Inflammatory　cytokines　can　induce　the　expression　of　cell　adhesion　molecules　(CAMs)　in　endothelial　cells.　The　induction　may　play　an　important　role　in　attracting　circulating　tumor　cells　(CTCs)　to　endothelial　cells.　S-nitrosocaptopril　(CapNO)　is　known　to　produce　vasorelaxation　and　interfere　the　hetero-adhesion　of　CTCs　to　vascular　endothelium　via　down-regulating　the　expression　of　CAMs.　To　elucidate　the　mechanisms　underlying　the　inhibition　of　CapNO　on　CAMs,　in　this　study,　we　examined　the　relationship　between　cytokines　and　CAMs　expression　and　investigated　the　effects　of　CapNO　on　cytokine-induced　NF-kappa　B　and　JAK/STAT　signal　pathways.　The　activation　of　CAMs　by　cytokines　was　dependent　on　concentrations　and　reaction　time　of　cytokines,　and　the　combination　of　cytokines　could　produce　a　strong　synergistic　effect.　IL-1　beta　induced　the　expression　of　CAMs　on　endothelial　cells　by　activating　NF-kappa　B　and　JAK/STAT　pathways.　CapNO　inhibited　IL-1　beta-stimulated　NF-kappa　B　pathway　by　down-regulating　IKK-alpha　and　inducing　Ix13-alpha　directly.　CapNO　also　inhibited　JAK/STAT　pathway　by　inhibiting　JAK2　and　STAT3　expressions.　These　effects　bring　about　down-regulating　CAMs　expression　on　endothelial　cells.　These　results　suggest　that　CapNO　may　interrupt　adhesion　of　cancer　cells　to　endothelium　by　suppressing　CAMs　via　inhibiting　the　NF-kappa　B　and　JAK/STAT　pathways　in　endothelial　cells.　(C)　2016　Elsevier　B.V.　All　rights　reserved.