Over-expression of beta-1,4-galactosyltransferase I, II, and V in human astrocytoma.
Over-expression of beta-1,4-galactosyltransferase I, II, and V in human astrocytoma.
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DOI：
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发表时间：
2001
影响因子：
3.6
通讯作者：
S. Xu;X. Zhu;S. Zhang;S. Yin;L. Zhou;C. Chen;J. Gu
中科院分区：
文献类型：
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作者：
S. Xu;X. Zhu;S. Zhang;S. Yin;L. Zhou;C. Chen;J. Gu
目的β-1，4-半乳糖基转移酶(β-1，4-GalT)I、II和V是通过将UDP-半乳糖转移到N-乙酰氨基葡萄糖(N-GlcNAc)末端形成β-1，4-键，在N-糖链上生物合成N-乙酰乳糖胺的酶。肿瘤在其糖偶联物的碳水化合物中经历不同的变化，这表明糖基转移酶本身可能发生变化。方法比较星形细胞瘤和正常脑组织中β-1，4-Galts的表达。结果我们的逆转录-聚合酶链式反应(RT-PCR)结果显示，β-1，4-GalT I在正常脑组织中缺失，但在II、III、IV级星形细胞瘤中可检测到；β-1，4-GalT II在II、III、IV级星形细胞瘤中表达增加，在正常脑组织中仅有少量表达；β-1，4-GalT V在星形细胞瘤进展过程中表达增加，在IV级星形细胞瘤中表达最高。通过蓖麻凝集素-1(RCA-1)凝集素印迹分析，我们还发现星形细胞瘤与正常脑组织相比有更广泛的半乳糖化条带。一个主要的61kD蛋白在星形细胞瘤中被半乳糖化，但在正常脑组织中没有。结论星形细胞瘤中半乳糖化水平的升高可能与β-1，4-GalT I、II、V基因表达改变有关，且星形细胞瘤的恶性程度与β-1，4-GalT V的表达密切相关。
PURPOSE beta-1,4-Galactosyltransferase (beta-1,4-GalT) I, II, and V are the enzymes responsible for the biosynthesis of N-acetyllactosamine on N-glycans by transferring UDP-galactose to the terminal N-acetylglucosamine (N-GlcNAc) residues with the formation of a beta-1,4-linkage. Neoplasms undergo various changes in the carbohydrate of their glycoconjugates, indicating the possible changes in glycosyltransferases themselves. METHOD Therefore, we compared the expression of beta-1,4-GalTs between astrocytoma and normal brain tissues. RESULTS Our reverse-transcription polymerase chain reaction (RT-PCR) results showed that beta-1,4-GalT I transcript was absent in normal adult brain but detectable in grade II, III, and IV astrocytomas; the level of beta-1,4-GalT II transcript was increased in grade II, III, and IV astrocytomas while only a trace amount was found in normal brain; beta-1,4-GalT V transcript existed in normal brain and increased in the process of astrocytoma progress, with the highest level in grade IV astrocytoma. By Ricinus communis agglutinin-1 (RCA-1) lectin blot assay, we also found the more extensive galactosylated bands in astrocytomas compared with normal brain. A major 61kD protein was galactosylated in astrocytoma but not in normal brain tissues. CONCLUSION These results indicate that the increase of galactosylation in astrocytomas may be caused by the alterations of gene expression of beta-1,4-GalT I, II, and V and that the malignant degree of astrocytoma is correlated with the expression of beta-1,4-GalT V.