乙肝病毒X蛋白激活NF-κB信号通路对AFP表达的影响
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陈孝平

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Hepatitis B virus X protein induces AFP expression by activation of NF-κB signaling pathway
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    摘要:

    目的: 研究乙肝病毒X蛋白(HBx)通过核因子-κB (NF-κB)信号通路对甲胎蛋白(AFP)的调节作用。
    方法:建立稳定转染HBx基因的L02细胞系(L02-HBx),用特异性的NF-κB信号通路阻断剂PDTC阻断该信号通路,荧光双标激光扫描共聚焦显微镜观察转染前后及加入PDTC前后NF-κB信号通路的激活、失活情况,同时用实时定量 PCR和Western Blot技术检测转染前后及加入PDTC前后AFP在mRNA及蛋白水平上的表达变化。
    结果:以L02细胞为参照,转染HBx基因后的L02-HBx细胞NF-κB信号通路被激活,AFP mRNA和蛋白水平较转染前分别增加(2.78±0.43)倍和(4.72±0.53)倍,差异有统计学意义(P<0.05);PDTC作用24 h后L02/HBx细胞NF-κB信号通路阻断,AFP mRNA和蛋白表达分别为(1.40±0.16)倍和(3.12±0.44)倍,与未加入PDTC作用的L02-HBx细胞相比,差异均有统计学意义(P<0.05)。
    结论:NF-κB信号通路是HBx上调AFP表达的途径之一。

    Abstract:

    Abstract:Objective:To study the effect of NF-κB signaling pathway for HBx on up-regulation of alpha-fetoprotein (AFP).
    Methods :On the basis of the establishment of LO2-HBx cell line with stable transfected HBx gene, NF-κB signaling pathway blocker PDTC was introduced to cut off its signal transduction, double fluorescent staining and laser scanning confocal microscopy were applied to study the activation and deactivation of NF-κB signaling pathway, and real-time PCR and Western Blot were facilitated to observe the expression of AFP gene before and after the HBx transfection as well as treating with PDTC.
    Results:The NF-κB signaling pathway of Lo2-HBx cells was activated after transfection with HBx gene. When compared with control Lo2 cells without treatment, the mRNA and protein levels of AFP in Lo2-HBx cells increased (2.78±0.43) and (4.72±0.53) times respectively, this difference was of statistical significance(P<0.05). But the mRNA levels of AFP decreased to (1.40±0.16), and at the same time the expression of AFP also reduced to (3.12±0.44)(P<0.05) when the NF-κB signaling pathway was blocked after treated by 50μmol/L PDTC for 24h respectively.
    Conclusions:NF-κB signaling pathway is one of the routes for HBx to up-regulate the expression of AFP.

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任利, 陈孝平, 张万广, 刘利平, 杨盛力, 梁慧芳.乙肝病毒X蛋白激活NF-κB信号通路对AFP表达的影响[J].中国普通外科杂志,2008,17(8):9-772.
DOI:10.7659/j. issn.1005-6947.2008.08.009

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  • 在线发布日期: 2008-08-25