降低miR-210的表達與Stmn1水平的提高和幽門螺桿菌感染蒙古沙鼠增值相關標記有關。

幽門螺桿菌與胃癌之間的密切關系已為大量研究所證實。日本東京大學的一個研究小組在新一期《自然—通訊》雜志發表論文稱，他們發現一種小核糖核酸對幽門螺桿菌感染導致胃癌發揮著關鍵作用。

這一成果促進了對胃部病態形成的了解，將有助于弄清幽門螺桿菌誘發炎癥的機制以及胃癌發病的原因。

幽門螺桿菌是一種單級、多鞭毛、螺旋形彎曲的細菌。感染這種細菌會導致胃部出現炎癥，引發胃炎、胃潰瘍和胃癌等。不過，其誘導細胞異常增殖的詳細機制則一直沒有弄清。

小核糖核酸是一類不編碼制造蛋白質的單鏈核糖核酸分子，主要參與控制基因表達，調節各種基因的功能。東京大學醫學研究所的研究人員讓長爪沙鼠感染幽門螺桿菌，約兩個月后收集了沙鼠的胃上皮細胞，全面調查了小核糖核酸的表達，發現一種名為miR-210的小核糖核酸表達顯著降低。

研究人員調查了miR-210的功能后，發現它在胃上皮細胞中表達后，細胞增殖就受到遏制，但是遏制其表達，則會促進細胞增殖。研究人員計劃今后通過更加精密的分析，弄清幽門螺桿菌如何影響miR-210的表達，為利用這種小核糖核酸進行胃癌檢查和治療作出貢獻。

原文摘要：

Epigenetic silencing of ?miR-210 increases the proliferation of gastric epithelium during chronicHelicobacter 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 & Chihiro Sasakawa

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 ?STMN1and ?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.

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