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Menin enhances c-Myc-mediated transcription to promote cancer progression

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  • Gongwei Wu

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Mengqiu Yuan

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Shengqi Shen

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Xiaoyu Ma

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Jingwen Fang

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Lianbang Zhu

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Linchong Sun

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Zhaoji Liu

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Xiaoping He

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • De Huang

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Tingting Li

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Chenchen Li

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Jun Wu

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Xin Hu

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Zhaoyong Li

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Libing Song

    (Sun Yat-sen University Cancer Center, Guangzhou)

  • Kun Qu

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Huafeng Zhang

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

  • Ping Gao

    (CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China)

Abstract

Menin is an enigmatic protein that displays unique ability to either suppress or promote tumorigenesis in a context-dependent manner. The role for Menin to promote oncogenic functions has been largely attributed to its essential role in forming the MLL methyltransferase complex, which mediates H3K4me3. Here, we identify an unexpected role of Menin in enhancing the transactivity of oncogene MYC in a way independent of H3K4me3 activity. Intriguingly, we find that Menin interacts directly with the TAD domain of MYC and co-localizes with MYC to E-Box to enhance the transcription of MYC target genes in a P-TEFb-dependent manner. We further demonstrate that, by transcriptionally promoting the expression of MYC target genes in cancer cells, Menin stimulates cell proliferation and cellular metabolism both in vitro and in vivo. Our results uncover a previously unappreciated mechanism by which Menin functions as an oncogenic regulatory factor that is critical for MYC-mediated gene transcription.

Suggested Citation

  • Gongwei Wu & Mengqiu Yuan & Shengqi Shen & Xiaoyu Ma & Jingwen Fang & Lianbang Zhu & Linchong Sun & Zhaoji Liu & Xiaoping He & De Huang & Tingting Li & Chenchen Li & Jun Wu & Xin Hu & Zhaoyong Li & Li, 2017. "Menin enhances c-Myc-mediated transcription to promote cancer progression," Nature Communications, Nature, vol. 8(1), pages 1-15, August.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15278
    DOI: 10.1038/ncomms15278
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