中文摘要：

肝炎 B 病毒 X 蛋白质(HBx ) 在 hepatocellular 癌的发展起一个关键作用。这里，我们寻求了识别 HBx 由调停的机制肝房间增长。我们发现那 HBx upregulated cyclooxygenase-2 (COX-2 ) 的层次， 5-lipoxygenase (5 哈鱼) 和 phosphorylated 在肝房间的细胞外的调整信号的蛋白质 kinases 1/2 (p-ERK1/2 ) 。导致 HBx 的 p-ERK1/2 被 Gi/o 蛋白质，艇长或哈鱼的抑制废除。另外， HBx 增加了前列腺素 E2 (PGE2 ) 的数量，免除房间线的 leukotriene B4 (LTB4 ) 源于 hepatocytes。而且，这些释放 arachidonic 酸代谢物能激活 ERK1/2。有趣地，激活 ERK1/2 能 upregulate 以一种积极反馈方式的 COX-2 和 5 哈鱼的表示。在结论， HBx 经由包含 COX-2， 5 哈鱼，释放 arachidonic 酸代谢物， Gi/o 蛋白质和 p-ERK1/2 的一个积极反馈环提高并且维持肝房间增长。

英文摘要：

Hepatitis B virus X protein （HBx） plays a crucial role in the development of hepatocellular carcinoma. Here, we sought to identify the mechanisms by which HBx mediates liver cell proliferation. We found that HBx upregulated the levels of cyclooxygenase-2 （COX-2）, 5-1ipoxygenase （5-LOX） and phosphorylated extracellular signal-regulated protein kinases 1/2 （p-ERK1/2） in liver cells. HBx-induced p-ERK1/2 was abolished by inhibition of Gi/o proteins, COX or LOX. In addition, HBx increased the amounts of prostaglandin E2 （PGE2） and leukotriene B4 （LTB4） released from cell lines derived from hepatocytes. Moreover, these released arachidonic acid metabolites were able to activate ERK1/2. Interestingly, activated ERK1/2 could upregulate the expression of COX-2 and 5-LOX in a positive feedback manner. In conclusion, HBx enhances and maintains liver cell proliferation via a positive feedback loop involving COX-2, 5-LOX, released arachidonic acid metabolites, Gi/o proteins and p-ERK1/2.