PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23135108-2 2012 METHODS: RT-PCR and Western blotting were used to detect the effect of NS-398, the COX-2 inhibitor on mRNA and protein expression of VEGF and Survivin in oral squamous carcinoma cell line Tca8113. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 71-77 vascular endothelial growth factor A Homo sapiens 133-137 26909300-9 2014 NS-398 also inhibited subcutaneous SK-N-AS tumor development with decreased angiogenesis and vascular endothelial growth factor-A expression. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 vascular endothelial growth factor A Homo sapiens 93-129 23135108-4 2012 RESULTS: NS-398 could down-regulate the expression of VEGF and Survivin in Tca8113 in a time-dependent manner. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 9-15 vascular endothelial growth factor A Homo sapiens 54-58 22009181-6 2012 RESULTS: NS-398 inhibited HCC proliferation and decreased the expression level of VEGF in HCC cells only under normoxia conditions. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 9-15 vascular endothelial growth factor A Homo sapiens 82-86 22009181-8 2012 The NS-398-induced increase in VEGF expression in SNU387 cell was associated with the up-regulation of the DDR2 gene. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 4-10 vascular endothelial growth factor A Homo sapiens 31-35 16861876-8 2006 DCA-induced VEGF protein expression was inhibited by pretreatment with NS-398 (COX-2 inhibitor), PDTC (NF-kappaB inhibitor), or tauroursodeoxycholic acid (TUDC). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 71-77 vascular endothelial growth factor A Homo sapiens 12-16 19210337-10 2009 The interleukin-1alpha-induced vascular endothelial growth factor mRNA and protein expression was inhibited to the same extent by indomethacin and NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 147-153 vascular endothelial growth factor A Homo sapiens 31-65 17302909-9 2007 NS-398, a COX-2 inhibitor, inhibited TGF-beta-induced VEGF production in a dose-dependent manner. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 vascular endothelial growth factor A Homo sapiens 54-58 20939988-6 2010 After inhibiting COX-2 expression with COX-2 specific inhibitor NS398, Hp-induced VEGF mRNA expression significantly reduced (P<0.01). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 64-69 vascular endothelial growth factor A Homo sapiens 82-86 18718465-6 2008 However, the COX-2-selective inhibitor, NS398, also attenuated VEGF-induced proliferation, implying a distinct role for endogenous COX-2 activity in regulating EC behaviour. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 40-45 vascular endothelial growth factor A Homo sapiens 63-67 17825254-2 2007 The LPS-stimulated COX-2 expression and PGI2 release were accompanied by production of the potent angiogenic cytokine, vascular endothelial growth factor (VEGF), and these effects were suppressed by NS-398, which is a COX-2 inhibitor. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 199-205 vascular endothelial growth factor A Homo sapiens 119-153 17825254-2 2007 The LPS-stimulated COX-2 expression and PGI2 release were accompanied by production of the potent angiogenic cytokine, vascular endothelial growth factor (VEGF), and these effects were suppressed by NS-398, which is a COX-2 inhibitor. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 199-205 vascular endothelial growth factor A Homo sapiens 155-159 15475935-4 2005 A papillary thyroid carcinoma cell line TPC-1 was also studied in vitro to determine the role of the specific COX-2 inhibitor NS-398 on COX-2 and vascular endothelial growth factor-A, since COX-2 also has a role in regulating tumor angiogenesis. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 126-132 vascular endothelial growth factor A Homo sapiens 146-182 16336951-10 2006 VEGF-induced cell proliferation was significantly reduced when HUVECs were either pre-treated with NS398 (21.52+/-3.6%) or transfected with COX-2 siRNA (34.12+/-5.81%). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 99-104 vascular endothelial growth factor A Homo sapiens 0-4 15705382-9 2005 The NS-398 treatment resulted in a statistically significant decrease in VEGF mRNA levels in adhesion (25%) and normal peritoneal (16%) fibroblasts. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 4-10 vascular endothelial growth factor A Homo sapiens 73-77 15475935-9 2005 In vitro studies with a COX-2 inhibitor, NS-398, showed inhibition of tumor growth along with increased levels of COX-2 and vascular endothelial growth factor-A mRNA expression. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 41-47 vascular endothelial growth factor A Homo sapiens 124-160 15838264-5 2004 The cyclooxygenase- 2 inhibitor, NS-398 drastically decreased the endothelin- 1-induced prostaglandin E2 production and vascular endothelial growth factor upregulation, indicating a role for cyclooxygenase-2 in endothelin-1-induced vascular endothelial growth factor-mediated angiogenesis. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 33-39 vascular endothelial growth factor A Homo sapiens 120-154 15838264-5 2004 The cyclooxygenase- 2 inhibitor, NS-398 drastically decreased the endothelin- 1-induced prostaglandin E2 production and vascular endothelial growth factor upregulation, indicating a role for cyclooxygenase-2 in endothelin-1-induced vascular endothelial growth factor-mediated angiogenesis. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 33-39 vascular endothelial growth factor A Homo sapiens 232-266 15246970-10 2004 NS-398 significantly suppressed VEGF and PGE(2) release from IL-1-stimulated gastric fibroblasts; concurrent addition of PGE(2) restored NS-398-inhibited VEGF release. