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Genome-wide functional screening of miR-23b as a pleiotropic modulator suppressing cancer metastasis

Author

Listed:
  • Hanshuo Zhang

    (College of Engineering, Peking University)

  • Yang Hao

    (College of Engineering, Peking University)

  • Junyu Yang

    (College of Engineering, Peking University)

  • Ying Zhou

    (College of Engineering, Peking University)

  • Juan Li

    (College of Engineering, Peking University)

  • Shenyi Yin

    (College of Engineering, Peking University)

  • Changhong Sun

    (College of Engineering, Peking University)

  • Ming Ma

    (College of Engineering, Peking University)

  • Yanyi Huang

    (College of Engineering, Peking University)

  • Jianzhong Jeff Xi

    (College of Engineering, Peking University)

Abstract

miRNA globally deregulates human carcinoma. A critical open question is how many miRNAs functionally participate in cancer development, particularly in metastasis. We systematically evaluate the capability of all known human miRNAs to regulate certain metastasis-relevant cell behaviours. To perform the high-throughput screen of miRNAs, which regulate cell migration, we developed a novel self-assembled cell microarray. Here we show that over 20% of miRNAs have migratory regulation activity in diverse cell types, indicating a general involvement of miRNAs in migratory regulation. MiR-23b, which is downregulated in human colon cancer samples, potently mediates the multiple steps of metastasis, including tumour growth, invasion and angiogenesis in vivo. It regulates a cohort of prometastatic targets, including FZD7 or MAP3k1. These findings provide new insight into the physiological and potential therapeutic importance of miRNAs as a new class of functional modulators.

Suggested Citation

  • Hanshuo Zhang & Yang Hao & Junyu Yang & Ying Zhou & Juan Li & Shenyi Yin & Changhong Sun & Ming Ma & Yanyi Huang & Jianzhong Jeff Xi, 2011. "Genome-wide functional screening of miR-23b as a pleiotropic modulator suppressing cancer metastasis," Nature Communications, Nature, vol. 2(1), pages 1-11, September.
    • Handle: RePEc:nat:natcom:v:2:y:2011:i:1:d:10.1038_ncomms1555
    DOI: 10.1038/ncomms1555
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