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首页> 外文期刊>Cell cycle >Differential stimulation of hepatitis C virus RNA translation by microRNA-122 in different cell cycle phases
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Differential stimulation of hepatitis C virus RNA translation by microRNA-122 in different cell cycle phases

机译：microRNA-122在不同细胞周期阶段对丙型肝炎病毒RNA翻译的差异刺激

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Hepatitis C virus (HCV) replicates preferentially in the liver, and in most cases the HCV infection becomes chronic and often results in hepatocellular carcinoma. When the HCV plus-strand RNA genome has been delivered to the cytosol of the infected cell, its translation is directed by the Internal Ribosome Entry Site (IRES) in the 5′-untranslated region (5′-UTR ) of the viral RNA. Thereby, IRES activity is modulated by several host factors. In particular, the liver-specific microRNA-122 (miR-122) interacts with two target sites in the HCV 5′-UTR and stimulates HCV translation, thereby most likely contributing to HCV liver tropism. Here we show that HCV IRES-dependent translation efficiency in the hepatoma cell line Huh7 is highest during the G 0 and G 1 phases of the cell cycle but significantly drops during the S phase and even more in the G2/M phase. The superimposed stimulation of HCV translation by ectopic miR-122 works best during the G 0, G 1 and G 2/M phases but is lower during the S phase. However, the levels of Ago2 protein do not substantially change during cell cycle phases, indicating that other cellular factors involved in HCV translation stimulation by miR-122 may be differentially expressed in different cell cycle phases. Moreover, the levels of endogenously expressed miR-122 in Huh7 cells are lowest in the S phase, indicating that the predominant G 0/G 1 state of non-dividing hepatocytes in the liver facilitates high expression of the HCV genome and stimulation by miR-122, with yet unknown factors involved in the differential extent of stimulation by miR-122.
机译：丙型肝炎病毒（HCV）在肝脏中优先复制，并且在大多数情况下，HCV感染会变成慢性，并经常导致肝细胞癌。当HCV正链RNA基因组已递送至感染细胞的胞质溶胶时，其翻译受病毒RNA的5'-非翻译区（5'-UTR）中的内部核糖体进入位点（IRES）指导。因此，IRES活性受到几种宿主因素的调节。特别是，肝脏特异性microRNA-122（miR-122）与HCV 5'-UTR中的两个靶位点相互作用并刺激HCV翻译，从而最有可能促进HCV肝向性。在这里，我们显示，在肝癌细胞系Huh7中，HCV IRES依赖性翻译效率在细胞周期的G 0和G 1期最高，而在S期则明显下降，而在G2 / M期则更高。异位miR-122对HCV翻译的叠加刺激在G 0，G 1和G 2 / M阶段效果最佳，但在S阶段效果较低。但是，Ago2蛋白的水平在细胞周期阶段基本没有变化，这表明与miR-122刺激HCV翻译刺激有关的其他细胞因子可能在不同的细胞周期阶段有所差异。此外，Huh7细胞中内源性表达的miR-122的水平在S期最低，表明肝脏中未分裂肝细胞的主要G 0 / G 1状态促进了HCV基因组的高表达和miR-的刺激。 122，与miR-122刺激差异程度有关的未知因素。

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