Different transformation pathways of murine fibroblast NIH 3T3 cells by hepatitis C virus core and NS3 proteins

2006 ◽  
Vol 30 (11) ◽  
pp. 915-919 ◽  
Author(s):  
I SMIRNOVA ◽  
N AKSENOV ◽  
M VONSKY ◽  
M ISAGULIANTS
2002 ◽  
Vol 83 (9) ◽  
pp. 2145-2151 ◽  
Author(s):  
Mi Nam Lee ◽  
Eun Young Jung ◽  
Hyun Jin Kwun ◽  
Hong Ki Jun ◽  
Dae-Yeul Yu ◽  
...  

The increased proliferation rate of hepatocytes is one of the major risk factors for the development of hepatocellular carcinoma. In this study, we investigated the mechanism by which hepatitis C virus (HCV) core protein represses transcription of the universal cyclin-dependent kinase inhibitor p21 gene in murine fibroblast NIH 3T3 cells. From the transient reporter assays of p21 promoter, we found that the TGF-β-responsive element (TβRE) located between −83 and −74 of the p21 promoter is responsible for the effect. The TGF-β-induced p21 promoter activity was specifically decreased by HCV core protein and in the presence of the inhibitory Smad7 the repression effect was almost completely abolished. Furthermore, HCV core protein stimulated the growth rate of NIH 3T3 cells and could overcome growth arrest by TGF-β but not by butyrate, suggesting that HCV core protein stimulates cell cycle progression by repressing p21 transcription through a TGF-β pathway.


2005 ◽  
Vol 149 (2) ◽  
pp. 393-396 ◽  
Author(s):  
Marica Theiszova ◽  
Sona Jantova ◽  
Jana Dragunova ◽  
Petra Grznarova ◽  
Martin Palou

2011 ◽  
Vol 13 (10) ◽  
pp. 2794 ◽  
Author(s):  
Martin McLaughlin ◽  
Martyn J. Earle ◽  
Manuela A. Gîlea ◽  
Brendan F. Gilmore ◽  
Sean P. Gorman ◽  
...  

2002 ◽  
Vol 196 (5) ◽  
pp. 641-653 ◽  
Author(s):  
Takafumi Yoshida ◽  
Toshikatsu Hanada ◽  
Takeshi Tokuhisa ◽  
Ken-ichiro Kosai ◽  
Michio Sata ◽  
...  

The signal transducer and activator of transcription (STAT) family proteins are transcription factors critical in mediating cytokine signaling. Among them, STAT3 is often constitutively phosphorylated and activated in human cancers and in transformed cell lines and is implicated in tumorigenesis. However, cause of the persistent activation of STAT3 in human tumor cells is largely unknown. The hepatitis C virus (HCV) is a major etiological agent of non-A and non-B hepatitis, and chronic infection by HCV is associated with development of liver cirrhosis and hepatocellular carcinoma. HCV core protein is proposed to be responsible for the virus-induced transformation. We now report that HCV core protein directly interacts with and activates STAT3 through phosphorylation of the critical tyrosine residue. Activation of STAT3 by the HCV core in NIH-3T3 cells resulted in rapid proliferation and up-regulation of Bcl-XL and cyclin-D1. Additional expression of STAT3 in HCV core-expressing cells resulted in anchorage-independent growth and tumorigenesis. We propose that the HCV core protein cooperates with STAT3, which leads to cellular transformation.


2003 ◽  
Vol 94 (2) ◽  
pp. 79-84 ◽  
Author(s):  
Eun Young Jung ◽  
Hae Kyung Kang ◽  
Jun Chang ◽  
Dae-Yeul Yu ◽  
Kyung Lib Jang

2018 ◽  
Vol 8 (1) ◽  
pp. 48-54
Author(s):  
Rashed Hassan ◽  
Abdelmonem Elshamy ◽  
Sameh Abdel Monem ◽  
Emad Moustafa ◽  
Essam Wahab

1994 ◽  
Vol 68 (6) ◽  
pp. 3631-3641 ◽  
Author(s):  
E Santolini ◽  
G Migliaccio ◽  
N La Monica

Author(s):  
Rin Yamaguchi ◽  
Seiya Momosaki ◽  
Guang Gao ◽  
Chu Hsia ◽  
Masamichi Kojiro ◽  
...  

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