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乙型肝炎病毒通过增强其启动子活性调节 HepG2.2.15 细胞中 Raf1 的表达。

Hepatitis B virus regulates Raf1 expression in HepG2.2.15 cells by enhancing its promoter activity.

机构信息

Key Laboratory of Molecular Biology on Infectious Diseases, Ministry of Education, Second Affiliated Hospital, Chongqing Medical University, China.

出版信息

Arch Virol. 2011 May;156(5):869-74. doi: 10.1007/s00705-010-0901-z. Epub 2011 Jan 5.

Abstract

Raf1 kinase is a central component of many signaling pathways that are involved in normal cell growth and oncogenic transformation. The expression of Raf1 is significantly increased in hepatocellular carcinoma (HCC). HBV is a major risk factor for HCC. HBx protein can increase the expression of Raf1; however, the mechanism of how HBV regulates Raf1 expression is still unknown. In this study, we showed the Raf1 expression was significantly higher in HepG2.2.15 cells than that in HepG2 cells in vitro. HBV could up-regulate Raf1 expression by enhancing the activity of its promoter in a dose-dependent manner, and HBs and HBx may be involved in this process. After silencing HBs and HBx by using RNA interference, the expression of Raf1 in HepG2.2.15 cells could be significantly inhibited. These results might provide useful information for understanding the mechanism of HCC induced by HBV infection.

摘要

Raf1 激酶是许多参与正常细胞生长和致癌转化的信号通路的核心组成部分。Raf1 的表达在肝细胞癌(HCC)中显著增加。HBV 是 HCC 的主要危险因素。HBx 蛋白可以增加 Raf1 的表达;然而,HBV 调节 Raf1 表达的机制尚不清楚。在这项研究中,我们发现在体外 HepG2.2.15 细胞中 Raf1 的表达明显高于 HepG2 细胞。HBV 可以通过增强其启动子的活性,以剂量依赖的方式上调 Raf1 的表达,HBs 和 HBx 可能参与了这一过程。用 RNA 干扰沉默 HBs 和 HBx 后,HepG2.2.15 细胞中 Raf1 的表达可以被显著抑制。这些结果可能为理解 HBV 感染诱导 HCC 的机制提供有用的信息。

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