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

FEBS Lett. 2020 Jan;594(2):358-366. doi: 10.1002/1873-3468.13596. Epub 2019 Sep 17.

Abstract

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.

Keywords: Glut1; MGAT1; cell proliferation; glioma; migration.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • ErbB Receptors / genetics
  • Gene Expression Regulation, Neoplastic / genetics
  • Gene Knockdown Techniques
  • Glioma / genetics*
  • Glioma / pathology
  • Glucose / metabolism
  • Glucose Transporter Type 1 / genetics*
  • Glycosylation
  • Humans
  • N-Acetylglucosaminyltransferases / genetics*
  • Oligosaccharides / genetics
  • Signal Transduction / genetics

Substances

  • Glucose Transporter Type 1
  • Oligosaccharides
  • SLC2A1 protein, human
  • MGAT1 protein, human
  • N-Acetylglucosaminyltransferases
  • EGFR protein, human
  • ErbB Receptors
  • Glucose