Diabetes is a common ailment among people who are at risk of pancreatic cancer. It arises from the endocrine glands of the pancreas, whereas pancreatic cancer arises from the exocrine glands. In diabetic retinopathy, leukocyte cell surface glycans are involved in leukocyte-endothelial cell adhesion and retinal endothelial cell death. Diabetes and pancreatic cancer caused by the oncogene KRAS mutation stimulate the hexosamine production pathway. The activities of 1-3 and 1-4fucosyltransferases were found to be significantly elevated in pancreatic cancer serum in this investigation. We looked at the incorporation of 14C or 3H monosaccharide (CPM) from 14C or 3H monosaccharide donors into particular acceptor catalysed by 1 mg protein of TritonX-100 solubilized tissue extract in 5 non-tumor and 14 tumour tissue specimens for quantitative alterations in glycosyltransferase (GTs) activities in pancreatic carcinogenesis. Pancreatic tumour specimens had 26.0, 42.9, 331.7, 121.0, and 62.8-fold of 1-2, 1-3, 1-4, 1-6 FTs and FT VI activities, respectively, as compared to pancreatic non-tumor tissue specimens with a very low level of GTs activities. N-glycan Man: 1-2GlcNAc-T, chain elongating Gal: 1-3 GlcNAc-T, and N-glycan GalNAc capping 1-3/1-4 GalNAc-T were respectively 95.0, 2.7, and 14.8-fold, and the mRNAs of FUT-4, 1-3, and 1-4 GalNAc-Ts were 8.3, 12.0, and 2.4-fold. 1-2-GlcNAc-T (9.0 fold), 1-3-GlcNAc-T (2.5), 1-3-FT (3.5), 1-6-FT (3.3), FTVII (1.9), GalNAc: 1-3-GalT (1.4), GalNAc: 1-4-Gal-T (2.1), 2-3-(O)ST (2.1), 2-3-(N)ST (4.5), 2-6-(N)ST (4.5), 2-6-(N)ST (8.1). Glycosyltransferase specificities shift when GalNAc replaces Gal in LacNAc terminals, and the transformed GalNAc 1-4GlcNAc by FTs and STs binds to lectins like WGA and SNA. A multifold rise in GTs in pancreatic tumour would indicate their important significance in invasion and intractability of pancreatic cancer, in contrast to a low-level expression-difference between tumour and non-tumor tissues from the stomach, prostate, and colon. High-level GT activities in diabetic neutrophils may play a role in diabetic retinopathy-related changes in cell-cell interactions.
Author(s) DetailsE. V. Chandrasekaran
Department of Cancer Biology, Roswell Park Cancer Institute, Buffalo, New York, USA.
Sriram Neelamegham
Department of Chemical & Biological Engineering, State University of New York at Buffalo, NY, USA.
Khushi L. Matta
Department of Cancer Biology, Roswell Park Cancer Institute, Buffalo, New York, USA and Department of Chemical & Biological Engineering, State University of New York at Buffalo, NY, USA.
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