Keloid　is　characterized　by　overactive　fibroblasts.　Forkhead　box　M1　(FOXM1)　is　transcription　factor　that　plays　important　roles　in　the　progression　of　fibrosis.　However,　the　role　of　FOXM1　in　keloid　has　not　been　elucidated.　In　the　present　study,　we　examined　the　expression　levels　of　FOXM1　in　clinical　keloid　tissue　specimens　and　primary　keloid　fibroblasts　(KFs).　The　results　showed　that　FOXM1　levels　were　significantly　increased　in　both　keloid　tissues　and　KFs.　To　further　investigate　the　biological　functions　of　FOXM1,　FOXM1　was　knocked　down　in　KFs　by　transfection　with　small　interfering　RNA　targeting　FOXM1　(si-FOXM1).　Knockdown　of　FOXM1　inhibited　transforming　growth　factor-beta　1　(TGF-beta　1)-induced　cell　proliferation　and　migration　of　KFs.　Besides,　the　increased　expressions　of　collagen　(coll　I),　connective　tissue　growth　factor　(CTGF),　and　alpha-smooth　muscle　actin　(alpha-SMA)　in　TGF-beta　1-induced　KFs　were　suppressed　by　si-FOXM1　transfection.　Furthermore,　TGF-beta　1-induced　increase　in　p-Smad2　and　p-Smad3　expressions　was　attenuated　by　FOXM1　knockdown.　These　data　indicated　that　knockdown　of　FOXM1　inhibited　TGF-beta　1-induced　KFs　activation　and　extracellular　matrix　(ECM)　accumulation,　which　was　attributed　to　the　inhibition　of　TGF-beta　1/Smad　pathway.