摘要
目的探究微小RNA-203(miR-203)靶向磷脂酰肌醇-3-激酶/蛋白激酶B(PI3K/Akt)通路抑制乙型肝炎病毒感染肝癌细胞迁移、侵袭的机制.方法检测肝细胞HL-7702、乙型肝炎病毒感染肝癌细胞HepG2中miR-203表达;人肝癌细胞HepG2传代培养后分为对照组,沉默组,过表达组;对照组为不做任何处理的人乙型肝炎病毒感染肝癌细胞,沉默组为人乙型肝炎病毒感染肝癌细胞做miR-203沉默质粒转染,过表达组为人乙型肝炎病毒感染肝癌细胞做miR-203过表达质粒转染;鉴定miR-203转染效率,分析上调miR-203对人乙型肝炎病毒感染肝癌细胞迁移、侵袭、MAPK通路蛋白表达量的影响.结果与正常肝细胞HL-7702相比,乙型肝炎病毒感染肝癌细胞HepG2中miR-203表达量上升(P<0.05);与对照组相比,沉默组miR-203、E-钙黏蛋白(E-cadherin)表达量下降,基质金属蛋白酶-9(MMP-9)、血管内皮生长因子(VEGF)、基质金属蛋白酶-2(MMP-2)、Slug、PI3K、Akt表达量上升,过表达组miR-203、E-cadherin表达量上升,MMP-9、VEGF、MMP-2、Slug、PI3K、Akt表达量下降(P<0.05);与沉默组相比,过表达组miR-203、E-cadherin表达量上升,MMP-9、VEGF、MMP-2、Slug、PI3K、Akt表达量下降(P<0.05).结论乙型肝炎病毒感染肝癌细胞经下调miR-203干预后迁移、侵袭数减少,迁移、侵袭相关蛋白表达量得到调节,其机制可能与PI3K/Akt通路得到抑制有关.
OBJECTIVE To investigate the mechanism of micrornA-203(miR-203)targeting phosphatidylinositol-3-kinase/protein kinase B(PI3K/Akt)pathway to inhibit the migration and invasion of hepatitis B virus-infected hepatocellular carcinoma cells.METHODS The expression of miR-203 in hepatocytes HL-7702 and hepatitis B virus-infected hepatocellular carcinoma cells HepG2 was detected.HepG2 human hepatocellular carcinoma cells were divided into control group,silencing group and overexpression group after passage cultivation.The control group was human hepatitis B virus-infected hepatocellular carcinoma cells without any treatment,the silencing group was human hepatitis B virus-infected hepatocellular carcinoma cells transfected with miR-203 silencing plasmid,and the overexpression group was human hepatitis B virus-infected hepatocellular carcinoma cells transfected with miR-203 overexpression plasmid.The transfection efficiency of miR-203 was evaluated,and the effects of up-regulation of miR-203 on the migration,invasion,and MAPK pathway protein expression of human hepatitis B virus-infected hepatocellular carcinoma cells were analyzed.RESULTS Compared with normal hepatocytes HL-7702,the expression of miR-203 in hepatitis B virus-infected hepatocellular carcinoma cell HepG2 was increased(P<0.05).Compared with the control group,the expression levels of miR-203 and E-cadherin decreased,while the expression levels of matrix metalloproteinase-9(MMP-9),vascular endothelial growth factor(VEGF),matrix metalloproteinase-2(MMP-2),Slug,PI3K and Akt increased in the silencing group.The expression levels of miR-203 and Ecadherin in the overexpression group were increased,while the expression levels of MMP-9,VEGF,MMP-2,Slug,PI3K and Akt were decreased(P<0.05).Compared with the silencing group,the expressions of miR-203 and E-cadherin in the overexpression group were increased,and the expressions of MMP-9,VEGF,MMP-2,Slug,PI3K and Akt were decreased(P<0.05).CONCLUSION After the intervention of down-regulated miR-203,the number of migration a
作者
盛盼
张荣贵
黄涛
刘成成
宋现宽
SHENG-Pan;ZHANG Rong-gui;HUANG Tao;LIU Cheng-cheng;SONG Xian-kuan(Dongrihu People's Hospital,Wuhan,Hubei 430000,China)
出处
《中华医院感染学杂志》
CAS
CSCD
北大核心
2024年第11期1611-1615,共5页
Chinese Journal of Nosocomiology
基金
武汉市医学科研项目立项基金资助项目(WG22D12)。
