Garcinol,　a　polyisoprenylated　benzophenone,　has　been　demonstrated　to　exert　anti-cancer　effects　in　various　tumor　cells.　However,　the　effect　of　garcinol　on　cervical　cancer　(CC)　cell　progression　and　the　related　molecular　mechanism　remains　poorly　understood.　Accumulating　evidence　has　verified　that　downregualtion　of　T-cadherin　is　closely　associated　with　tumorigenesis,　suggesting　that　T-cadherin　might　be　a　potential　therapeutic　target　for　cancer　treatment.　In　the　present　study,　Hela　and　SiHa　cells　were　treated　with　different　concentrations　of　garcinol　(0,　5,　10,　and　25　uM),　and　T-cadherin　siRNA　was　synthesized　and　transfected　into　Hela　and　SiHa　cells　combined　with　garcinol　(25　uM)　treatment.　We　found　that　garcinol　dose-dependently　suppressed　cell　viability,　colony　formation,　invasion,　migration,　cell　cycle　progression,　and　promoted　cell　apoptosis　in　CC　cell　lines,　as　well　as　inhibited　tumor　growth　in　xenograft　model.　Importantly,　our　results　showed　that　garcinol　treatment　increased　the　expression　of　T-cadherin　both　in　vitro　and　in　vivo,　and　knockdown　of　T-cahderin　partially　reversed　garcinol-induced　inhibition　of　CC　development　via　activating　P13　K/AKT　signaling　pathway　in　CC　cell　lines.　Thus,　these　findings　demonstrated　the　tumor　suppressive　function　of　garcinol　on　CC　progression,　and　emphasized　that　the　T-cadherin/P13　K/AKT　was　a　potential　mechanism　involved　in　the　antumor　effects　of　garcinol.