OBJECTIVE:　To　explore　how　GLI-1　affects　the　EMT　induced　by　TGF-beta　1　in　gastric　cancer.　MATERIALS　AND　METHODS:　Following　24　hours　of　culture　of　SGC-7901　cells　in　presence　of　TGF-beta　1,　we　observed　the　changes　in　morphology　as　well　as　mRNA　and　protein　expressions　of　GLI-1,　E-cadherin　and　Vimentin　by　RT-PCR　and　Western　blot.　Transwell　assay　was　conducted　to　evaluate　the　changes　in　invasion　ability　of　SGC-7901　cells.　Then.　SGC-7901　cells　were　co-treated　with　TGF-beta　1　and　GANT　61,　and　changes　of　the　above　indexes　were　also　detected　using　the　corresponding　methods.　RESULTS:　In　presence　of　TGF-beta　1,　EMT　was　initiated　in　SGC-7901　cells　EMT　with　increased　cell　invasion　ability,　and　the　mRNA　and　protein　expressions　of　E-cadherin　were　downregulated,　while　those　of　the　GLI-1　and　Vimentin　were　upregulated.　Conversely,　the　co-treatment　of　TGF-beta　1　and　GANT　61　suppressed　the　increased　cell　invasion　ability　induced　only　by　TGF-beta　1,　and　the　changes　in　mRNA　and　protein　expressions　of　these　factors　were　abolished.　CONCLUSIONS:　We　found　that　GLI-1　facilitates　the　EMT　induced　by　TGF-beta　1　in　SGC-7901　cells,　which　may　serve　as　a　potential　target　in　developing　the　clinical　treatment　of　gastric　cancer.