A secreted type of β1,6-N-acetylglucosaminyltransferase V (GnT-V) induces tumor angiogenesis without mediation of glycosylation -: A novel function of GnT-V distinct from the original glycosyltransferase activity
A secreted type of β1,6-N-acetylglucosaminyltransferase V (GnT-V) induces tumor angiogenesis without mediation of glycosylation -: A novel function of GnT-V distinct from the original glycosyltransferase activity
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DOI：
10.1074/jbc.m200521200
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发表时间：
2002-05-10
影响因子：
4.8
通讯作者：
Taniguchi, N
中科院分区：
文献类型：
--
作者：
Saito, T;Miyoshi, E;Taniguchi, N
血管生成是肿瘤进展的第一个调节步骤。在此，我们报告的一些发现表明，β 1，6-N-乙酰氨基葡萄糖转移酶V（GnT-V）的功能作为一种诱导剂的血管生成，有一个新的和完全不同的功能从原来的功能的糖基转移酶。分泌型GnT-V蛋白本身在生理浓度下促进体外和体内血管生成。GnT-V的高碱性结构域诱导成纤维细胞生长因子-2从细胞表面和/或细胞外基质上的硫酸乙酰肝素蛋白聚糖释放，导致血管生成。这些发现为GnT-V与肿瘤转移的关系提供了新的信息。抑制GnT-V的分泌或其表达代表了抑制肿瘤血管生成的新的潜在策略。
Angiogenesis is the first regulatory step of tumor progression. Herein, we report on some findings that show that beta1,6-N-acetylglucosaminyltransferase V (GnT-V) functions as an inducer of angiogenesis that has a novel and completely different function from the original function of glycosyltransferase. A secreted type of GnT-V protein itself promoted angiogenesis in vitro and in vivo at physiological concentrations. The highly basic domain of GnT-V induced the release of fibroblast growth factor-2 from heparan sulfate proteoglycan on the cell surface and/or extracellular matrix, leading to angiogenesis. These findings provide some novel information on the relationship between GnT-V and tumor metastasis. The inhibition of GnT-V secretion or its expression represents a novel potential strategy for the inhibition of tumor angiogenesis.