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Human hepatitis B virus x protein is a possible mediator of hypoxia-induced angiogenesis in hepatocarcinogenesis

Title
Human hepatitis B virus x protein is a possible mediator of hypoxia-induced angiogenesis in hepatocarcinogenesis
Authors
Lee S.-W.Lee Y.M.Bae S.-K.Murakami S.Yun Y.Kim K.-W.
Ewha Authors
윤영대
SCOPUS Author ID
윤영대scopus
Issue Date
2000
Journal Title
Biochemical and Biophysical Research Communications
ISSN
0006-291XJCR Link
Citation
vol. 268, no. 2, pp. 456 - 461
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
The hepatitis B virus (HBV)-encoded transcriptional activator HBV-X protein (HBx) was known to be involved in hepatocarcinogenesis. Hepatocarcinogenesis generally included an active angiogenesis that was mainly considered to be due to a local hypoxia in liver tissues. However, the exact mechanisms of HBx-induced hepatocarcinogenesis were poorly understood. In this study, we examined the role of HBx in the increased angiogenesis and the possible regulating mechanisms of HBx by hypoxia. We demonstrated that HBx stimulated the transcription of vascular endothelial growth factor (VEGF), a potent angiogenic factor, in HBx-stable transfectants. HBx-induced angiogenesis was confirmed by in vivo tumor angiogenesis assay, resulting in that the HBx transfectants increased the formation of new blood vessels compared to the control transfectants. Then, we demonstrated that the expression of HBx was enhanced after incubating HBV-infected hepatoma cells under hypoxia. Moreover, the activity of HBV enhancer 1 (Enh1) was increased when hepatoma cells transfected with the reporter plasmid containing HBV Enh1 were exposed to hypoxic conditions. These results strongly suggest that HBx may play a critical role in the hypoxia-induced angiogenesis through transcriptional activation of VEGF during hepatocarcinogenesis. (C) 2000 Academic Press.
DOI
10.1006/bbrc.2000.2093
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자연과학대학 > 생명과학전공 > Journal papers
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