Synergy between transforming growth factor-α and hepatitis B virus surface antigen in hepatocellular proliferation and carcinogenesis Jakobczak, J.L., Chisari, F.V., Merlino G. Laboratory of Molecular Biology, National Cancer Institute, Building 37, 37 Convent Drive, Bethesda, MD 20892-4255, USA Cancer Research 1997; 57 (16): 3606–3611

1997 ◽  
Vol 9 (1) ◽  
pp. 68-69
Keyword(s):  
Cancer Research ◽  
Hepatitis B Virus ◽  
Growth Factor ◽  
Molecular Biology ◽  
Hepatitis B ◽  
Transforming Growth Factor ◽  
Virus Surface ◽  
Transforming Growth Factor Α ◽  
B Virus ◽  
Factor Α

scholarly journals Hepatitis B virus X antigen promotes transforming growth factor-β1 (TGF-β1) activity by up-regulation of TGF-β1 and down-regulation of α 2-macroglobulin

2004 ◽  
Vol 85 (2) ◽  
pp. 275-282 ◽  
Author(s):  
Jingbo Pan ◽  
Marcy Clayton ◽  
Mark A. Feitelson
Keyword(s):  
Hepatitis B Virus ◽  
Growth Factor ◽  
Hepatitis B ◽  
Target Genes ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Sensitive Cell Line ◽  
Cdna Subtraction ◽  
B Virus ◽  
Tgf Β1

Hepatitis B virus (HBV) X antigen (HBxAg) may contribute to the development of hepatocellular carcinoma (HCC) by activation of signalling pathways such as NF-κB. To identify NF-κB target genes differentially expressed in HBxAg-positive compared to -negative cells, HepG2 cells consistently expressing HBxAg (HepG2X cells) were stably transfected with pZeoSV2 or pZeoSV2-IκBα. mRNA from each culture was isolated and compared by PCR select cDNA subtraction. The results showed lower levels of α 2-macroglobulin (α 2-M) in HepG2X-pZeoSV2 compared to HepG2X-pZeoSV2-IκBα cells. This was confirmed by Northern and Western blotting, and by measurement of extracellular α 2-M levels. Elevated transforming growth factor-β1 (TGF-β1) levels were also seen in HepG2X compared to control cells. Serum-free conditioned medium (SFCM) from HepG2X cells suppressed DNA synthesis in a TGF-β-sensitive cell line, Mv1Lu. The latter was reversed when the SFCM was pretreated with exogenous, activated α 2-M or with anti-TGF-β. Since elevated TGF-β1 promotes the development of many tumour types, these observations suggest that the HBxAg-mediated alteration in TGF-β1 and α 2-M production may contribute importantly to the pathogenesis of HCC.

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