Gastric　cancer　remains　a　leading　cause　of　cancer-related　mortality　worldwide,　characterized　by　poor　prognosis　due　to　its　aggressive　nature　and　high　metastatic　potential.　While　the　E2-conjugating　enzyme　UBE2I　(UBC9),　essential　for　SUMOylation,　has　been　implicated　in　various　cancers,　its　precise　role　in　gastric　cancer　remains　poorly　understood.　In　the　study,　we　demonstrate　significant　UBC9　overexpression　in　gastric　cancer　tissues,　which　correlates　with　poor　clinical　outcomes.　Functional　analyses　revealed　that　UBC9　knockdown　significantly　suppressed　gastric　cancer　cell　proliferation,　migration,　and　invasion　in　vitro　and　in　vivo,　whereas　UBC9　overexpression　enhanced　these　malignant　phenotypes.　Through　integrated　transcriptomic　and　proteomic　analyses,　we　identified　ATF2　(Activating　Transcription　Factor　2)　as　a　crucial　downstream　effector　of　UBC9-mediated　oncogenic　signaling.　The　mechanistic　relationship　between　these　factors　was　confirmed　as　ATF2　knockdown　substantially　attenuated　the　oncogenic　effects　of　UBC9　overexpression.　This　newly　identified　UBC9-ATF2　regulatory　axis　promotes　gastric　cancer　progression　by　enhancing　cellular　proliferation　and　metastatic　potential.　Our　findings　establish　UBC9　and　ATF2　as　promising　prognostic　biomarkers　and　potential　therapeutic　targets,　suggesting　that　intervention　in　the　UBC9-ATF2　axis　may　provide　novel　therapeutic　strategies　for　inhibiting　gastric　cancer　progression　and　improving　patient　outcomes.