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H3 ubiquitination by NEDD4 regulates H3 acetylation and tumorigenesis

Author

Listed:
  • Xian Zhang

    (Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USA
    The University of Texas MD Anderson Cancer Center
    The University of Texas Graduate School of Biomedical Sciences at Houston)

  • Binkui Li

    (The University of Texas MD Anderson Cancer Center)

  • Abdol Hossein Rezaeian

    (The University of Texas MD Anderson Cancer Center)

  • Xiaohong Xu

    (The University of Texas MD Anderson Cancer Center)

  • Ping-Chieh Chou

    (Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USA
    The University of Texas MD Anderson Cancer Center)

  • Guoxiang Jin

    (Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USA
    The University of Texas MD Anderson Cancer Center)

  • Fei Han

    (Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USA
    The University of Texas MD Anderson Cancer Center
    The University of Texas Graduate School of Biomedical Sciences at Houston)

  • Bo-Syong Pan

    (Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USA
    The University of Texas MD Anderson Cancer Center)

  • Chi-Yun Wang

    (Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USA
    The University of Texas MD Anderson Cancer Center)

  • Jie Long

    (Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USA
    The University of Texas MD Anderson Cancer Center)

  • Anmei Zhang

    (Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USA
    The University of Texas MD Anderson Cancer Center)

  • Chih-Yang Huang

    (Graduate Institute of Basic Medical Science, China Medical University
    Asia University)

  • Fuu-Jen Tsai

    (College of Chinese Medicine, China Medical University
    Pediatrics and Medical Research, China Medical University Hospital)

  • Chang-Hai Tsai

    (Asia University
    Center of Molecular Medicine, China Medical University Hospital)

  • Christopher Logothetis

    (University of Texas MD Anderson Cancer Center)

  • Hui-Kuan Lin

    (Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USA
    The University of Texas MD Anderson Cancer Center
    The University of Texas Graduate School of Biomedical Sciences at Houston
    Graduate Institute of Basic Medical Science, China Medical University)

Abstract

Dynamic changes in histone modifications under various physiological cues play important roles in gene transcription and cancer. Identification of new histone marks critical for cancer development is of particular importance. Here we show that, in a glucose-dependent manner, E3 ubiquitin ligase NEDD4 ubiquitinates histone H3 on lysine 23/36/37 residues, which specifically recruits histone acetyltransferase GCN5 for subsequent H3 acetylation. Genome-wide analysis of chromatin immunoprecipitation followed by sequencing reveals that NEDD4 regulates glucose-induced H3 K9 acetylation at transcription starting site and enhancer regions. Integrative analysis of ChIP-seq and microarray data sets also reveals a consistent role of NEDD4 in transcription activation and H3 K9 acetylation in response to glucose. Functionally, we show that NEDD4-mediated H3 ubiquitination, by transcriptionally activating IL1α, IL1β and GCLM, is important for tumour sphere formation. Together, our study reveals the mechanism for glucose-induced transcriptome reprograming and epigenetic regulation in cancer by inducing NEDD4-dependent H3 ubiquitination.

Suggested Citation

  • Xian Zhang & Binkui Li & Abdol Hossein Rezaeian & Xiaohong Xu & Ping-Chieh Chou & Guoxiang Jin & Fei Han & Bo-Syong Pan & Chi-Yun Wang & Jie Long & Anmei Zhang & Chih-Yang Huang & Fuu-Jen Tsai & Chang, 2017. "H3 ubiquitination by NEDD4 regulates H3 acetylation and tumorigenesis," Nature Communications, Nature, vol. 8(1), pages 1-15, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14799
    DOI: 10.1038/ncomms14799
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