Helicobacter pylori targets cancer-associated apical-junctional constituents in gastroids and gastric epithelial cells.

ABSTRACT:

Objective

Helicobacter pylori strains that express the oncoprotein CagA augment risk for gastric cancer. However, the precise mechanisms through which cag(+) strains heighten cancer risk have not been fully delineated and model systems that recapitulate the gastric niche are critical for understanding pathogenesis. Gastroids are three-dimensional organ-like structures that provide unique opportunities to study host-H. pylori interactions in a preclinical model. We used gastroids to inform and direct in vitro studies to define mechanisms through which H. pylori modulates expression of the cancer-associated tight junction protein claudin-7.

Design

Gastroids were infected by luminal microinjection, and MKN28 gastric epithelial cells were cocultured with H. pylori wild-type cag(

SUBMITTER: Wroblewski LE 

PROVIDER: S-EPMC4329117 | biostudies-literature | 2015 May

REPOSITORIES: biostudies-literature