Matsumoto Yuko, Marusawa Hiroyuki, Kinoshita Kazuo, Endo Yoko, Kou Tadayuki, Morisawa Toshiyuki, Azuma Takeshi, Okazaki Il-Mi, Honjo Tasuku, Chiba Tsutomu
Department of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan.
Nat Med. 2007 Apr;13(4):470-6. doi: 10.1038/nm1566. Epub 2007 Apr 1.
Infection with Helicobacter pylori (H. pylori) is a risk factor for the development of gastric cancer. Here we show that infection of gastric epithelial cells with 'cag' pathogenicity island (cagPAI)-positive H. pylori induced aberrant expression of activation-induced cytidine deaminase (AID), a member of the cytidine-deaminase family that acts as a DNA- and RNA-editing enzyme, via the IkappaB kinase-dependent nuclear factor-kappaB activation pathway. H. pylori-mediated upregulation of AID resulted in the accumulation of nucleotide alterations in the TP53 tumor suppressor gene in gastric cells in vitro. Our findings provide evidence that aberrant AID expression caused by H. pylori infection might be a mechanism of mutation accumulation in the gastric mucosa during H. pylori-associated gastric carcinogenesis.
幽门螺杆菌（H. pylori）感染是胃癌发生的一个危险因素。在此我们表明，“cag”致病岛（cagPAI）阳性的幽门螺杆菌感染胃上皮细胞会通过依赖IκB激酶的核因子κB激活途径，诱导激活诱导的胞苷脱氨酶（AID）异常表达，AID是胞苷脱氨酶家族的一员，作为一种DNA和RNA编辑酶发挥作用。幽门螺杆菌介导的AID上调导致体外培养的胃细胞中TP53肿瘤抑制基因的核苷酸改变积累。我们的研究结果提供了证据，表明幽门螺杆菌感染引起的AID异常表达可能是幽门螺杆菌相关胃癌发生过程中胃黏膜突变积累的一种机制。
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