N-acetylglucosaminyltransferase I promotes glioma cell proliferation and migration through increasing the stability of the glucose transporter GLUT1

被引:19
作者
Li, Yinan [1 ]
Liu, Yingchao [2 ]
Zhu, Hongda [3 ]
Chen, Xiaoning [1 ]
Tian, Mi [3 ,4 ]
Wei, Yuanyan [1 ]
Gong, Ye [3 ,4 ]
Jiang, Jianhai [1 ]
机构
[1] Fudan Univ, Sch Basic Med Sci, Dept Biochem & Mol Biol, NHC Key Lab Glycoconjugates Res, Shanghai, Peoples R China
[2] Shandong Univ, Prov Hosp, Dept Neurosurg, Jinan, Shandong, Peoples R China
[3] Fudan Univ, Huashan Hosp, Dept Neurosurg, Shanghai, Peoples R China
[4] Fudan Univ, Huashan Hosp, Dept Crit Care Med, Shanghai, Peoples R China
基金
国家重点研发计划; 中国国家自然科学基金;
关键词
cell proliferation; glioma; Glut1; MGAT1; migration; EPIDERMAL-GROWTH-FACTOR; FACTOR RECEPTOR; GLYCOSYLATION; OLIGOSACCHARIDES; ACTIVATION; EXPRESSION; INVASION; COMPLEX;
D O I
10.1002/1873-3468.13596
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Abnormal alteration of N-glycosylation structure contributes to glioma progression. N-acetylglucosaminyltransferase I (MGAT1) plays an essential role in the conversion of processed high-mannose cores into complex or hybrid N-linked oligosaccharide structures. The function of MGAT1 in glioma development remains largely unknown. Here, we found that the expression of MGAT1 is higher in glioblastoma compared to normal brain tissues. Inhibition of EGFR signalling pathway or serum starvation reduces MGAT1 expression. Knockdown of MGAT1 inhibits glioma cell proliferation and migration. Furthermore, MGAT1 promotes complex N-glycosylation of glucose transporter 1 (Glut1) and increases Glut1 protein levels. In summary, our findings indicate that MGAT1 is highly expressed in glioblastoma and promotes glioma cells at least partly through upregulation of Glut1 protein.
引用
收藏
页码:358 / 366
页数:9
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