NF-κB activation by hepatitis B virus X (HBx) protein shifts the cellular fate toward survival

Chawon Yun, Hae Ryun Um, Young Hee Jin, Jin Hee Wang, Mi Ock Lee, Sun Park, Jae Ho Lee, Hyeseong Cho*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

64 Scopus citations


In this paper, we examined the cellular effect of hepatitits B virus X (HBx) in ChangX-34 cells, inducible HBx-expressing cells. High expression of HBx protein in ChangX-34 cells resulted in approximately three-fold increase in DNA synthesis and did not show apoptotic changes. Expression of HBx in these cells was accompanied by the NF-κB-mediated transcription. Interestingly, inhibition of NF-κB activity either by treatment with sulfasalazine, a specific inhibitor of NF-κB, or by expressing IκBα super-repressor significantly increased cell death in ChangX-34 cells but had no influence on parental Chang cells. Thus, the activation of NF-κB in HBx-expressing cells may play a critical role in shifting the balance toward cell survival.

Original languageEnglish (US)
Pages (from-to)97-104
Number of pages8
JournalCancer Letters
Issue number1
StatePublished - Oct 8 2002


  • Apoptosis
  • Hepatitis B virus
  • Hepatitis B virus X
  • NF-κB
  • Proliferation

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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