Mifepristone　(RU486),　a　synthetic　steroid　compound　used　as　an　abortifacient　drug,　has　received　considerable　attention　to　its　anticancer　activity　recently.　To　explore　the　possibility　of　using　mifepristone　as　a　cancer　metastasis　chemopreventive,　we　performed　a　systems　pharmacology　analysis　of　mifepristone-related　molecules　in　the　present　study.　Data　were　collected　by　using　Natural　Language　Processing　(NLP)　and　513　mifepristone-related　genes　were　dug　out　and　classified　functionally　using　a　gene　ontology　(GO)　hierarchy,　followed　by　KEGG　pathway　enrichment　analysis.　Potential　signal　pathways　and　targets　involved　in　cancer　were　obtained　by　integrative　network　analysis.　Total　thirty-three　proteins　were　involved　in　focal　adhesion-the　key　signaling　pathway　associated　with　cancer　metastasis.　Molecular　and　cellular　assays　further　demonstrated　that　mifepristone　had　the　ability　to　prevent　breast　cancer　cells　from　migration　and　interfere　with　their　adhesion　to　endothelial　cells.　Moreover,　mifepristone　inhibited　the　expression　of　focal　adhesion　kinase　(FAK),　paxillin,　and　the　formation　of　FAK/Src/Paxillin　complex,　which　are　correlated　with　cell　adhesion　and　migration.　This　study　set　a　good　example　to　identify　chemotherapeutic　potential　seamlessly　from　systems　pharmacology　to　cellular　pharmacology,　and　the　revealed　hub　genes　may　be　the　promising　targets　for　cancer　metastasis　chemoprevention.