Helicobacter pylori infection triggers aberrant expression of activation-induced cytidine deaminase in gastric epithelium
Helicobacter pylori infection triggers aberrant expression of activation-induced cytidine deaminase in gastric epithelium
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DOI：
10.1038/nm1566
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发表时间：
2007-04-01
期刊：
影响因子：
82.9
通讯作者：
Chiba, Tsutomu
中科院分区：
文献类型：
--
作者：
Matsumoto, Yuko;Marusawa, Hiroyuki;Chiba, Tsutomu
幽门螺杆菌（Helicobacter pylori，H.幽门螺杆菌）是胃癌发生的危险因素。在这里，我们表明，感染胃上皮细胞与'cag'致病岛（cagPAI）阳性H。幽门螺杆菌通过I κ B激酶依赖性核因子-κ B激活途径诱导激活诱导的胞苷脱氨酶（AID）的异常表达，AID是胞苷脱氨酶家族的成员，其作为DNA和RNA编辑酶发挥作用。H. pylori介导的AID上调导致体外胃细胞中TP 53肿瘤抑制基因核苷酸改变的积累。我们的研究结果提供了证据表明，由H。pylori感染可能是H.幽门相关胃癌发生
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 I kappa B kinase-dependent nuclear factor-kappa B 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.