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 137-143 vascular endothelial growth factor A Homo sapiens 154-158 15010822-12 2004 Treatment of the COX-2 overexpressing cells with a COX-2-selective inhibitor, NS-398 (10 microM), decreased PGE2 level and attenuated VEGF expression. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 78-84 vascular endothelial growth factor A Homo sapiens 134-138 12107271-4 2002 Pretreatment of HMEC-1 with a selective COX-2 inhibitor, NS-398, abolished VEGF-induced PGE(2) synthesis, suggesting specific up-regulation of COX-2 activity by VEGF in HMEC-1. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 57-63 vascular endothelial growth factor A Homo sapiens 75-79 12107271-4 2002 Pretreatment of HMEC-1 with a selective COX-2 inhibitor, NS-398, abolished VEGF-induced PGE(2) synthesis, suggesting specific up-regulation of COX-2 activity by VEGF in HMEC-1. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 57-63 vascular endothelial growth factor A Homo sapiens 161-165 11158990-6 2001 The nonselective cyclooxygenase (COX) inhibitor indomethacin (5 microM) and the selective COX-2 inhibitor NS-398 (5 microM) potentiated the stimulatory effect of VEGF, whereas the selective COX-1 inhibitor resveratrol (5 microM) was without effect. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 106-112 vascular endothelial growth factor A Homo sapiens 162-166 15705382-10 2005 CONCLUSION(S): Stimulation of aerobic metabolism by DCA or inhibition of COX-2 by NS-398 reduces VEGF expression. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 82-88 vascular endothelial growth factor A Homo sapiens 97-101 15864753-10 2005 In addition, pretreatment with NS-398 to reduce PGE2 also effectively suppressed HIF-1alpha protein accumulation and achieved a similar inhibitory effect on VEGF production as did antisense HIF-1alpha transfection. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 31-37 vascular endothelial growth factor A Homo sapiens 157-161 16015035-0 2005 Autocrine vascular endothelial growth factor/vascular endothelial growth factor receptor-2 growth pathway represents a cyclooxygenase-2-independent target for the cyclooxygenase-2 inhibitor NS-398 in colon cancer cells. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 190-196 vascular endothelial growth factor A Homo sapiens 10-44 16015035-0 2005 Autocrine vascular endothelial growth factor/vascular endothelial growth factor receptor-2 growth pathway represents a cyclooxygenase-2-independent target for the cyclooxygenase-2 inhibitor NS-398 in colon cancer cells. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 190-196 vascular endothelial growth factor A Homo sapiens 45-79 16015035-10 2005 CONCLUSION: The autocrine VEGF/VEGFR-2 growth pathway could be a COX-2-independent target of the COX-2 inhibitor, NS-398, in colon cancer cells. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 114-120 vascular endothelial growth factor A Homo sapiens 26-30 15246970-10 2004 NS-398 significantly suppressed VEGF and PGE(2) release from IL-1-stimulated gastric fibroblasts; concurrent addition of PGE(2) restored NS-398-inhibited VEGF release. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 vascular endothelial growth factor A Homo sapiens 32-36 14532971-8 2003 Treatment with NS398, a specific COX-2 inhibitor, reduced VEGF expression in COX-2 expressing Kato III cells by 25%. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 15-20 vascular endothelial growth factor A Homo sapiens 58-62 12010778-4 2002 NS-398 (1 microM), a cyclo-oxygenase-2 (COX-2) inhibitor, inhibited IL-6 and VEGF production (35+/-4% and 26+/-2%, respectively) but enhanced M-CSF production (38+/-4%) by IL-1beta (1 ng ml(-1)) in synovial fibroblasts isolated from patients with osteoarthritis (OA) and rheumatoid arthritis (RA). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 vascular endothelial growth factor A Homo sapiens 77-81 11381123-12 2001 Treatment of LMP1-expressing cells with the COX-2-specific inhibitor (NS-398) dramatically decreased production of VEGF, suggesting that LMP1-induced VEGF production is mediated, at least in part, by COX-2. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 70-76 vascular endothelial growth factor A Homo sapiens 115-119 11381123-12 2001 Treatment of LMP1-expressing cells with the COX-2-specific inhibitor (NS-398) dramatically decreased production of VEGF, suggesting that LMP1-induced VEGF production is mediated, at least in part, by COX-2. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 70-76 vascular endothelial growth factor A Homo sapiens 150-154 11595463-5 2001 This study aimed to determine whether indomethacin (IND) and/or the selective COX-2 inhibitor, NS-398, interfere with egr-1 gene expression in human microvascular endothelial cells (HMVEC) in response to vascular endothelial growth factor (VEGF) stimulation. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 95-101 vascular endothelial growth factor A Homo sapiens 204-238 11595463-5 2001 This study aimed to determine whether indomethacin (IND) and/or the selective COX-2 inhibitor, NS-398, interfere with egr-1 gene expression in human microvascular endothelial cells (HMVEC) in response to vascular endothelial growth factor (VEGF) stimulation. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 95-101 vascular endothelial growth factor A Homo sapiens 240-244 11595463-10 2001 NS-398 inhibited VEGF-induced Egr-1 mRNA and protein expression by 23+/-3% and 35+/-4%, respectively (both P<0.01). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 vascular endothelial growth factor A Homo sapiens 17-21 10919714-11 1999 Moreover, the increases in VEGF mRNA and protein secretion induced by CoCl2 in PC-3ML cells were significantly suppressed following exposure to NS398, a selective COX-2 inhibitor. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 144-149 vascular endothelial growth factor A Homo sapiens 27-31