Utilizing experimental mouse model to identify effectors of hepatocellular carcinoma induced by HBx antigen

Ming Hui Yang, Marcelo Chen, Hsiao Hsuan Mo, Wan Chi Tsai, Yu Chi Chang, Chin Chuan Chang, Ko Chin Chen, Hsin Yi Wu, Cheng Hui Yuan, Che Hsin Lee, Yi Ming Arthur Chen, Yu Chang Tyan

Research output: Contribution to journalArticlepeer-review

15 Citations (Scopus)


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.
Original languageEnglish
Article number409
Issue number2
Publication statusPublished - Feb 10 2020


  • HBx
  • Hepatocellular carcinoma
  • Missing proteins

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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