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Hepatitis C virus core protein‐induced loss of LZIP function correlates with cellular transformation
Author(s) -
Jin DongYan,
Wang HaiLin,
Zhou Yuan,
Chun Abel C.S.,
Kibler Karen V.,
Hou YunDe,
Kung Hsiangfu,
Jeang KuanTeh
Publication year - 2000
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/19.4.729
Subject(s) - biology , transcription factor , hepatitis c virus , virology , viral transformation , hepatocellular carcinoma , neoplastic transformation , transcription (linguistics) , transformation (genetics) , virus , microbiology and biotechnology , cancer research , gene , genetics , carcinogenesis , linguistics , philosophy
Hepatitis C virus (HCV) is the major etiological agent of blood‐borne non‐A non‐B hepatitis and a leading cause of liver cirrhosis and hepatocellular carcinoma worldwide. HCV core protein is a multifunctional protein with regulatory functions in cellular transcription and virus‐induced transformation and pathogenesis. Here we report on the identification of a bZIP nuclear transcription protein as an HCV core cofactor for transformation. This bZIP factor, designated LZIP, activates CRE‐dependent transcription and regulates cell proliferation. Loss of LZIP function in NIH 3T3 cells triggers morphological transformation and anchorage‐independent growth. We show that HCV core protein aberrantly sequesters LZIP in the cytoplasm, inactivates LZIP function and potentiates cellular transformation. Our findings suggest that LZIP might serve a novel cellular tumor suppressor function that is targeted by the HCV core.