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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.

Original publication




Journal article


Cancer Cell

Publication Date





597 - 609


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