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A model for p53-induced apoptosis

Author

Listed:
  • Kornelia Polyak

    (The Howard Hughes Medical Institute
    The Johns Hopkins Oncology Center)

  • Yong Xia

    (Johns Hopkins University School of Medicine)

  • Jay L. Zweier

    (Johns Hopkins University School of Medicine)

  • Kenneth W. Kinzler

    (The Johns Hopkins Oncology Center)

  • Bert Vogelstein

    (The Howard Hughes Medical Institute
    The Johns Hopkins Oncology Center)

Abstract

The inactivation of the p53 gene in a large proportion of human cancers has inspired an intense search for the encoded protein's physiological and biological properties. Expression of p53 induces either a stable growth arrest or programmed cell death (apoptosis). In human colorectal cancers, the growth arrest is dependent on the transcriptional induction of the protein p21WAF1/CIP1(ref. 1), but the mechanisms underlying the development of p53-dependent apoptosis are largely unknown2. As the most well documented biochemical property of p53 is its ability to activate transcription of genes, we examined in detail the transcripts induced by p53 expression before the onset of apoptosis. Of 7,202 transcripts identified, only 14 (0.19%) were found to be markedly increased in p53-expressing cells compared with control cells. Strikingly, many of these genes were predicted to encode proteins that could generate or respond to oxidative stress, including one that is implicated in apoptosis in plant meristems. These observations stimulated additional biochemical and pharmacological experiments suggesting that p53 results in apoptosis through a three-step process: (1) the transcriptional induction of redox-related genes; (2) the formation of reactive oxygen species; and (3) the oxidative degradation of mitochondrial components, culminating in cell death.

Suggested Citation

  • Kornelia Polyak & Yong Xia & Jay L. Zweier & Kenneth W. Kinzler & Bert Vogelstein, 1997. "A model for p53-induced apoptosis," Nature, Nature, vol. 389(6648), pages 300-305, September.
    • Handle: RePEc:nat:nature:v:389:y:1997:i:6648:d:10.1038_38525
    DOI: 10.1038/38525
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    Cited by:

    1. Shuji Ito & Xiaoxi Liu & Yuki Ishikawa & David D. Conti & Nao Otomo & Zsofia Kote-Jarai & Hiroyuki Suetsugu & Rosalind A. Eeles & Yoshinao Koike & Keiko Hikino & Soichiro Yoshino & Kohei Tomizuka & Mo, 2023. "Androgen receptor binding sites enabling genetic prediction of mortality due to prostate cancer in cancer-free subjects," Nature Communications, Nature, vol. 14(1), pages 1-10, December.
    2. Arielle S. Strasser & Ana Silvia Gonzalez-Reiche & Xianxiao Zhou & Braulio Valdebenito-Maturana & Xiaoqian Ye & Bin Zhang & Meng Wu & Harm Bakel & Ethylin Wang Jabs, 2024. "Limb reduction in an Esco2 cohesinopathy mouse model is mediated by p53-dependent apoptosis and vascular disruption," Nature Communications, Nature, vol. 15(1), pages 1-17, December.

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