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降低miR-210的表達(dá)與Stmn1水平的提高和幽門螺桿菌感染蒙古沙鼠增值相關(guān)標(biāo)記有關(guān)。

幽門螺桿菌與胃癌之間的密切關(guān)系已為大量研究所證實(shí)。日本東京大學(xué)的一個(gè)研究小組在新一期《自然—通訊》雜志發(fā)表論文稱，他們發(fā)現(xiàn)一種小核糖核酸對(duì)幽門螺桿菌感染導(dǎo)致胃癌發(fā)揮著關(guān)鍵作用。

這一成果促進(jìn)了對(duì)胃部病態(tài)形成的了解，將有助于弄清幽門螺桿菌誘發(fā)炎癥的機(jī)制以及胃癌發(fā)病的原因。

幽門螺桿菌是一種單級(jí)、多鞭毛、螺旋形彎曲的細(xì)菌。感染這種細(xì)菌會(huì)導(dǎo)致胃部出現(xiàn)炎癥，引發(fā)胃炎、胃潰瘍和胃癌等。不過，其誘導(dǎo)細(xì)胞異常增殖的詳細(xì)機(jī)制則一直沒有弄清。

小核糖核酸是一類不編碼制造蛋白質(zhì)的單鏈核糖核酸分子，主要參與控制基因表達(dá)，調(diào)節(jié)各種基因的功能。東京大學(xué)醫(yī)學(xué)研究所的研究人員讓長(zhǎng)爪沙鼠感染幽門螺桿菌，約兩個(gè)月后收集了沙鼠的胃上皮細(xì)胞，全面調(diào)查了小核糖核酸的表達(dá)，發(fā)現(xiàn)一種名為miR-210的小核糖核酸表達(dá)顯著降低。

研究人員調(diào)查了miR-210的功能后，發(fā)現(xiàn)它在胃上皮細(xì)胞中表達(dá)后，細(xì)胞增殖就受到遏制，但是遏制其表達(dá)，則會(huì)促進(jìn)細(xì)胞增殖。研究人員計(jì)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(dá)，為利用這種小核糖核酸進(jìn)行胃癌檢查和治療作出貢獻(xiàn)。

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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