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Global proteome analysis of hepatitis B virus expressing human hepatoblastoma cell line HepG2
Author(s) -
Huang Qingling,
Wang Lin,
Bai Shiyu,
Lin Wansong,
Chen Wannan,
Lin Jianyin,
Lin Xu
Publication year - 2009
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.21593
Subject(s) - hepatoblastoma , hepatitis b virus , hepatocellular carcinoma , biology , virology , proteome , pathogenesis , cell culture , cell cycle , hepatitis b , virus , cell , microbiology and biotechnology , cancer research , immunology , genetics , medicine , radiology
In countries where hepatitis B virus (HBV) is endemic, a high incidence of hepatocellular carcinoma (HCC) occur in HBV carriers and the prolonged replication and expression of HBV proteins in the liver is considered an important risk factor for progression to malignancy. However, the mechanism of pathogenesis of HBV‐associated carcinoma remains elusive. In this study, the human hepatoblastoma HepG2 cell line harboring 1.2 × unit‐length of the HBV genome was generated and subjected to a proteomic approach analyzing the global protein expression profiles of HepG2 cells with and without HBV replication and protein expression. By using fluorescence two‐dimensional difference gel electrophoresis (2D‐DIGE), followed by MALDI‐TOF‐MS and database searching, a total of 50 differentially expressed proteins were identified, including some cell cycle‐related proteins. These cycle‐related proteins may lead to accumulation of HepG2‐HBV cells in the G2/M phase, and an increase in the proportion of HepG2 cells with tripolar or multipolar spindles. This study described the proteomic alterations in HepG2 cells HBV‐harboring, which may provide new insights into the underlying molecular mechanisms involved in HBV replication and pathogenesis. J. Med. Virol. 81:1539–1550, 2009. © 2009 Wiley‐Liss, Inc.