Beta1,4-galactosyltransferase V functions as a positive growth regulator in glioma.

Hongliang Zong

Research output: Contribution to journalArticlepeer-review

30 Citations (Scopus)

Abstract

beta1,4-galactosyltransferase V (GalT V; EC 2.4.1.38) can effectively galactosylate the GlcNAcbeta1-->6Man arm of the highly branched N-glycans that are characteristic of glioma. Previously, we have reported that the expression of GalT V is increased in the process of glioma. However, currently little is known about the role of GalT V in this process. In this study, the ectopic expression of GalT V could promote the invasion and survival of glioma cells and transformed astrocytes. Furthermore, decreasing the expression of GalT V in glioma cells promoted apoptosis, inhibited the invasion and migration and the ability of tumor formation in vivo, and reduced the activation of AKT. In addition, the activity of GalT V promoter could be induced by epidermal growth factor, dominant active Ras, ERK1, JNK1, and constitutively active AKT. Taken together, our results suggest that GalT V functioned as a novel glioma growth activator and might represent a novel target in glioma therapy.
Original languageEnglish
Pages (from-to)9482-9489
Number of pages8
JournalJournal of Biological Chemistry
Volume281(14)
Issue number14
DOIs
Publication statusPublished - 07 Apr 2006

ASJC Scopus subject areas

  • Biochemistry

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