PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 21993002-6 2011 We found that MK886 reversed celecoxib-induced increases in 5-LOX gene expression and Erk1/2 activation in pancreatic tumor cells. Celecoxib 29-38 mitogen-activated protein kinase 3 Homo sapiens 86-92 21738696-5 2011 Treatment of cells with 12-O-tetradecanoylphorbol-13-acetate, an inducer of COX-2, enhanced the phosphorylation of ERK1/2, a protein of mitogen-activated protein kinase family, and subsequently cell migration whereas both GSPs and celecoxib significantly inhibited 12-O-tetradecanoylphorbol-13-acetate-promoted cell migration as well as phosphorylation of ERK1/2. Celecoxib 231-240 mitogen-activated protein kinase 3 Homo sapiens 115-121 19157634-4 2009 In this study, we characterize the role of celecoxib in the cytotoxicity, ERK1/2 activation and Rad51 expression affected by gefitinib in NSCLC cells. Celecoxib 43-52 mitogen-activated protein kinase 3 Homo sapiens 74-80 21044953-6 2010 Because Elk1 is an ERK-regulated protein, we accordingly found that celecoxib increased the levels of phosphorylated ERK1/2, RSK2, and Elk1. Celecoxib 68-77 mitogen-activated protein kinase 3 Homo sapiens 117-123 21044953-7 2010 Inhibition of either ERK signaling with a MEK inhibitor or ERK1/2 siRNA, or RSK2 signaling with an RSK2 inhibitor or RSK2 siRNA abrogated DR5 up-regulation by celecoxib as well as other agents. Celecoxib 159-168 mitogen-activated protein kinase 3 Homo sapiens 59-65 19157634-8 2009 Furthermore, blocking ERK1/2 activation by U0126 (MKK1/2 inhibitor) and knocking down Rad51 expression by transfection with small interfering RNA of Rad51 can enhance the cytotoxicity of celecoxib. Celecoxib 187-196 mitogen-activated protein kinase 3 Homo sapiens 22-28 17936723-9 2008 Celecoxib upregulated p-ERK1/2 in H134 cells, but not in WiDr cells. Celecoxib 0-9 mitogen-activated protein kinase 3 Homo sapiens 24-30 33152664-7 2021 In vivo pharmacological inhibition of COX-2 by celecoxib decreased tissue fibrosis and increased skeletal muscle fiber preservation reflected by less ECM formation and myofibroblast accumulation with decreased p-ERK1/2, p-Smad2/3, TGF-betaR1, VEGF, NOX2 and NOX4 expression. Celecoxib 47-56 mitogen-activated protein kinase 3 Homo sapiens 212-218 18296338-5 2008 ET-18-O-CH3 also inhibited constitutive activation of ERK1/2, p38 MAPK, and Akt/protein kinase B, which was blunted by a selective COX-2 inhibitor SC58635. Celecoxib 147-154 mitogen-activated protein kinase 3 Homo sapiens 54-60 31518663-8 2019 Moreover, in the xenograft models, inhibition of PTGS2 by celecoxib significantly augmented the cytotoxic efficacy of cisplatin in the resistant gastric cancer via suppression of PTGS2 and BCL2 expressions regulated by ERK1/2 and P38 signal axis, suggesting PTGS2 might be employed as an adjunctive therapeutic target for reversal of the chemoresistance in a subset of cisplatin resistant gastric cancer. Celecoxib 58-67 mitogen-activated protein kinase 3 Homo sapiens 219-225 25987127-1 2015 We previously demonstrated that non-toxic doses of Celecoxib induced the immediate phosphorylation of Erk1-2 in colon tumor associated fibroblasts (TAFs), increasing their responsiveness to epidermal growth factor (EGF). Celecoxib 51-60 mitogen-activated protein kinase 3 Homo sapiens 102-108 27821910-0 2016 Celecoxib alleviates oxaliplatin-induced hyperalgesia through inhibition of spinal ERK1/2 signaling. Celecoxib 