Objective To investigate the mechanism by which hsa _ circ _0005692 adsorbs miR - 625 - 5p to regulate the expression of CXXC4 and to inhibit gastric cancer metastasis. Methods Human gastric cancer cell lines, BGC-803, SNU-1, NCI-N87, and hs-746 t were cultured in GES-1, and hsa_circ_0005692, miR-625-5p and CXXC4 mRNA were detected by qRT-PCR. hsa-cirC-0005692 and miR - 625 - 5p were identified by double luciferase assays. CXXC4 was targeted by miR-625-5p. hsa_circ_0005692 and Ago2 were identified by radioimmunoprecipitation assays. RNA pull-down result showed that hsa _ circ _ 0005692 combined with miR - 625 - 5p. MTT was used to detect cell proliferation. Transwell assays were used to detect cell migration and invasion ability. Cell flow cytometry was used to detect apoptosis rate. Western blot was used to detect CXXC4 and the migration- and invasion-related factors, N-cadherin and MMP9. Results The expression of HSA in gastric cancer cells was significantly higher than that in gastric cancer cells_ circ_0005692 and CXXC4 showed low expression, while mir - 625 - 5p showed high expression. Dual luciferase assay verified that mir-625-5p could interact with hsa_circ_0005692 and cxxc4 binding, rip test verified that ago2 protein and hsa_ circ _ 0005692, and RNA pull-down test proved that hsa _ circ _ 0005692 specifically binds to mir - 625 - 5p. Overexpression of hsa_circ _0005692 or silencing mir - 625 - 5p can inhibit the proliferation, migration and invasion of gastric cancer cells, and promote their apoptosis. The expression of N-cadherin and MMP9 related to migration and invasion decreased, while overexpression of mir - 625 - 5p or silencing CXXC4 can reverse hsa _ circ _ 0005692 overexpression inhibited the biological activity of gastric cancer cells. Conclusions hsa_circ_0005692 may up-regulate the CXXC4 gene by adsorbing miR-625-5p, thereby inhibiting proliferation, migration and invasion, and promoting the apoptosis of gastric cancer cells.