α1,4-Linked N-acetylglucosamine suppresses gastric cancer development by inhibiting Mucin-1-mediated signaling.

ABSTRACT: Gastric cancer is the second leading cause of cancer deaths worldwide, and more understanding of its molecular basis is urgently needed. 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 α1,4-linked N-acetylglucosamine (αGlcNAc) residues. We previously reported that αGlcNAc loss correlated positively with poor outcomes for patients with differentiated-type gastric cancer. However, the molecular mechanisms underlying these outcomes remained poorly understood. Here, we examined the effects of upregulated αGlcNAc expression on malignant phenotypes of the differentiated-type gastric cancer cell lines, AGS and MKN7. Upregulation of αGlcNAc following ectopic expression of its biosynth

SUBMITTER: Fujii C 

PROVIDER: S-EPMC9633294 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature