p53 mutants suppress ZBP-89 function

Morihiro Okada, Arthur Tessier, Longchuan Bai, Juanita L. Merchant

Research output: Contribution to journalArticlepeer-review

6 Scopus citations


Background: ZBP-89 is a widely expressed Krüppel-type zinc finger transcription factor that binds to GC-rich elements and represses or activates known target genes. ZBP-89 stabilizes wild-type p53 and can induce apoptosis independently of p53. Tissues with p53 mutations are predisposed to transformation and are more resistant to chemotherapy. Materials and Methods: The effect of ZBP-89 on seven sporadic p53 mutants was investigated. It was then examined whether a cell null for p53 in comparison to one expressing mutated p53 is more sensitive or resistant to chemotherapy in the presence of increased levels of ZBP-89. Results: None of the p53 mutations were stabilized by ZBP-89 except for the A161T p53 mutation, which exhibited constitutive transcriptional activity. ZBP-89 potentiated p53-mediated cell death with 10 nM staurosporine and 100 nM etoposide, but did not in the presence of the R273H p53 mutation. Conclusion: ZBP-89 is an important co-activator of wild-type p53 and both proteins are negatively affected by functionally inactive p53 mutants.

Original languageEnglish (US)
Pages (from-to)2023-2028
Number of pages6
JournalAnticancer research
Issue number3 A
StatePublished - May 2006
Externally publishedYes


  • Apoptosis
  • Cell cycle
  • Colon cancer
  • Etoposide
  • Staurosporine

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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