title: Proteome responses to stable hepatitis B virus transfection and following interferon alpha treatment in human liver cell line HepG2.
abstract: Hepatitis B virus (HBV) infection is a worldwide health problem and may develop to liver fibrosis, cirrhosis, and even hepatocellular carcinoma. To investigate the global proteome responses of liver-derived cells to HBV infection and IFNalpha treatment, 2-DE and MS-based analysis were performed to compare the proteome changes between HBV stably transfected cell line HepG2.2.15 and its parental cell line HepG2, as well as HepG2.2.15 before and after IFNalpha treatment (5000 IU/mL for 72 h). Compared to HepG2, 12 of 18 down-regulated and 27 of 32 up-regulated proteins were identified in HepG2.2.15. After IFNalpha treatment, 6 of 7 down-regulated and 11 of 14 up-regulated proteins were identified. Differentially expressed proteins caused by HBV infection were involved with cytoskeletal matrix, heat shock stress, kinases/signal transduction, protease/proteasome components, etc. Prohibitin showed a dose-dependent up-regulation during IFNalpha treatment and might play a potent role in anti-HBV activities of IFNalpha by enhancing the crossbinding p53 expression to achieve the apoptosis of HBV infected liver cells. Down-regulation of interferon-stimulated gene 15 (ISG15) in HepG2.2.15 and recovery by IFNalpha suggested its relationship with IFNalpha's anti-HBV effect.
authors.affiliation: Peking University Hepatology Institute, Peking University People's Hospital, Beijing, China.
authors.forename: Jianghua
authors.initials: J
authors.lastname: Wang
authors.forename: Dong
authors.initials: D
authors.lastname: Jiang
authors.forename: Henghui
authors.initials: H
authors.lastname: Zhang
authors.forename: Sa
authors.initials: S
authors.lastname: Lv
authors.forename: Huiying
authors.initials: H
authors.lastname: Rao
authors.forename: Ran
authors.initials: R
authors.lastname: Fei
authors.forename: Lai
authors.initials: L
authors.lastname: Wei
mesh_terms: D017304:Annexin A5 / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D053179:Caspase 7 / Q000235:genetics / Q000378:metabolism; D045744:Cell Line, Tumor; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D015536:Down-Regulation / Q000187:drug effects; D016650:Fluorescein-5-isothiocyanate / Q000378:metabolism; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D006515:Hepatitis B virus / Q000187:drug effects* / Q000378:metabolism*; D006801:Humans; D016898:Interferon-alpha / Q000494:pharmacology*; D008099:Liver / Q000473:pathology* / Q000821:virology*; D009363:Neoplasm Proteins / Q000032:analysis; D000091402:Prohibitins; D020543:Proteome / Q000032:analysis*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism; D015203:Reproducibility of Results; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014162:Transfection; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism; D014452:Ubiquitins / Q000235:genetics / Q000378:metabolism
chemical_list: D017304:Annexin A5; D016207:Cytokines; D016898:Interferon-alpha; D009363:Neoplasm Proteins; D000091402:Prohibitins; D020543:Proteome; D012333:RNA, Messenger; D012097:Repressor Proteins; D016159:Tumor Suppressor Protein p53; D014452:Ubiquitins; C074034:ISG15 protein, human; D053179:Caspase 7; D016650:Fluorescein-5-isothiocyanate