CAJ | 학술논문

糖鞘脂由糖链、长链脂肪酸和神经鞘氨醇3部分组成，是细胞结构的重要组成部分，广泛参与细胞的生长、增殖、分化、凋亡、黏附及信号转导等过程。研究发现小鼠胸腺上皮细胞（ Normal murine mammary gland epithelial ， NMuMG）发生上皮间质转化（ Epithelial-mesenchymal transition ， EMT）后，糖鞘脂Gg4的表达显著下降；Gg4能够巩固E-钙黏蛋白和β-连锁蛋白的相互作用，增加细胞粘附，明显抑制上皮间质转化。运用基因工程技术将Gg4的合成酶基因β3GalT4（ UDP-galactose：β-N-acetyl-galacosamine β-1，3 galactosyltransferase ）在NMuMG细胞中过表达及沉默，构建了相应的永久转染细胞株。在上调Gg4的表达后，NMuMG细胞迁移能力降低，而下调Gg4的表达后，细胞迁移能力增强，实验结果证实了Gg4在调节细胞粘附和迁移方面具有重要的生物学功能。
당초지유당련、장련지방산화신경초안순3부분조성，시세포결구적중요조성부분，엄범삼여세포적생장、증식、분화、조망、점부급신호전도등과정。연구발현소서흉선상피세포（ Normal murine mammary gland epithelial ， NMuMG）발생상피간질전화（ Epithelial-mesenchymal transition ， EMT）후，당초지Gg4적표체현저하강；Gg4능구공고E-개점단백화β-련쇄단백적상호작용，증가세포점부，명현억제상피간질전화。운용기인공정기술장Gg4적합성매기인β3GalT4（ UDP-galactose：β-N-acetyl-galacosamine β-1，3 galactosyltransferase ）재NMuMG세포중과표체급침묵，구건료상응적영구전염세포주。재상조Gg4적표체후，NMuMG세포천이능력강저，이하조Gg4적표체후，세포천이능력증강，실험결과증실료Gg4재조절세포점부화천이방면구유중요적생물학공능。
Glycosphingolipids ( GSLs) composed of carbohydrate chain , long fatty acid and sphingosine are important components in cellular structure .GSLs widely participate in processes like cell growth , proliferation , differentiation , apoptosis , cell-cell adhesion , and signal transduction .The previous findings suggested that the expression of Gg 4 in mouse mammary gland cells ( NMuMG ) de-creased significantly in the process of Epithelial-mesenchymal transition ( EMT) .Gg4 may consolidate the interaction between E-cad-herin andβ-catenin, increase the cell-cell adhesion, and inhibit the EMT process .In this study, the expression of β3GalT4 encodeing UDP-galactose:β-N-acetyl-galacosamine β-1, 3 galactosyltransferase (β3GalT4, the synthetase of Gg4), in NMuMG cell was overex-pressed and silenced .Overexpression of Gg4 inhibiting the cell motility and vice versa was confirmed by colloidal gold assay .All the data proved the biological function role of Gg 4.