Hepatitis C virus core protein-induced loss of LZIP function correlates with cellular transformation

Dong Yan Jin, Hai Lin Wang, Yuan Zhou, Abel C.S. Chun, Karen V. Kibler, Hou Yun-De, Hsiang Fu Kung, Kuan Teh Jeang

Research output: Contribution to journalArticlepeer-review

122 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)729-740
Number of pages12
JournalEMBO Journal
Volume19
Issue number4
DOIs
StatePublished - Feb 15 2000

Keywords

  • Hepatitis C virus
  • Hepatitis C virus core protein
  • Hepatocellular carcinoma
  • LZIP
  • bZIP transcription factor

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

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