Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Rua Dr Roberto Frias s/n, 4200-465 Porto, Portugal; Institute of Biomedical Sciences of Abel Salazar (ICBAS), University of Porto, Rua de Jorge Viterbo Ferreira n.° 228, 4050-313 Porto, Portugal.
Trends Mol Med. 2013 Nov;19(11):664-76. doi: 10.1016/j.molmed.2013.07.003. Epub 2013 Aug 8.
Gastric cancer has a high incidence and mortality, so there is a pressing need to understand the underlying molecular mechanisms in order to discover novel biomarkers. Glycosylation alterations are frequent during gastric carcinogenesis and cancer progression. This review describes the role of glycans from the initial steps of the carcinogenesis process, in which Helicobacter pylori adheres to host mucosa glycans and modulates the glycophenotype, as well as how glycans interfere with epithelial cell adhesion by modulating epithelial cadherin functionality in gastric cancer progression. Other mechanisms regulating gastric cancer malignant behavior are discussed, such as increased sialylation interfering with key signaling pathways and integrin glycosylation leading to an invasive phenotype. Applications of these glycosylation alterations in the clinical management of gastric cancer patients are discussed.
胃癌发病率和死亡率高，因此迫切需要了解潜在的分子机制，以便发现新的生物标志物。在胃癌的发生和发展过程中，糖基化改变很常见。本综述描述了糖链在癌变过程初始步骤中的作用，包括幽门螺杆菌黏附于宿主黏膜糖链并调节糖表型，以及糖链如何通过调节上皮钙黏蛋白功能干扰上皮细胞黏附从而促进胃癌进展。还讨论了其他调节胃癌恶性行为的机制，如增加唾液酸化干扰关键信号通路和整合素糖基化导致侵袭表型。讨论了这些糖基化改变在胃癌患者临床管理中的应用。
