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通过改变细胞生长、黏附和运动来控制肿瘤细胞表型的糖基突触微域。

Glycosynaptic microdomains controlling tumor cell phenotype through alteration of cell growth, adhesion, and motility.

机构信息

Division of Biomembrane Research, Pacific Northwest Research Institute, Seattle, WA 98122, USA.

出版信息

FEBS Lett. 2010 May 3;584(9):1901-6. doi: 10.1016/j.febslet.2009.10.065. Epub 2009 Oct 27.

DOI:10.1016/j.febslet.2009.10.065
PMID:19874824
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2867360/
Abstract

Glycosphingolipids (GSLs) GM3 (NeuAcalpha3Galbeta4Glcbeta1Cer) and GM2 (GalNAcbeta4[NeuAcalpha3]Galbeta4Glcbeta1Cer) inhibit (i) cell growth through inhibition of tyrosine kinase associated with growth factor receptor (GFR), (ii) cell adhesion/motility through inhibition of integrin-dependent signaling via Src kinases, or (iii) both cell growth and motility by blocking "cross-talk" between integrins and GFRs. These inhibitory effects are enhanced when GM3 or GM2 are in complex with specific tetraspanins (TSPs) (CD9, CD81, CD82). Processes (i)-(iii) occur through specific organization of GSLs with key molecules (TSPs, caveolins, GFRs, integrins) in the glycosynaptic microdomain. Some of these processes are shared with epithelial-mesenchymal transition induced by TGFbeta or under hypoxia, particularly that associated with cancer progression.

摘要

糖鞘脂 (Glycosphingolipids, GSLs) GM3 (NeuAcalpha3Galbeta4Glcbeta1Cer) 和 GM2 (GalNAcbeta4[NeuAcalpha3]Galbeta4Glcbeta1Cer) 通过抑制与生长因子受体 (Growth Factor Receptor, GFR) 相关的酪氨酸激酶，抑制细胞生长；通过Src 激酶抑制整合素依赖性信号转导，抑制细胞黏附和迁移；通过阻断整合素和 GFR 之间的“串扰”，同时抑制细胞生长和迁移。当 GM3 或 GM2 与特定的四跨膜蛋白 (Tetraspanins, TSPs) (CD9、CD81、CD82) 形成复合物时，这些抑制作用会增强。这些过程通过糖基突触微域中 GSL 与关键分子（TSPs、小窝蛋白、GFRs、整合素）的特定组织来实现。其中一些过程与 TGFbeta 诱导的上皮-间充质转化或缺氧有关，特别是与癌症进展相关的过程。

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