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Intracellular CD24 disrupts the ARF–NPM interaction and enables mutational and viral oncogene-mediated p53 inactivation

Author

Listed:
  • Lizhong Wang

    (University of Alabama at Birmingham)

  • Runhua Liu

    (University of Alabama at Birmingham)

  • Peiying Ye

    (Children’s Research Institute, Children’s National Medical Center)

  • Chunshu Wong

    (Children’s Research Institute, Children’s National Medical Center
    Program of Immunology, Integrated Biomedical Graduate Program, University of Michigan School of Medicine)

  • Guo-Yun Chen

    (Children’s Research Institute, Children’s National Medical Center)

  • Penghui Zhou

    (Dana-Farber Cancer Institute, Harvard Medical School)

  • Kaoru Sakabe

    (Children’s Research Institute, Children’s National Medical Center)

  • Xincheng Zheng

    (OncoImmune, Inc.)

  • Wei Wu

    (OncoImmune, Inc.)

  • Peng Zhang

    (Institute of Biophysics, Chinese Academy of Science)

  • Taijiao Jiang

    (Institute of Biophysics, Chinese Academy of Science)

  • Michael F. Bassetti

    (School of Medicine, University of Michigan)

  • Sandro Jube

    (Children’s Research Institute, Children’s National Medical Center)

  • Yi Sun

    (School of Medicine, University of Michigan)

  • Yanping Zhang

    (University of North Carolina)

  • Pan Zheng

    (Children’s Research Institute, Children’s National Medical Center)

  • Yang Liu

    (Children’s Research Institute, Children’s National Medical Center)

Abstract

CD24 is overexpressed in nearly 70% human cancers, whereas TP53 is the most frequently mutated tumour-suppressor gene that functions in a context-dependent manner. Here we show that both targeted mutation and short hairpin RNA (shRNA) silencing of CD24 retard the growth, progression and metastasis of prostate cancer. CD24 competitively inhibits ARF binding to NPM, resulting in decreased ARF, increase MDM2 and decrease levels of p53 and the p53 target p21/CDKN1A. CD24 silencing prevents functional inactivation of p53 by both somatic mutation and viral oncogenes, including the SV40 large T antigen and human papilloma virus 16 E6-antigen. In support of the functional interaction between CD24 and p53, in silico analyses reveal that TP53 mutates at a higher rate among glioma and prostate cancer samples with higher CD24 mRNA levels. These data provide a general mechanism for functional inactivation of ARF and reveal an important cellular context for genetic and viral inactivation of TP53.

Suggested Citation

  • Lizhong Wang & Runhua Liu & Peiying Ye & Chunshu Wong & Guo-Yun Chen & Penghui Zhou & Kaoru Sakabe & Xincheng Zheng & Wei Wu & Peng Zhang & Taijiao Jiang & Michael F. Bassetti & Sandro Jube & Yi Sun &, 2015. "Intracellular CD24 disrupts the ARF–NPM interaction and enables mutational and viral oncogene-mediated p53 inactivation," Nature Communications, Nature, vol. 6(1), pages 1-15, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms6909
    DOI: 10.1038/ncomms6909
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    Cited by:

    1. Song Gao & Shuaibin Wang & Zhiying Zhao & Chao Zhang & Zhicao Liu & Ping Ye & Zhifang Xu & Baozhu Yi & Kai Jiao & Gurudatta A. Naik & Shi Wei & Soroush Rais-Bahrami & Sejong Bae & Wei-Hsiung Yang & Gu, 2022. "TUBB4A interacts with MYH9 to protect the nucleus during cell migration and promotes prostate cancer via GSK3β/β-catenin signalling," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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