Hepatitis B virus X protein protects hepatoma and hepatic cells from complement‐dependent cytotoxicity by up‐regulation of CD46
Hepatitis B virus X protein protects hepatoma and hepatic cells from complement‐dependent cytotoxicity by up‐regulation of CD46
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DOI：
10.1016/j.febslet.2013.01.019
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发表时间：
2013-03
期刊：
影响因子：
3.5
通讯作者：
Shuai Zhang;Changliang Shan;Wenjing Cui;Xiaona You;Yumei Du;G. Kong;F. Gao;L. Ye;Xiao-dong Zhang
中科院分区：
文献类型：
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作者：
Shuai Zhang;Changliang Shan;Wenjing Cui;Xiaona You;Yumei Du;G. Kong;F. Gao;L. Ye;Xiao-dong Zhang
乙肝病毒X蛋白(HBX)在肝癌发生过程中参与抗补体依赖性细胞毒(CDC)活性的机制尚不清楚。在此，我们报道HBx能够通过激活涉及cAMP反应元件结合蛋白(CREB)/环氧合酶-2(COX-2)/前列腺素E2(PGE2)/信号转导和转录激活因子3(STAT3)信号通路的启动子活性，上调肝癌细胞和人永生化肝细胞膜结合补体调节蛋白CD46的表达。而CD46的表达下调则使肝癌细胞对CDC的耐药能力丧失。因此，我们得出结论，HBx通过上调CD46的表达来保护肝癌和肝细胞免受CDC的侵袭。
The involvement of hepatitis B virus X protein (HBx) in anti-complement-dependent cytotoxicity (CDC) activity during hepatocarcinogenesis is poorly understood. Here, we report that HBx is able to up-regulate membrane-bound complement regulatory protein CD46 in hepatoma cells and human immortalized liver cells through activating the promoter activity involving cAMP response element-binding protein (CREB)/cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2)/signal transducers and activators of transcription 3 (STAT3) signaling pathway. In contrast, the down-regulation of CD46 abolishes the resistance capability of hepatoma cells to CDC. Thus, we conclude that HBx contributes to the protection of hepatoma and hepatic cells from CDC by up-regulation of CD46.