W. Zhang et al., Regulation of expression of the human beta-1,2-N-acetylglucosaminyltransferase II gene (MGAT2) by Ets transcription factors, BIOCHEM J, 347, 2000, pp. 511-518
Oncogenic transformation of fibroblasts by the src oncogene has long been k
nown to cause an increase in the size of cell-surface protein-bound oligosa
ccharides, owing primarily to increased N-glycan branching mediated by incr
eased beta-1,6-N-acetylglucosaminyltransferase V (GnT V) activity. The src-
responsive element of the GnT V promoter was localized to Ets-binding sites
and the promoter was transcriptionally stimulated by both ets-1 and ets-2
expression [Buckhaults, Chen, Fregien and Pierce (1997) J. Biol. Chem. 272,
19575-19581; Kang, Saito, Ihara, Miyoshi, Koyama, Sheng and Taniguchi (199
6) J. Biol. Chem. 271, 26706-26712]. Because GnT V action requires the prio
r action of beta-1,2-N-acetylglucosaminyltransferase II (GnT II) and the hu
man GnT II promoter contains four putative Ets-binding sites [Chen, Zhou, T
an and Schachter (1998) Glycoconj. J. 15, 301-308], GnT II might also be un
der oncogenic control via Ets transcription factors. We now report that co-
transfection into HepG2 or COS-1 cells of either ets-1 or ets-2 expression
plasmids together with chimaeric GnT II promoter-chloramphenicol acetyltran
sferase plasmids results in a 2-4-fold stimulation of promoter activity. Mo
bility-shift assays and South-Western blots localized the functional Ets-bi
nding site to one of the four putative sites on the GnT II promoter, The Gn
T II promoter, unlike the GnT V promoter, is not activated by either src or
neu. Therefore although both promoters are stimulated by a member of the E
ts family of transcription factors, the functional role of this Ets transcr
iptional control seems to be different for the two genes.