Journal
HISTOCHEMISTRY AND CELL BIOLOGY
Volume 149, Issue 6, Pages 569-575Publisher
SPRINGER
DOI: 10.1007/s00418-018-1667-8
Keywords
Barrett's esophagus; Chronic atrophic gastritis; Immunohistochemistry; IPMN/PanIN; O-glycan; Pyloric gland adenoma
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Funding
- Japan Society for the Promotion of Science [15H04712, 17K15640]
- Grants-in-Aid for Scientific Research [15H04712, 17K15640] Funding Source: KAKEN
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Gastric gland mucin secreted from pyloric gland cells, mucous neck cells, and cardiac gland cells of the gastric mucosa harbors unique O-glycans carrying terminal alpha 1,4-linked N-acetylglucosamine residues (alpha GlcNAc), which are primarily attached to the scaffold mucin core protein MUC6. alpha GlcNAc acts as an antibiotic against Helicobacter pylori (H. pylori), a microbe causing gastric cancer. In addition, mice deficient in A4gnt, which encodes the enzyme alpha 1,4-N-acetylglucosaminyltransferase (alpha 4GnT) that catalyzes alpha GlcNAc biosynthesis, spontaneously develop gastric differentiated-type adenocarcinoma, even if not infected by H. pylori. Thus, alpha GlcNAc prevents gastric cancer as both an antibiotic and a tumor suppressor (Nakayama in Acta Histochem Cytochem 47:1-9, 2014b). Indeed, in humans alpha GlcNAc loss on MUC6 in differentiated-type adenocarcinoma is closely associated with poor patient prognosis (Shiratsu et al. in Cancer Sci 105:126-133, 2014). Recently, we reported reduced alpha GlcNAc expression on MUC6 in both pyloric gland adenoma of the stomach and chronic atrophic gastritis, in Barrett's esophagus, and in pancreatic intraductal papillary-mucinous neoplasm (IPMN)/pancreatic intraepithelial neoplasia (PanIN), all potentially premalignant conditions. This review discusses whether relatively reduced levels of alpha GlcNAc in these lesions could serve as a biomarker to predict malignant potential and cancer progression.
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