癌症是一种难以治愈的疾病，在世界范围内发病率和死亡率很高，很大程度上是由于耐药性和疾病复发。糖基化是细胞生物分子的一种常见修饰，几十年前就被发现，由于其影响细胞功能和促进癌变的能力而引起了癌症研究的兴趣。多种糖基化类型和结构调节生物分子的功能，是研究和治疗癌症的潜在靶标。最近，p53 在能量代谢中的作用揭示了糖基化与致癌之间的联系，包括 p53 靶基因 α-L-岩藻糖苷酶 1 (FUCA1)，它在岩藻糖基化中发挥着重要作用。在这篇综述中，我们总结了聚糖结构和糖基化相关酶在癌症发展中的作用。还讨论了糖基化与肿瘤微环境因素之间的相互作用，以及糖基化与已知的促癌机制的关系，例如表皮生长因子受体 (EGFR)、磷脂酰肌醇-3-激酶/蛋白激酶 B (PI3K/Akt) ）和 p53 介导的途径。聚糖结构还调节细胞-基质相互作用、细胞-细胞粘附以及细胞迁移和沉降，这些功能障碍可能导致癌症。因此，进一步研究糖基化、相关酶和癌症进展之间的机制关系可能会为潜在的新型癌症治疗提供见解。

Cancer is a difficult-to-cure disease with high worldwide incidence and mortality, in large part due to drug resistance and disease relapse. Glycosylation, which is a common modification of cellular biomolecules, was discovered decades ago and has been of interest in cancer research due to its ability to influence cellular function and to promote carcinogenesis. A variety of glycosylation types and structures regulate the function of biomolecules and are potential targets for investigating and treating cancer. The link between glycosylation and carcinogenesis has been more recently revealed by the role of p53 in energy metabolism, including the p53 target gene alpha-L-fucosidase 1 (FUCA1), which plays an essential role in fucosylation. In this review, we summarize roles of glycan structures and glycosylation-related enzymes to cancer development. The interplay between glycosylation and tumor microenvironmental factors is also discussed, together with involvement of glycosylation in well-characterized cancer-promoting mechanisms, such as the epidermal growth factor receptor (EGFR), phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) and p53-mediated pathways. Glycan structures also modulate cell-matrix interactions, cell-cell adhesion as well as cell migration and settlement, dysfunction of which can contribute to cancer. Thus, further investigation of the mechanistic relationships among glycosylation, related enzymes and cancer progression may provide insights into potential novel cancer treatments.