proteins of the knockout group were significantly lower than those of the blank group,the expression levels of JNK,p-JNK proteins were significantly elevated,and the expression le

关 键 词：Piwil4基因敲除 乙型肝炎病毒感染 肝癌 JNK/p38MAPK信号通路 

分 类 号：R510.2[医药卫生—内科学]