Hepatitis B virus X gene mutants might play a key role in the development of HBV-related hepatocellular carcinoma by modifying the biological functions of HBx. However, its mechanism remains unclear. We confirmed that HBx protein over expression and deletion in the distal C-terminal region of HBx gene may be characterized as a common feature of HBx in the tumor tissue by immunohistochemistry and DNA direct sequencing approach. So we designed artifical mutants of the C-terminal deletions of HBx to explore the effects on the cytobiological characteristics of HCC cell line by transfection. We found that the function, which involved in p53 pathway by Western blot, were distinct in different mutants truncated HBx. Besides, we have first time taken the advantage of cDNA microarray and two-dimensional gel electrophoresis approach to compare HBx3'-30 and HBx3'-40 with wtHBx at gene and protein level which will help us to determine the distinct role of HBx and its deletion forms on cell proliferation. Those results are very significant to demonstrate the mechanism of HBx on carcinogenesis.
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