Role of tumor-associated gangliosides in cancer progression
Role of tumor-associated gangliosides in cancer progression
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DOI：
10.1016/s0300-9084(03)00006-3
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发表时间：
2003-03-01
期刊：
影响因子：
3.9
通讯作者：
Aubry, J
中科院分区：
文献类型：
--
作者：
Birklé, S;Zeng, G;Aubry, J
神经外胚层肿瘤的主要特征是肿瘤相关的神经节苷脂抗原的存在，如神经节苷脂，由单抗定义。最近，越来越多的证据表明，神经节苷脂在体外和体内改变了几种营养因子的生物学效应，以及这些因子产生的促有丝分裂信号级联反应。神经节苷脂在肿瘤进展中的功能作用可以被重新审视：(I)神经节苷脂抗原在细胞表面或从细胞中脱落，充当免疫抑制剂，如通常观察到的抑制细胞毒性T细胞和树突状细胞，(Ii)某些神经节苷脂，如GD3或GM2，促进肿瘤相关血管生成，(Iii)神经节苷脂强烈调节细胞黏附/运动，从而启动肿瘤转移，(Iv)神经节苷脂抗原与微域中的转导分子直接连接，启动黏附与信号耦合，和(V)神经节苷脂抗原及其分解代谢产物是通过与生长因子受体或其他蛋白激酶相关的酪氨酸激酶相互作用而调节信号转导的分子。鉴于这些唾液酸化神经节苷脂的潜在重要性及其对体内生物学行为的调节，有必要对神经节苷脂的作用进行进一步的研究。(C)2003年版《Elsevier SAS和Societe Francaise de Biochie et Biologie Moleculaire》。版权所有。
Neuroectodermic tumors can mostly be characterized by the presence of tumor-associated glycosphingolipid antigens, such as gangliosides, defined by monoclonal antibodies. Recently, cumulative evidence indicates that gangliosides modify the biological effects of several trophic factors, in vitro and in vivo, as well as the mitogenic signaling cascade that these factors generate. The functional roles of gangliosides in tumor progression can be revisited: (i) ganglioside antigens on the cell surface, or shed from the cells, act as immunosuppressors, as typically observed for the suppression of cytotoxic T cells and dendritic cells, (ii) certain gangliosides, such as GD3 or GM2, promote tumor-associated angiogenesis, (iii) gangliosides strongly regulate cell adhesion/motility and thus initiate tumor metastasis, (iv) ganglioside antigens are directly connected with transducer molecules in microdomains to initiate adhesion coupled with signaling, and (v) ganglioside antigens and their catabolites are modulators of signal transduction through interaction with tyrosine kinases associated with growth factor receptors or other protein kinases. Given the potential importance of these sialylated gangliosides and their modulating biological behavior in vivo, further studies on the role of gangliosides are warranted. (C) 2003 Editions scientifiques et medicales Elsevier SAS and Societe francaise de biochimie et biologie moleculaire. All rights reserved.