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Epigenetic silencing of miR-210 increases the proliferation of gastric epithelium during chronic Helicobacter pylori infection

Author

Listed:
  • Kotaro Kiga

    (International Research Center for Infectious Diseases, The Institute of Medical Science, The University of Tokyo
    Max-Planck-Institute of Immunobiology and Epigenetics)

  • Hitomi Mimuro

    (International Research Center for Infectious Diseases, The Institute of Medical Science, The University of Tokyo)

  • Masato Suzuki

    (Institute of Medical Science, The University of Tokyo)

  • Aya Shinozaki-Ushiku

    (Graduate School of Medicine, The University of Tokyo)

  • Taira Kobayashi

    (International Research Center for Infectious Diseases, The Institute of Medical Science, The University of Tokyo)

  • Takahito Sanada

    (International Research Center for Infectious Diseases, The Institute of Medical Science, The University of Tokyo)

  • Minsoo Kim

    (Institute of Medical Science, The University of Tokyo)

  • Michinaga Ogawa

    (Institute of Medical Science, The University of Tokyo)

  • Yuka W. Iwasaki

    (Max-Planck-Institute of Immunobiology and Epigenetics)

  • Hiroyuki Kayo

    (Max-Planck-Institute of Immunobiology and Epigenetics)

  • Yoko Fukuda-Yuzawa

    (Max-Planck-Institute of Immunobiology and Epigenetics)

  • Masakazu Yashiro

    (Osaka City University Graduate School of Medicine)

  • Masashi Fukayama

    (Graduate School of Medicine, The University of Tokyo)

  • Taro Fukao

    (Max-Planck-Institute of Immunobiology and Epigenetics)

  • Chihiro Sasakawa

    (Institute of Medical Science, The University of Tokyo
    Institute of Medical Science, The University of Tokyo
    Nippon Institute for Biological Science
    Medical Mycology Research Center, Chiba University)

Abstract

Persistent colonization of the gastric mucosa by Helicobacter pylori (Hp) elicits chronic inflammation and aberrant epithelial cell proliferation, which increases the risk of gastric cancer. Here we examine the ability of microRNAs to modulate gastric cell proliferation in response to persistent Hp infection and find that epigenetic silencing of miR-210 plays a key role in gastric disease progression. Importantly, DNA methylation of the miR-210 gene is increased in Hp-positive human gastric biopsies as compared with Hp-negative controls. Moreover, silencing of miR-210 in gastric epithelial cells promotes proliferation. We identify STMN1 and DIMT1 as miR-210 target genes and demonstrate that inhibition of miR-210 expression augments cell proliferation by activating STMN1 and DIMT1. Together, our results highlight inflammation-induced epigenetic silencing of miR-210 as a mechanism of induction of chronic gastric diseases, including cancer, during Hp infection.

Suggested Citation

  • Kotaro Kiga & Hitomi Mimuro & Masato Suzuki & Aya Shinozaki-Ushiku & Taira Kobayashi & Takahito Sanada & Minsoo Kim & Michinaga Ogawa & Yuka W. Iwasaki & Hiroyuki Kayo & Yoko Fukuda-Yuzawa & Masakazu , 2014. "Epigenetic silencing of miR-210 increases the proliferation of gastric epithelium during chronic Helicobacter pylori infection," Nature Communications, Nature, vol. 5(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5497
    DOI: 10.1038/ncomms5497
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