Hepatocellular carcinoma (HCC) is among the ten most commonly diagnosed
cancers and the fourth leading cause of
cancer-related death. Patients with hepatitis B virus (HBV)
infection are prone to developing chronic
liver diseases (i.e.,
fibrosis and
cirrhosis), and the HBV X
antigen plays an important role in the development of HCC. The difficulty in detecting HCC at the early stages is one of the main reasons that the death rate approximates the incidence rate. The regulators controlling the downstream liver
protein expression from HBV
infection are unclear. Mass spectrometric techniques and customized programs were used to identify differentially expressed
proteins which may be involved in the development of
liver fibrosis and HCC progression in
hepatitis B virus X protein transgenic mice (HBx mice). FSTL1, CTSB, and TGF-β enhanced the signaling pathway
proteins during the pathogenesis of HBx. Missing
proteins can be essential in cell growth, differentiation, apoptosis, migration,
metastasis or angiogenesis. We found that LHX2,
BMP-5 and GDF11 had complex interactions with other missing
proteins and
BMP-5 had both
tumor suppressing and tumorigenic roles.
BMP-5 may be involved in
fibrosis and tumorigenic processes in the liver. These results provide us an understanding of the mechanism of HBx-induced disorders, and may serve as molecular targets for liver treatment.