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Bnip3L is induced by p53 under hypoxia, and its knockdown promotes tumor growth.

p53-dependent apoptosis is a major determinant of its tumor suppressor activity and can be triggered by hypoxia. No p53 target is known to be induced by p53 or to mediate p53-dependent apoptosis during hypoxia. We report that p53 can directly upregulate expression of Bnip3L, a cell death inducer. During hypoxia, Bnip3L is highly induced in wild-type p53-expressing cells, in part due to increased recruitment of p53 and CBP to Bnip3L. Apoptosis is reduced in hypoxia-exposed cells with functional p53 following Bnip3L knockdown. In vivo, Bnip3L knockdown promotes tumorigenicity of wild-type versus mutant p53-expressing tumors. Thus, Bnip3L, capable of attenuating tumorigenicity, mediates p53-dependent apoptosis under hypoxia, which provides a novel understanding of p53 in tumor suppression.

Pubmed ID: 15607964


  • Fei P
  • Wang W
  • Kim SH
  • Wang S
  • Burns TF
  • Sax JK
  • Buzzai M
  • Dicker DT
  • McKenna WG
  • Bernhard EJ
  • El-Deiry WS


Cancer cell

Publication Data

December 20, 2004

Associated Grants

  • Agency: NCI NIH HHS, Id: CA105008
  • Agency: NCI NIH HHS, Id: CA75138
  • Agency: NCI NIH HHS, Id: CA75454

Mesh Terms

  • Animals
  • Apoptosis
  • Blotting, Western
  • CREB-Binding Protein
  • Caspase 3
  • Caspases
  • Cell Hypoxia
  • Cell Line, Tumor
  • Cell Proliferation
  • Chromatin Immunoprecipitation
  • Cisplatin
  • Doxycycline
  • Fluorouracil
  • Gene Expression Regulation, Neoplastic
  • Genes, Reporter
  • Glucose Transporter Type 1
  • Humans
  • Immunohistochemistry
  • In Situ Hybridization
  • Membrane Proteins
  • Mice
  • Mice, Nude
  • Monosaccharide Transport Proteins
  • Neoplasms
  • Nuclear Proteins
  • Oligonucleotide Array Sequence Analysis
  • Protein Binding
  • Proto-Oncogene Proteins
  • RNA Interference
  • RNA, Small Interfering
  • Repressor Proteins
  • Trans-Activators
  • Transfection
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins
  • Xenograft Model Antitumor Assays