Objective:To investigate the effects and possible mechanisms of action of Curcurna wenyujin Y.H.Chen et C.Ling n-Butyl alcohol extract (CWNAE) on repression of human gastric cancer (GC) AGS cell invasion induced by co-culturing with Helicobacter pylori (HP).Methods:AGS cells were cultured with HP of positive or negative cytotoxin-associated gene A (CagA) and vacuolating cytotoxin gene A (VacA) expression (CagA+/-or VacA+/-) and divided into 5 group.Group A was cultured without HP as a control,Group B with HPCagA+VacA+,Group C with HPCagA+VacA-,Group D with HPCagA+VacA+ and CWNAE,and Group E with HPCagA+VacA-and CWNAE.Methylthiazolyldiphenyl-tetrazolium bromide (MTT) and tumor invasion assays,examinations of morphology and ultramicroscopic structures,quantitative real-time polymerase chain reaction and Westem blots were performed to measure the effects and uncover the mechanisms behind these effects of HPCagA+VacA+ and CWNAE on the epithelial-mesenchymal transition (EMT) of AGS cells.Results:The 10% inhibitory concentration of CWNAE against AGS cells after a 48 h incubation was 19.73± 1.30 μg/mL.More AGS cells were elongated after co-culturing with HPCagA+VacA+ than after culturing with HPCagA+VacA-.In tumor invasion assays,HPCagA+VacA+ significantly enhanced the invasiveness of AGS cells compared to the other experimental groups (all P value <0.05),and this effect was inhibited by CWNAE.Treatment with CWNAE normalized tight junctions and reduced the number of pseudopodia of AGS cells co-cultured with HPCagA+VacA+.HPCagA+VacA+ up-regulated zincfinger ebox binding homeobox 1 (ZEB1) in AGS cells after co-culturing for 24 h.Expression of caudal type homeobox transcription factor (CDX-2) and claudin-2 was significantly increased by HPCagA+VacA+ (P<0.05),but not by HPCagA+VacA-.Conclusions:HPCagA+VacA+ promoted the invasiveness of AGS cells through up-regulation of ZEB1 transcription and claudin-2 and CDX-2 expression.CWNAE inhibited these effects of HPCagA+VacA+ on AGS cells by down-regulating ZEB1 transcription,and CDX-2 and claudin-2 expression.