Regulation of N-acetylglucosaminyltransferase V and Asn-linked oligosaccharide beta(1,6) branching by a growth factor signaling pathway and effects on cell adhesion and metastatic potential.

Abstract

Recent evidence demonstrates that the changes in the size of N-linked oligosaccharides that correlate with cell transformation and tumorigenicity are due at least in part to the regulation of expression of a glycosyltransferase involved in the branching of N-linked structures, N-acetylglucosaminyltransferase V or GlcNAc-T V. Studies have shown that the increases in GlcNAc-T V expression after oncogenic transformation are most likely caused by direct effects on the GlcNAc-T V promoter by the Ets family of transcriptional activators, which are up-regulated by a cellular proliferation signaling pathway. This pathway begins with growth factor receptors that activate tyrosine kinases at the cell surface and proceeds through src, ras, and raf. Additional evidence for the association between cellular proliferation and GlcNAc-T V expression will be presented, as well as a discussion of the effects of beta(1,6) branching on several of the phenotypes of oncogenically transformed cells, including metastatic potential.