Epigenetic downregulation of MUC17 by H. pylori infection facilitates NF-κB-mediated expression of CEACAM1-3S in human gastric cancer.

ABSTRACT:

Background and aims

Helicobacter pylori invades the mucosal barrier and infects the mucins of gastric epithelial cells. However, whether gastric carcinogenesis caused by H. pylori infection involves the membrane-bound mucins is unclear. This study explored the role of mucin 17 (MUC17) in gastric cancer (GC) associated with H. pylori infection.

Methods

The expression of MUC17 and carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) was examined in human GC cells and tissues with H. pylori infection. Gain- and loss-of-function assays were performed to assess the role of MUC17 in regulating CEACAM1 in H. pylori-infected GC cells.

Results

MUC17 was downregulated in H. pylori-infected GC cells and tissues in association with poor survival of GC patients. Dow

SUBMITTER: Lin S 

PROVIDER: S-EPMC8320707 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature