Helicobacter pylori-Mediated Immunity and Signaling Transduction in Gastric Cancer.
Helicobacter pylori-Mediated Immunity and Signaling Transduction in Gastric Cancer.
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DOI：
10.3390/jcm9113699
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发表时间：
2020-11-18
影响因子：
3.9
通讯作者：
Shinomiya N
中科院分区：
文献类型：
--
作者：
Ito N;Tsujimoto H;Ueno H;Xie Q;Shinomiya N
幽门螺杆菌感染是导致胃癌的主要原因，胃癌是世界上第二大常见的癌症相关死亡。H.幽门螺杆菌感染刺激细胞内信号通路，即炎症信号，这可能导致癌细胞的促进和进展。我们在此报告两个重要的信号转导途径，LPS-TLR 4和CagA-MET途径。在H。pylori刺激后，脂多糖（LPS）主要与巨噬细胞和胃上皮细胞上的Toll样受体4（TLR 4）结合。这在胃上皮中诱导炎症反应以上调转录因子，如NF-κB、AP-1和IRF，所有这些都有助于胃癌细胞的发生和进展。与其它细菌LPS相比，H. pylori LPS具有抑制单核细胞（MNC）产生IL-12和IFN-γ的独特功能。这种机制在降低免疫细胞炎症反应程度的同时，也促进了胃癌细胞的存活。HGF/SF-MET信号传导在促进细胞增殖、运动、迁移、存活和血管生成中起主要作用，所有这些都是癌症进展的必要因素。H.幽门螺杆菌感染可能通过其CagA蛋白经由磷酸化依赖性和/或磷酸化非依赖性途径促进胃癌细胞中MET下游信号传导。H. pylori感染包括EGFR、FAK和Wnt/β-Catenin。这些通路在胃上皮粘膜的炎症过程中发挥作用，以及胃癌细胞的进展。因此，H.幽门螺杆菌感染介导的慢性炎症在胃癌的发生和发展中起重要作用。
Helicobacter pylori infection is a leading cause of gastric cancer, which is the second-most common cancer-related death in the world. The chronic inflammatory environment in the gastric mucosal epithelia during H. pylori infection stimulates intracellular signaling pathways, namely inflammatory signals, which may lead to the promotion and progression of cancer cells. We herein report two important signal transduction pathways, the LPS-TLR4 and CagA-MET pathways. Upon H. pylori stimulation, lipopolysaccharide (LPS) binds to toll-like receptor 4 (TLR4) mainly on macrophages and gastric epithelial cells. This induces an inflammatory response in the gastric epithelia to upregulate transcription factors, such as NF-κB, AP-1, and IRFs, all of which contribute to the initiation and progression of gastric cancer cells. Compared with other bacterial LPSs, H. pylori LPS has a unique function of inhibiting the mononuclear cell (MNC)-based production of IL-12 and IFN-γ. While this mechanism reduces the degree of inflammatory reaction of immune cells, it also promotes the survival of gastric cancer cells. The HGF/SF-MET signaling plays a major role in promoting cellular proliferation, motility, migration, survival, and angiogenesis, all of which are essential factors for cancer progression. H. pylori infection may facilitate MET downstream signaling in gastric cancer cells through its CagA protein via phosphorylation-dependent and/or phosphorylation-independent pathways. Other signaling pathways involved in H. pylori infection include EGFR, FAK, and Wnt/β-Catenin. These pathways function in the inflammatory process of gastric epithelial mucosa, as well as the progression of gastric cancer cells. Thus, H. pylori infection-mediated chronic inflammation plays an important role in the development and progression of gastric cancer.
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影响因子：
4.4
作者：
Hishida, Asahi;Matsuo, Keitaro;Hamajima, Nobuyuki
通讯作者：
Hamajima, Nobuyuki
影响因子：
6.7
作者：
Botham, Crystal M.;Wandler, Anica M.;Guillemin, Karen
通讯作者：
Guillemin, Karen
Toll像受体（TLR）自由基周期在慢性炎症中的作用：针对TLR4途径的可能治疗方法。
影响因子：
5.1
作者：
Lucas K;Maes M
通讯作者：
Maes M
影响因子：
4.4
作者：
Hitzler, Iris;Sayi, Ayca;Mueller, Anne
通讯作者：
Mueller, Anne
DOI：
10.1111/j.1749-6632.2012.06622.x
发表时间：
2012-01-01
期刊：
NEUROIMMUNOMODULATION IN HEALTH AND DISEASE II
影响因子：
--
作者：
Benson, Sven;Engler, Harald;Elsenbruch, Sigrid
通讯作者：
Elsenbruch, Sigrid