Inhibitory Effect of Astaxanthin on Gene Expression Changes in Helicobacter pylori -Infected Human Gastric Epithelial Cells.

Helicobacter pylori ( H. pylori ) infection promotes gastric carcinogenesis by increasing oxidative stress, inflammation, and dysregulation of cell survival and proliferation of gastric epithelial cells. Astaxanthin (ASTX), a bioactive carotenoid, exhibits antioxidant and anticancer effects by modulating aberrant signaling pathways that lead to dysregulation of cell death and proliferation. To elucidate the molecular mechanism of H. pylori -induced gastric carcinogenesis and to examine the inhibitory effect of ASTX on H. pylori -induced gastric epithelial cell gene expression changes, we performed comparative RNA-sequencing (RNA-Seq) analysis for H. pylori -infected gastric epithelial cells treated with or without ASTX. RNA-Seq results reveal that differentially expressed genes (DEGs) in H. pylori -infected cells were mainly associated with the Wnt/β-catenin signaling pathway, which is related to cell proliferation. ASTX significantly reversed H. pylori -induced transcriptional alterations of the key mediators involved in β-catenin signaling, notably, porcupine (gene symbol, PORCN) , spermine oxidase ( SMOX ), bone morphogenetic protein (BMP) and activin membrane-bound inhibitor ( BAMBI ), SMAD family member 4 ( SMAD4 ), transforming growth factor-β1 ( TGFB1) , Fos-like 1 ( FOSLI) , and c-myc ( MYC) . We suggest that ASTX may be a potential therapeutic agent that can suppress H. pylori -induced proliferation-associated gene expression changes, in part, by counter-regulating the Wnt/β-catenin signaling pathway.