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Quantitative Transcriptome Analysis of the Stomach Neck Mucosa from Control vs Claudin (CLDN)-18 knockout mice.

ABSTRACT: Purpose: To determine early changes in gene expression that drive gastric cancer development in the landscape of CLDN18 loss using RNAseq. Results: Although claudin-18 is a tight junction protein and should regulate paracellular permeabiity and/or ion flux across the mucosa, we showed this protein is rather a potent tumor suppressor that regulates cellular signaling and differentiation pathways in gastric epithelial cells. Methods: Stomach neck region mRNA profiles of 7-day-old wild-type (WT) and claudin-18 knockout (CLDN18−/−) mice were generated by deep sequencing, in triplicate, using the Illumina HiSeq2000 sequencing system. The resulting sequences were mapped to the Mouse genome (mm10) using STAR aliger and P-values were adjusted using the Benjamini-Hochberg procedure (J R Statist Soc B 1995;57:289-300). Conclusions: Loss of claudin-18 promotes gastric cancer development by modulating the expression program of gastric epithelial cells, including cellular signaling and differentiation pathways that are required for mucosal homeostasis.

ORGANISM(S): Mus musculus

PROVIDER: GSE93774 | GEO | 2017/01/19

SECONDARY ACCESSION(S): PRJNA362346

REPOSITORIES: GEO

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Knockout mice reveal key roles for claudin-18 in alveolar fluid homeostasis.

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2014-04-06 | E-GEOD-48443 | biostudies-arrayexpress

Knockout mice reveal key roles for claudin-18 in alveolar fluid homeostasis.

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