COBRE: RIH: THEME B: H PYLORI IN GASTRIC CARCINOGENESIS

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 慢性幽门螺杆菌感染是胃癌最重要的危险因素，但幽门螺杆菌持续定植与胃癌发生之间的分子和细胞机制尚不清楚。我们发现，胃上皮细胞的慢性幽门螺杆菌感染会导致与 p27（一种具有肿瘤抑制特性的细胞周期蛋白依赖性激酶抑制剂）表达减少相关的凋亡抵抗状态。该项目研究幽门螺杆菌降低 p27 表达的机制（目标 1），确定胃上皮细胞中 p27 缺失的功能后果（目标 2），并探索胃上皮细胞中伴随其对幽门螺杆菌诱导的细胞凋亡的抵抗的其他分子变化，作为候选胃癌生物标志物（目标 3）。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Chronic H. pylori infection is the most important risk factor for gastric cancer, but the molecular and cellular mechanisms linking sustained H. pylori colonization with gastric carcinogenesis are poorly defined. We showed that chronic H. pylori infection of gastric epithelial cells leads to a state of apoptosis-resistance associated with decreased expression of p27 - a cyclin-dependent kinase inhibitor with tumor suppressor properties. This project examines the mechanisms by which H. pylori decreases p27 expression (aim 1), determines the functional consequences of p27 loss in gastric epithelial cells (aim 2) and explores other molecular changes in gastric epithelial cells accompanying their resistant to H. pylori-induced apoptosis, as candidate gastric cancer biomarkers (aim 3).