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Abstract
X protein (HBx), a product of hepatitis B virus, has been closely associated with the development of hepatocellular carcinoma (HCC). Based on observations that the COOH-terminal truncated HBx was frequently detected in HCC, the aim of this study is to evaluate the function of COOH-terminal truncated HBx in hepatocarcinogenesis. Expression pattern of HBx was analyzed by immunohistochemistry on tissue microarray containing 194 pairs of HCCs and their matched nontumor liver tissues. MIHA and HepG2 cells transfected with full-length (X2) and COOH-terminal truncated HBx (X1) were tested for their ability to grow in soft agar and form tumors in vivo. Proliferation and apoptosis were assessed using 2,3-bis[2-methoxy-4-nitro-5-sulfophenyl]-2H-tetrazolium-5-carboxanilide inner salt and terminal deoxyribonucleotidyl transferase-mediated dUTP nick-end labeling assays, respectively. To gain additional insight, the expression profile of HepG2-X2 and HepG2-X1 were compared using cDNA microarray. COOH-terminal truncated HBx was frequently detected in HCCs (79.3%, n = 111), and our in vitro and in vivo studies showed that the truncated rather than the full-length HBx could effectively transform immortalized liver cell line MIHA. Interestingly, expression profiling revealed differential expression of key genes implicated in the control of cell cycle and apoptosis. These findings strongly suggest that the COOH-terminal truncated HBx plays a critical role in the HCC carcinogenesis via the activation of cell proliferation.
Highlights
X protein (HBx), a product of hepatitis B virus, has been closely associated with the development of hepatocellular carcinoma (HCC)
We and others reported observations that integration of hepatitis B virus (HBV) was detected in 80% to 90% of host genome of HBV-infected HCC cases, suggesting that viral DNA integration plays a critical role in the HCC carcinogenesis [13, 14]
We investigated the HBx expression in 140 cases of HBV-related HCCs paired with the adjacent nontumor tissues, and compared an oncogenic role of the COOH-terminal truncated HBx with the full-length HBx protein
Summary
X protein (HBx), a product of hepatitis B virus, has been closely associated with the development of hepatocellular carcinoma (HCC). Results: COOH-terminal truncated HBx was frequently detected in HCCs (79.3%, n = 111), and our in vitro and in vivo studies showed that the truncated rather than the full-length HBx could effectively transform immortalized liver cell line MIHA. Conclusions: These findings strongly suggest that the COOH-terminal truncated HBx plays a critical role in the HCC carcinogenesis via the activation of cell proliferation. We proposed here that the truncated HBx protein plays a key role in the HCC carcinogenesis. To test this hypothesis, we investigated the HBx expression in 140 cases of HBV-related HCCs paired with the adjacent nontumor tissues, and compared an oncogenic role of the COOH-terminal truncated HBx with the full-length HBx protein. Our results reported here showed that the COOH-terminal truncated HBx, rather than the full-length HBx, is required and sufficient to cause HCC
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