The　present　study　emphasized　on　the　anti-cancerous　effects　of　dioscin　and　its　underlying　molecular　mechanism　in　human　endometrial　cancer　Ishikawa　cells.　Dioscin　significantly　suppressed　the　proliferation　of　Ishikawa　cells　at　IC50　of　2.37　mu　M.　Besides,　dioscin　could　inhibit　the　proliferation　of　Ishikawa　cells　by　blocking　the　G0/G1　cell　cycle　through　up-regulation　of　p16,　p21,　and　p27　and　down-regulation　of　cycle-cellular　protein　(Cyclin　A/D/E)　and　cyclin-dependent　kinase　(CDK2/4/6).　Also,　it　promoted　apoptosis　through　the　mitochondrial　pathway,　including　the　regulation　of　Bcl　family　proteins,　the　increase　of　ROS　levels,　the　activation　of　caspases　(Caspase　9/3),　and　the　decrease　of　mitochondrial　membrane　permeability.　Whereas　dioscin　also　effectively　activated　the　marker　genes　and　proteins　(Fas,　TNF-R1,　and　Caspase　8)　related　to　the　death　receptor-mediated　pathway　which　confirmed　the　involvement　of　both　the　pathways　for　dioscin-induced　apoptosis.　The　current　results　demonstrated　that　dioscin　possessed　potential　health　benefits　with　respect　to　endometrial　cancer　prevention　and　treatment.