Augmentation of UDP-GalNAc: Fuc alpha 1-2Gal alpha 1-3 N-acetylgalactosaminyl transferase activity in nitrosamine-induced hamster pancreatic cancers

Citation
M. Hirota et al., Augmentation of UDP-GalNAc: Fuc alpha 1-2Gal alpha 1-3 N-acetylgalactosaminyl transferase activity in nitrosamine-induced hamster pancreatic cancers, J EXP CL C, 19(2), 2000, pp. 235-239
Citations number
34
Categorie Soggetti
Oncology
Journal title
JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
ISSN journal
03929078 → ACNP
Volume
19
Issue
2
Year of publication
2000
Pages
235 - 239
Database
ISI
SICI code
0392-9078(200006)19:2<235:AOUFA1>2.0.ZU;2-O
Abstract
Pancreatic cancers induced by N-nitrosobis(2-oxopropyl)amine (BOP) in hamst ers produce blood group-A antigen (BG-A Ag), which is not present in the no rmal pancreas. To understand the neo-expression mechanism of BG-A Ag, we ex amined uridine diphosphate (UDP)-N-acetylgalactosamine (GalNAc): fucose (Fu c) alpha 1-2 galactose (Gal) alpha 1-3 GalNAc transferase (alpha 1-3 GalNAc Tf) activity, the enzyme responsible for BG-A production. The specific act ivity of alpha 1-3 GalNAc Tf in pancreatic cancers was similar to 8,000 nmo le/g protein/h, whereas it was absent from the normal pancreas. Although th e antrum and colon express A-Tf and BG-A Ag, the divalent cation requiremen ts of alpha 1-3 GalNAc Tf in these tissues were different from those of can cers. These results suggest that alpha 1-3 GalNAc Tf is activated during BO P-induced pancreatic carcinogenesis, and that there are multiple alpha 1-3 GalNAc Tf isozymes present in hamster tissues.