Objective To investigate the effects of Weichang’an（ 胃肠安） on the invasion and metastasis of gastric cancer and its possible mechanism. Methods The cell proliferation assay was used to screen the drug concentration of Weichang’ an. Samples were divided into blank group

Weichang’ an high dose group

Weichang’ an low dose group and 5-FU group. After cell culture for 24 h

the Weichang’an high and low dose groups were treated with the screening concentration of Weichang’an 100 μl for intervention. The 5-FU group was added with 32 mg/L 5-FU injection 100 μl. The blank group was treated with serum-free culture base 100 μl. The cell proliferation was detected by cell counting kit-8（ CCK8） method

and the migration and invasion ability of gastric cancer cells were detected by scratch test and Transwell invasion assay. RUN and FYVE domain protein 3（ RUFY3）

phosphorylated extracellular signal-regulated kinase（ p-ERK）

mitogen-activated protein kinase（ MEK）

phosphorylated mitogen-activated protein kinase（ p-MEK）

Twist1

E-cadherin

vimentin

N-cadherin

vascular endothelial growth factor（ VEGF）

matrix metalloproteinase 2（ MMP2）

matrix metalloproteinase 9（ MMP9） protein expression levels were detected by Western blot. Results The concentrations of 500 mg/L and 1000 mg/L Weichang’ an were screened and set as Weichang’an low and high treated dose. After drug administration for 48 h

the cell migration rate of Weichang’ an high

low dose group and 5-FU group was significantly lower than that of the blank group（ P < 0. 01）. The number of transmembrane cells in the Weichang’an high dose group and 5-FU group was significantly lower than that in the blank group and Weichang’an low dose group（ P < 0. 01）. The invasive inhibition rates of Weichang’an high and low dose groups were 54. 11% and 7. 65%

respectively

and the invasion inhibition rate of 5-FU group was 47. 88%. Compared with the blank group

the expression of p-ERK and Twist1 protein was decreased in Weichang’ an low dose group

and the expression of E-cadherin protein was increased（ P < 0. 05）. The expression of RUFY3

p-ERK

pMEK

Twist1. N-cadherin and Vimentin protein in the Weichang’an high dose group was decreased

and the expression of E-cadherin protein was increased（ P < 0. 05）. Compared with Weichang’an low dose group

the expression of RUFY3

p-MEK and N-cadherin protein in Weichang’ an high dose group was more significantly decreased（ P <0. 05）. Conclusion Weichang’an can inhibit the invasion and metastasis of gastric cancer

and the effect is best at the concentration of 1000 mg/L. The mechanism may be related to the regulation of invasion and metastasis-related proteins and inhibition of epithelial mesenchymal transition in gastric cancer cells by regulating RUFY3 and MAPKs pathways.