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

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 Yashiro, Masashi Fukayama, Taro Fukao () and Chihiro Sasakawa ()
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Kotaro Kiga: International Research Center for Infectious Diseases, The Institute of Medical Science, The University of Tokyo
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

Nature Communications, 2014, vol. 5, issue 1, 1-11

Abstract: 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.

Date: 2014
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DOI: 10.1038/ncomms5497

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