Bile acids have been linked to pathomechanism and prognosis in various types of
cancers. The present study aimed to investigate the effect of
bile acids on the molecular change in gastric epithelial
cancer cells and to evaluate gastric
bile acid concentration in patients with early
gastric cancer (EGC). Human
gastric cancer cells (AGS and NCI‑N87 cell lines) were treated with several
bile acid types to determine their effect on molecular changes in the cells. Gastric levels of individual
bile acids were measured (primary unconjugated or conjugated
bile acids and secondary
bile acids) in 39 participants (20 controls and 19 patients with EGC). Exposing gastric epithelial
cancer cells to primary
bile acids in vitro upregulated the expression of early growth response factor 1 (Egr‑1) and the oncogenes including c‑Jun, c‑Myc and Snail, whereas a p42/44 MAPK inhibitor exposure reduced their expression. There was a significant difference in age and presence of
atrophic gastritis with intestinal
metaplasia in background mucosa between controls and patients with EGC. There were significant differences in the levels of unconjugated or conjugated primary
bile acids between controls and EGC patients except
lithocholic acid. After adjustment of age and presence of
atrophic gastritis with intestinal
metaplasia, the levels of
cholic acid [adjusted odds ratio (aOR) 4.3; 95% confidence interval (CI): 1.2‑16.2; P=0.029] and
glycochenodeoxycholic acid [aOR 9.9; 95% CI: 1.3‑75.3; P=0.027] were significantly higher in patients with EGC compared with controls. In conclusion,
bile acids upregulate Egr‑1 in
gastric cancer cells via the MAPK signaling pathway, and higher gastric levels of primary
bile acids are associated with EGC. Therefore, exposure of gastric cells to primary
bile acids may play a role in gastric
carcinogenesis.