Gastric Carcinogenesis and Underlying Molecular Mechanisms: Helicobacter pylori and Novel Targeted Therapy.

Gastric Carcinogenesis and Underlying Molecular Mechanisms: Helicobacter pylori and Novel Targeted Therapy.
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胃癌发生及其潜在分子机制:幽门螺杆菌和新型靶向治疗。

DOI:
10.1155/2015/794378
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发表时间:
2015
影响因子:
--
通讯作者:
Suzuki H
Suzuki H
中科院分区:
生物学3区
文献类型:
--
作者:
Nishizawa T;Suzuki H

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活化的中性粒细胞释放的氧自由基是幽门螺杆菌诱导的胃黏膜损伤的细胞毒性因子之一。幽门螺杆菌感染的胃组织中胞苷脱氨酶活性增加促进了各种突变的积累,并可能促进胃癌发生。细胞毒素相关基因A(CagA)通过细菌Ⅳ型分泌系统被递送到胃上皮细胞中,它引起炎症和致癌途径的激活。幽门螺杆菌感染诱导表观遗传改变,例如肿瘤抑制基因中的启动子异常甲基化。据报道,微小RNA的异常表达也与胃肿瘤发生有关。此外,分子靶向治疗的最新进展为通过抗人表皮生长因子受体2(HER - 2)疗法治疗晚期胃癌提供了一种新的有效手段。这篇更新的综述文章强调了包括幽门螺杆菌相关因素在内的胃癌发生的可能机制。
The oxygen-derived free radicals that are released from activated neutrophils are one of the cytotoxic factors of Helicobacter pylori-induced gastric mucosal injury. Increased cytidine deaminase activity in H. pylori-infected gastric tissues promotes the accumulation of various mutations and might promote gastric carcinogenesis. Cytotoxin-associated gene A (CagA) is delivered into gastric epithelial cells via bacterial type IV secretion system, and it causes inflammation and activation of oncogenic pathways. H. pylori infection induces epigenetic transformations, such as aberrant promoter methylation in tumor-suppressor genes. Aberrant expression of microRNAs is also reportedly linked to gastric tumorogenesis. Moreover, recent advances in molecular targeting therapies provided a new interesting weapon to treat advanced gastric cancer through anti-human epidermal growth factor receptor 2 (HER-2) therapies. This updated review article highlights possible mechanisms of gastric carcinogenesis including H. pylori-associated factors.
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