ZBP-89 enhances Bak expression and causes apoptosis in hepatocellular carcinoma cells

Ann K.Y. To, George G. Chen, Ursula P.F. Chan, Caiguo Ye, Jing P. Yun, Rocky L.K. Ho, Art Tessier, Juanita L. Merchant, Paul B.S. Lai

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


ZBP-89 can enhance tumor cells to death stimuli. However, the molecular mechanism leading to the inhibitory effect of ZBP-89 is unknown. In this study, 4 liver cell lines were used to screen for the target of ZBP-89 on cell death pathway. The identified Bak was further analyzed for its role in ZBP-89-mediated apoptosis. The result showed that ZBP-89 significantly and time-dependently induced apoptosis. It significantly upregulated the level of pro-apoptotic Bak. ZBP-89 targeted a region between -457 and -407 of human Bak promoter to stimulate Bak expression based on the findings of Bak promoter luciferase report gene assay and electrophoretic mobility shift assay. ZBP-89-induced Bak increase and ZBP-89-mediated apoptosis were markedly suppressed by Bak siRNA, confirming that Bak was specifically targeted by ZBP-89 to facilitate apoptosis. In conclusion, this study demonstrated that ZBP-89 significantly induced apoptosis of HCC cells via promoting Bak level.

Original languageEnglish (US)
Pages (from-to)222-230
Number of pages9
JournalBiochimica et Biophysica Acta - Molecular Cell Research
Issue number1
StatePublished - Jan 2011
Externally publishedYes


  • Apoptosis
  • Bak
  • Hepatocellular carcinoma
  • Proliferation
  • ZBP-89

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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