Gorelik E, Galili U, Raz A
University of Pittsburgh Cancer Institute and Department of Pathology, PA 15213, USA.
Cancer Metastasis Rev. 2001;20(3-4):245-77. doi: 10.1023/a:1015535427597.
This review focuses on the recent advances in investigations of the role of cell surface carbohydrates in tumor metastasis. It also summarizes the results of extensive studies of endogenous lectins, their structure, carbohydrate specificity and biological functions with the major emphasis on the significance of lectin-cell surface carbohydrate interactions in a metastatic process. Numerous data demonstrate that malignant transformation is associated with various and complex alterations in the glycosylation process. Some of these changes might provide a selective advantage for tumor cells during their progression to more invasive and metastatic phenotype. Cell glycosylation depends on the expression and function of various glycosyltransferases and glycosidases. Recently, transfection of genes encoding various glysosyltransferases gene in sense and antisense orientation helped to bring direct evidence that changes in cell surface carbohydrates are important for the metastatic behavior of tumor cells. Cell surface carbohydrates affect tumor cell interactions with normal cells or with the extracellular matrix during metastatic spread and growth. These interactions can be mediated via tumor cell carbohydrates and their binding proteins known as endogenous lectins. The family of the discovered endogenous lectins is rapidly expanding. The number of C-type lectins has reached 50 and at least 10 galectins have been identified. The biological significance of the endogenous lectins and their possible role in tumor growth and metastasis formation has started to unravel. Some lectins recognize the 'foreign' patterns of cell surface carbohydrates expressed by microorganisms and tumor cells, and play a role in innate and adaptive immunity. It was shown that lectins affect tumor cell survival, adhesion to the endothelium or extracellular matrix, as well as tumor vascularization and other processes that are crucial for metastatic spread and growth.
本综述聚焦于细胞表面碳水化合物在肿瘤转移中作用的研究进展。它还总结了对内源凝集素的广泛研究结果，包括其结构、碳水化合物特异性和生物学功能，重点强调凝集素 - 细胞表面碳水化合物相互作用在转移过程中的重要性。大量数据表明，恶性转化与糖基化过程中各种复杂的改变相关。其中一些变化可能为肿瘤细胞向更具侵袭性和转移性表型发展提供选择性优势。细胞糖基化取决于各种糖基转移酶和糖苷酶的表达与功能。最近，以正义和反义方向转染编码各种糖基转移酶基因的实验有助于直接证明细胞表面碳水化合物的变化对肿瘤细胞的转移行为很重要。在转移扩散和生长过程中，细胞表面碳水化合物会影响肿瘤细胞与正常细胞或细胞外基质的相互作用。这些相互作用可通过肿瘤细胞碳水化合物及其结合蛋白（即内源凝集素）介导。已发现的内源凝集素家族正在迅速扩大。C 型凝集素的数量已达 50 种，且已鉴定出至少 10 种半乳糖凝集素。内源凝集素的生物学意义及其在肿瘤生长和转移形成中的可能作用已开始被揭示。一些凝集素识别微生物和肿瘤细胞表达的细胞表面碳水化合物的“外来”模式，并在先天免疫和适应性免疫中发挥作用。研究表明，凝集素会影响肿瘤细胞的存活、与内皮或细胞外基质的黏附，以及肿瘤血管生成和其他对转移扩散和生长至关重要的过程。
