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J Gen Virol 85 (2004), 275-282; DOI 10.1099/vir.0.19650-0

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© 2004 Society for General Microbiology

Hepatitis B virus X antigen promotes transforming growth factor-{beta}1 (TGF-{beta}1) activity by up-regulation of TGF-{beta}1 and down-regulation of {alpha}2-macroglobulin

Jingbo Pan1, Marcy Clayton1 and Mark A. Feitelson1,2

1 Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Room 222 Alumni Hall, 1020 Locust Street, Philadelphia, PA 19107, USA
2 Department of Microbiology and Immunology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA

Correspondence
Mark A. Feitelson
Mark.Feitelson{at}jefferson.edu

Hepatitis B virus (HBV) X antigen (HBxAg) may contribute to the development of hepatocellular carcinoma (HCC) by activation of signalling pathways such as NF-{kappa}B. To identify NF-{kappa}B 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-I{kappa}B{alpha}. mRNA from each culture was isolated and compared by PCR select cDNA subtraction. The results showed lower levels of {alpha}2-macroglobulin ({alpha}2-M) in HepG2X-pZeoSV2 compared to HepG2X-pZeoSV2-I{kappa}B{alpha} cells. This was confirmed by Northern and Western blotting, and by measurement of extracellular {alpha}2-M levels. Elevated transforming growth factor-{beta}1 (TGF-{beta}1) levels were also seen in HepG2X compared to control cells. Serum-free conditioned medium (SFCM) from HepG2X cells suppressed DNA synthesis in a TGF-{beta}-sensitive cell line, Mv1Lu. The latter was reversed when the SFCM was pretreated with exogenous, activated {alpha}2-M or with anti-TGF-{beta}. Since elevated TGF-{beta}1 promotes the development of many tumour types, these observations suggest that the HBxAg-mediated alteration in TGF-{beta}1 and {alpha}2-M production may contribute importantly to the pathogenesis of HCC.






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