Helicobacter pylori regulates cellular migration and apoptosis by activation of phosphatidylinositol 3-kinase signaling.
Helicobacter pylori regulates cellular migration and apoptosis by activation of phosphatidylinositol 3-kinase signaling.
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DOI：
10.1086/596660
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发表时间：
2009-03-01
期刊：
影响因子：
--
通讯作者：
Peek RM Jr
中科院分区：
文献类型：
--
作者：
Nagy TA;Frey MR;Yan F;Israel DA;Polk DB;Peek RM Jr
幽门螺杆菌是胃腺癌最强的危险因素。一个H增加癌症风险的幽门螺杆菌毒力成分是cag分泌系统，其将CagA和肽聚糖易位到宿主细胞中，最终激活信号转导途径。AKT是磷脂酰肌醇3-磷酸激酶（PI 3 K）的靶点，在胃癌中被激活，但PI 3 K-AKT与H.具有致癌潜力的幽门诱导的细胞反应仍不清楚。我们确定了介导H.幽门螺旋杆菌刺激的AKT激活和这些事件在胃上皮细胞中的生物学后果。H. pylori以Src和EGFR依赖的方式增强PI 3 K-AKT信号传导，这也是由功能性cag分泌系统和肽聚糖介导的。PI 3 K活化可减弱感染引起的细胞凋亡，并且是H.幽门诱导的细胞迁移。这些结果表明，PI 3 K-AKT信号调节H的病理生理反应。幽门螺杆菌，这可能会降低致癌的门槛。
Helicobacter pylori is the strongest identified risk factor for gastric adenocarcinoma. One H. pylori virulence constituent that augments cancer risk is the cag secretion system, which translocates CagA and peptidoglycan into host cells, eventuating in activation of signal transduction pathways. AKT is a target of phosphatidylinositol 3-phosphate kinase (PI3K) and is activated in gastric cancer, but the relationship between PI3K-AKT and H. pylori-induced cellular responses with carcinogenic potential remains unclear. We defined the molecular pathways mediating H. pylori-stimulated AKT activation and the biological consequences of these events in gastric epithelial cells. H. pylori enhanced PI3K-AKT signaling in a Src and EGFR-dependent manner, which was also mediated by a functional cag secretion system, and peptidoglycan. PI3K activation attenuated apoptosis in response to infection and was required for H. pylori-induced cell migration. These results indicate that PI3K-AKT signaling regulates pathophysiologic responses to H. pylori that may lower the threshold for carcinogenesis.
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影响因子：
3.4
作者：
Backert, S;Ziska, E;Meyer, TF
通讯作者：
Meyer, TF
DOI：
10.1016/j.bbrc.2004.07.199
发表时间：
2004-09-24
影响因子：
3.1
作者：
Al-Ghoul, L;Wessler, S;Naumann, M
通讯作者：
Naumann, M
影响因子：
56.9
作者：
Franke, TF;Kaplan, DR;Toker, A
通讯作者：
Toker, A
影响因子：
4.8
作者：
Keates, S;Sougioultzis, S;Kelly, CP
通讯作者：
Kelly, CP
影响因子：
5.5
作者：
Allen, LAH;Allgood, JA;Wittine, LM
通讯作者：
Wittine, LM