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Morphological alteration and biological properties of hepatocytes not related to tumorigenesis following transfection with HCV core protein *
Author(s) -
Gu J.,
Wang L.,
Che Y.,
Liu L.,
Jiang L.,
Dong S.,
Li W.,
Li Q.
Publication year - 2005
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1111/j.1365-2893.2005.00539.x
Subject(s) - transfection , carcinogenesis , western blot , hepatocellular carcinoma , hepatitis c virus , biology , pathogenesis , hepatocyte , microbiology and biotechnology , gene , immunofluorescence , virus , virology , cancer research , antibody , immunology , in vitro , genetics
Summary. The hepatitis C virus (HCV) core protein is supposed to play a critical role in HCV‐mediated human liver disease with its capabilities to regulate the growth rate of hepatocytes and to partially contribute to the pathogenesis of hepatocellular carcinoma in association with cellular oncogenes. In this study, to analyse the possible pathological mechanism of the HCV core protein, human primary embryo hepatocytes transfected with HCV core were monitored by immunofluorescence, reverse transcriptase‐polymerase chain reaction (RT‐PCR) and Western blot. The morphological changes and biological properties of the transfected hepatocytes were also studied. The results showed that the HCV core gene integrated in the cellular genome and the protein expressed in the transfected hepatocyte, could be detected following serial passage at both the mRNA and protein level. The proliferation assays indicated that hepatocytes transfected with the HCV core gene alone did not exhibit any tumorigenic tendency. Meanwhile, the morphological alterations of these cells demonstrated obvious changes in size, and large vacuolar degeneration. In conclusion, the hepatocytes transfected with the HCV core gene revealed that the core protein expressed induced pathological changes of degeneration, probably related indirectly to tumorigenicity.