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Vol. 273, Issue 1, 381-385, January 2, 1998
From the Signal Transduction Laboratory, Mogam Biotechnology
Research Institute, 341 Pojungri, Koosungmyon, Yonginsi,
Kyunggido 449-910, Korea
Hepatitis B virus is a causative agent of
hepatocellular carcinoma, and in the course of tumorigenesis, the
X-gene product (HBx) is known to play important roles. Here, we
investigated the transforming potential of HBx by conventional focus
formation assay in NIH3T3 cells. Cells were cotransfected with the HBx
expression plasmid along with other oncogenes including
Ha-ras, v-src, v-myc, v-fos, and E1a. Unexpectedly, the introduction of HBx
completely abrogated the focus-forming ability of all five tested
oncogenes. In addition, the cotransfection of Bcl-2, an apoptosis
inhibitor, reversed the HBx-mediated inhibition of focus formation,
suggesting that the observed repression of focus formation by HBx is
through the induction of apoptosis. Next, to test unequivocally whether HBx induces apoptosis in liver cells, we established stable Chang liver
cell lines expressing HBx under the control of a tetracycline-inducible promoter. Induction of HBx in these cells in the presence of 1% calf
serum resulted in typical apoptosis phenomena such as DNA fragmentation, nuclear condensation, and fragmentation. Based on these
results, we propose that HBx sensitizes liver cells to apoptosis upon
hepatitis B virus infection, contributing to the development of
hepatitis and the subsequent generation of hepatocellular carcinoma.
X-gene Product of Hepatitis B Virus Induces Apoptosis in
Liver Cells
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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