Development of a recombinant murine tumour model using hepatoma cells expressing hepatitis C virus nonstructural antigens

2018 ◽  
Vol 25 (6) ◽  
pp. 649-660 ◽  
Author(s):  
K. G. Young ◽  
K. Haq ◽  
S. MacLean ◽  
R. Dudani ◽  
S. M. Elahi ◽  
...  
Hepatology ◽  
2007 ◽  
Vol 47 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Jennifer M. Timpe ◽  
Zania Stamataki ◽  
Adam Jennings ◽  
Ke Hu ◽  
Michelle J. Farquhar ◽  
...  

2010 ◽  
Vol 30 (10) ◽  
pp. 1490-1504 ◽  
Author(s):  
Nury M. Steuerwald ◽  
Judith C. Parsons ◽  
Kristen Bennett ◽  
Tonya C. Bates ◽  
Herbert L. Bonkovsky

PLoS ONE ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. e61089 ◽  
Author(s):  
Tzu-Yue Shiu ◽  
Shih-Ming Huang ◽  
Yu-Lueng Shih ◽  
Heng-Cheng Chu ◽  
Wei-Kuo Chang ◽  
...  

2009 ◽  
Vol 83 (19) ◽  
pp. 9824-9834 ◽  
Author(s):  
Nan Wang ◽  
Yuqiong Liang ◽  
Santhana Devaraj ◽  
Jie Wang ◽  
Stanley M. Lemon ◽  
...  

ABSTRACT Toll-like receptor-3 (TLR3) senses double-stranded RNA, initiating signaling that activates NF-κB and interferon regulatory factor 3 (IRF-3), thereby inducing the synthesis of proinflammatory cytokines, type I interferons, and numerous interferon-stimulated genes (ISGs). This pathway has not been extensively investigated in human hepatocytes, and its role in sensing and protecting against hepatitis virus infections is uncertain. We show here that primary human hepatocytes express TLR3 and robustly upregulate ISGs upon poly(I·C) stimulation. We also show that TLR3 senses hepatitis C virus (HCV) infection when expressed in permissive hepatoma cells, acting independently of retinoic acid-inducible gene I and inducing IRF-3 activation and the synthesis of ISGs that restrict virus replication. In turn, HCV infection reduces the abundance of TRIF, an essential TLR3 adaptor, and impairs poly(I·C)-induced signaling. The induction and disruption of TLR3 signaling by HCV may be important factors in determining the outcome of infection and the ability of HCV to establish persistent infections.


2013 ◽  
Vol 14 (12) ◽  
pp. 24230-24241 ◽  
Author(s):  
Yuan Liu ◽  
Ziying Zou ◽  
Bing Zhu ◽  
Zonghai Hu ◽  
Ping Zeng

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 908 ◽  
Author(s):  
Chen-Jei Tai ◽  
Alagie Jassey ◽  
Ching-Hsuan Liu ◽  
Cheng-Jeng Tai ◽  
Christopher D. Richardson ◽  
...  

Hepatocellular carcinoma (HCC), including hepatitis C virus (HCV)-induced HCC, is a deadly disease highly refractory to chemotherapy, thus requiring the continuous identification of novel treatment strategies. Berberine (BBR) has been previously reported to inhibit hepatoma cell growth, but the main type of cell death elicited by BBR, and whether the alkaloid can inhibit hepatoma cells carrying HCV genomes, is unclear. Herein, we show that BBR treatment induced a biphasic cell death irrespective of the presence of HCV subgenomic replicon RNA, first triggering apoptosis that then progressed to necrosis between 24 and 48 h post-treatment. Furthermore, BBR treatment potentiated the HCV replicon-induced reactive oxygen species (ROS) production, inhibition of which with an antioxidant attenuated the cell death that was elicited by BBR in these cells. Moreover, BBR dampened the autophagic response in HCV RNA-positive or negative hepatoma cells, and pharmacological inhibition of autophagy conversely augmented the BBR-induced cell death. Finally, BBR inhibited the growth of Huh-7 cells that were persistently infected with the full-length genome HCV particles, and concomitant pharmacological inhibition of autophagy potentiated the killing of these cells by BBR. Our findings suggest that combining BBR with the inhibition of autophagy could be an attractive treatment strategy against HCC, irrespective of the presence of the HCV genome.


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