0-9 mitogen-activated protein kinase 3 Homo sapiens 83-89 23010081-0 2013 Celecoxib induces proliferation and Amphiregulin production in colon subepithelial myofibroblasts, activating erk1-2 signaling in synergy with EGFR. Celecoxib 0-9 mitogen-activated protein kinase 3 Homo sapiens 110-116 23010081-6 2013 Celecoxib induces erk1-2 and Akt phosphorylation within 5". Celecoxib 0-9 mitogen-activated protein kinase 3 Homo sapiens 18-24 23010081-10 2013 According to these results the association with EGFR (or erk1-2) inhibitors could abolish the off-target activity of Celecoxib, possibly extending the potential of this drug for colon cancer prevention. Celecoxib 117-126 mitogen-activated protein kinase 3 Homo sapiens 57-63 22209876-4 2012 The results indicated that celecoxib could suppress cell proliferation stimulated by FGF-2 (IC(50) FGF+group, 75+-1.9mumol/l) and TGF-beta1 (IC(50) TGF+group, 48+-1.4mumol/l), by inhibiting ERK1/2 phosphorylation but not ERK1/2 expression. Celecoxib 27-36 mitogen-activated protein kinase 3 Homo sapiens 190-196 22415852-8 2012 Moreover, CXB up-regulated the cell cycle negative regulator p21(CIP/WAF1) and the cell cycle positive regulator Cyclin A, blocked ERK1/2 phosphorylation, induced apoptotic factors (Bax and caspase-3) and reduced Bcl-2. Celecoxib 10-13 mitogen-activated protein kinase 3 Homo sapiens 131-137 22209876-4 2012 The results indicated that celecoxib could suppress cell proliferation stimulated by FGF-2 (IC(50) FGF+group, 75+-1.9mumol/l) and TGF-beta1 (IC(50) TGF+group, 48+-1.4mumol/l), by inhibiting ERK1/2 phosphorylation but not ERK1/2 expression. Celecoxib 27-36 mitogen-activated protein kinase 3 Homo sapiens 221-227 22209876-6 2012 The suppression of NIH/3T3 fibroblast proliferation and collagen expression upon stimulation by FGF-2 and TGF-beta1 is likely a result of the inhibition of ERK1/2 and SMAD2/3 phosphorylation by celecoxib. Celecoxib 194-203 mitogen-activated protein kinase 3 Homo sapiens 156-162 22200683-0 2012 Celecoxib suppresses fibroblast proliferation and collagen expression by inhibiting ERK1/2 and SMAD2/3 phosphorylation. Celecoxib 0-9 mitogen-activated protein kinase 3 Homo sapiens 96-102 22200683-1 2012 This study aimed to investigate whether celecoxib suppresses fibroblast proliferation and collagen expression by inhibiting extracellular signal-regulated kinase 1/2 (ERK1/2) and SMAD2/3 phosphorylation. Celecoxib 40-49 mitogen-activated protein kinase 3 Homo sapiens 167-173 22200683-4 2012 The results indicated that celecoxib suppressed cell proliferation (IC50 FGF+ group, 75 +- 1.9 micromol/l) stimulated by FGF-2, and also inhibited cell viability (IC50 FGF- group, 252 +- 2.3 micromol/l) by inhibiting ERK1/2 phosphorylation but not ERK1/2 expression. Celecoxib 27-36 mitogen-activated protein kinase 3 Homo sapiens 217-223 22200683-4 2012 The results indicated that celecoxib suppressed cell proliferation (IC50 FGF+ group, 75 +- 1.9 micromol/l) stimulated by FGF-2, and also inhibited cell viability (IC50 FGF- group, 252 +- 2.3 micromol/l) by inhibiting ERK1/2 phosphorylation but not ERK1/2 expression. Celecoxib 27-36 mitogen-activated protein kinase 3 Homo sapiens 248-254 22200683-7 2012 Celecoxib is capable of inhibiting ERK1/2 and SMAD2/3 phosphorylation, which is responsible for NIH/3T3 fibroblast proliferation and collagen expression. Celecoxib 0-9 mitogen-activated protein kinase 3 Homo sapiens 35-41