Abstract: This work aims to elucidate the function of gene Wnt10A during the proliferation and migration of gastric cancer cells and the underlying molecular mechanism，for providing new target molecule in the diagnosis and treatment of gastric cancer. Real-time quantitative PCR and Western bolt analysis were used to detect gene expression；RNAi technology was applied to knockdown and decrease the expression of Wnt10A，and MTT assay，wound healing assay and transwell assay were employed to detect the biological behavior of gastric cancer cells. Results showed that gene Wnt10A expressed more highly in tumor tissues than that in adjacent normal tissues，approximately 3 times. The level of Wnt10A in gastric cancer cell lines was also higher than the normal cells GES. The proliferation rate of AGS cells reduced by 40%，the migration rate decreased by 40%，and the invasive ability was also downregulated about 70%，when the expression level of gene Wnt10A in AGS cells decreased about 60%. Furthermore，Western blot analysis demonstrated that the expressions of β-catenin，Cyclin D，TCF and gene Myc reduced after Wnt10A knockdown in AGS cells，while the expression levels of DKK1 and GSK3β increased，which was in consistent with the results by the treatment of LGK-974，a specific inhibitor against Wnt/β-catenin signaling. Conclusively，gene Wnt10A promotes the proliferation and migration of gastric cancer cells through simulating activation of Wnt/β-catenin/Myc signaling pathway，i.e.，functions as cancer-promoting gene.

Key words: Wnt10A, gastric cancer, AGS, Wnt/β-catenin signaling