Kallistatin　has　been　recognized　as　an　endogenous　angiogenesis　inhibitor　and　exerts　pleiotropic　effects　in　inhibiting　tumor　growth,　migration,　apoptosis,　and　inflammation.　The　purpose　of　the　present　study　was　to　investigate　the　potential　role　and　mechanisms　of　kallistatin　in　cervical　cancer.　We　demonstrated　that　kallistatin　effectively　inhibited　cell　proliferation　and　enhanced　apoptosis　in　a　dose-dependent　manner.　Additionally,　kallistatin　suppressed　migration　and　invasion　activities　and　markedly　reduced　the　expression　of　matrix-degrading　metalloproteinases,　progelatinase　(MMP-2),　MMP-9,　and　urokinase-type　PA　(uPA).　Kallistatin　reversed　the　epithelial　mesenchymal　transition　(EMT)　and　caused　the　upregulation　of　epithelial　markers　such　as　E-cadherin　and　inhibited　mesenchymal　markers　such　as　N-cadherin　and　vimentin.　Moreover,　kallistatin　led　to　a　marked　decrease　in　the　expression　of　vascular　endothelial　growth　factor　(VEGF)　and　HIF-I　alpha.　In　a　xenograft　mouse　model,　kallistatin　treatment　reduced　tumor　growth.　Importantly,　kallistatin　strikingly　impeded　NF-kappa　B　activation　by　suppressing　I　kappa　B　alpha　degradation　and　the　level　of　phosphorylation　of　p65.　Interestingly,　similar　to　kallistatin,　treatment　with　PDTC　(an　inhibitor　of　NF-kappa　B)　also　attenuated　cell　invasion　and　migration.　Taken　together,　these　findings　suggest　that　kallistatin　suppresses　cervical　cancer　cell　proliferation,　migration,　and　EMT　and　promotes　cell　apoptosis　by　blocking　the　NF-kappa　B　signaling　pathway,　suggesting　that　kallistatin　may　be　a　novel　therapeutic　target　for　cervical　cancer　treatment.