Ma Hui-Ying, Liu Xin-Zhou, Liang Chun-Min
Hui-Ying Ma, Xin-Zhou Liu, Chun-Min Liang, Lab of Tumor Immunology, Department of Anatomy and Histology and Embryology, Shanghai Medical College of Fudan University, Shanghai 200032, China.
World J Gastroenterol. 2016 Aug 7;22(29):6619-28. doi: 10.3748/wjg.v22.i29.6619.
Gastric cancer (GC) is the fifth most common malignancy in the world. The major cause of GC is chronic infection with Helicobacter pylori (H. pylori). Infection with H. pylori leads to an active inflammatory microenvironment that is maintained by immune cells such as T cells, macrophages, natural killer cells, among other cells. Immune cell dysfunction allows the initiation and accumulation of mutations in GC cells, inducing aberrant proliferation and protection from apoptosis. Meanwhile, immune cells can secrete certain signals, including cytokines, and chemokines, to alter intracellular signaling pathways in GC cells. Thus, GC cells obtain the ability to metastasize to lymph nodes by undergoing the epithelial-mesenchymal transition (EMT), whereby epithelial cells lose their epithelial attributes and acquire a mesenchymal cell phenotype. Metastasis is a leading cause of death for GC patients, and the involved mechanisms are still under investigation. In this review, we summarize the current research on how the inflammatory environment affects GC initiation and metastasis via EMT.
胃癌（GC）是全球第五大常见恶性肿瘤。胃癌的主要病因是幽门螺杆菌（H. pylori）的慢性感染。幽门螺杆菌感染会导致一个由T细胞、巨噬细胞、自然杀伤细胞等免疫细胞维持的活跃炎症微环境。免疫细胞功能障碍会使胃癌细胞发生突变并积累，诱导异常增殖并防止细胞凋亡。同时，免疫细胞可分泌某些信号，包括细胞因子和趋化因子，以改变胃癌细胞内的信号通路。因此，胃癌细胞通过上皮-间质转化（EMT）获得转移至淋巴结的能力，在此过程中上皮细胞失去其上皮特性并获得间充质细胞表型。转移是胃癌患者死亡的主要原因，其相关机制仍在研究中。在本综述中，我们总结了目前关于炎症环境如何通过EMT影响胃癌发生和转移的研究。
