ISG12a mediates cell response to Newcastle disease viral infection
ISG12a mediates cell response to Newcastle disease viral infection
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ISG12a介导细胞对新城疫病毒感染的反应
DOI：
10.1016/j.virol.2014.06.014
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发表时间：
2014-08-01
期刊：
影响因子：
3.7
通讯作者：
Zhu, Haizhen
中科院分区：
文献类型：
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作者：
Liu, Nianli;Long, Ying;Zhu, Haizhen
新城疫病毒 (NDV) 溶瘤被认为是由缺陷的 I 型干扰素 (IFN) 反应促进的。我们比较了肝细胞癌 (HCC) 来源的细胞系，发现 TRAIL 抗性细胞比 TRAIL 敏感细胞更容易受到 NDV 溶瘤作用。在检查 IFN 反应时，我们发现 IFN 刺激基因 (ISG)-12a 的基础表达在 TRAIL 抗性细胞中较低，但在 TRAIL 敏感细胞中较高，并且 ISG12a 过表达或沉默分别增强或降低了 TRAIL 敏感性。此外，TRAIL 抗性细胞中 ISG12a 的过度表达降低了 NDV 复制，但令人惊讶地增加了溶瘤作用，而 ISG12a 沉默对 TRAIL 敏感细胞具有相反的效果。最后，RIG-I 和 Noxa 似乎也有助于 NDV 溶瘤作用。总之，这些结果表明，高基础 ISG12a 可能会抑制 NDV 复制和溶瘤，而低基础 ISG12a 可能允许足够的 NDV 复制以诱导 ISG12a，以及 NDV 溶瘤所需的其他因素，这对未来的治疗具有影响。 (C) 2014 Elsevier Inc. 保留所有权利。
Newcastle disease virus (NDV) oncolysis is believed to be facilitated by a defective Type I interferon (IFN) response. We compared hepatocellular carcinoma (HCC)-derived cell lines and found that TRAIL-resistant cells were more susceptible to NDV oncolysis than were TRAIL-sensitive cells. In examining the IFN response, we found that basal expression of the IFN-stimulated gene (ISG)-12a was low in TRAIL-resistant but high in TRAIL-sensitive cells, and ISG12a over-expression or silencing enhanced or reduced their TRAIL sensitivities, respectively. Moreover, ISG12a over-expression in TRAIL-resistant cells decreased NDV replication but surprisingly increased oncolysis while ISG12a silencing had the opposite effect on TRAIL-sensitive cells. Finally, RIG-I and Noxa appear to also contribute to NDV oncolysis. Together, these results suggest that high basal ISG12a may inhibit NDV replication and oncolysis, while low basal ISG12a may allow sufficient NDV replication for induction of ISG12a, and other factors required for NDV oncolysis, with implications for future therapeutics. (C) 2014 Elsevier Inc. All rights reserved.