Selective COX-2 inhibitor regulates the MAP kinase signaling pathway in human osteoarthritic chondrocytes after induction of nitric oxide

Takahashi, Toshiaki; Ogawa, Yasuhiro; Kitaoka, Kenichi; Tani, Tohru; Uemura, Yoshiki; Taguchi, Hirokuni; Kobayashi, Toshihiro; Seguchi, Harumichi; Yamamoto, Haruyasu; Shoji, Yasuhiro

doi:10.3892/ijmm.15.2.213

Cited by 11 publications

(9 citation statements)

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“…42). Previously, celecoxib was found to either activate or reduce p38-MAPK activity depending on the cellular context (43)(44)(45). In our study, celecoxib activates p38-MAPK and assessment of various signaling inhibitors, including those targeting p38-MAPK, MEK, PI-3K, and Src kinase, suggest that celecoxib-induced VEGF expression is mainly dependent on p38-MAPK acting upstream of Sp1.…”

Section: Discussionsupporting

confidence: 49%

Celecoxib Can Induce Vascular Endothelial Growth Factor Expression and Tumor Angiogenesis

Gao

Shu

2011

Molecular Cancer Therapeutics

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Section: Discussionsupporting

confidence: 49%

Celecoxib Can Induce Vascular Endothelial Growth Factor Expression and Tumor Angiogenesis

Gao

Shu

2011

Molecular Cancer Therapeutics

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“…These include proteins with crucial roles in cell cycle regulation such as cyclins, cyclin-dependent kinases, inhibitory proteins p21 and p27, and Rb, as well as proteins believed to be involved in celecoxib-induced apoptosis in cancer cell lines such as various caspases, Apaf-1, survivin, nuclear factor nB, and peroxisome proliferator -activated receptor g (8,12,17,19,23). There is also evidence that celecoxib affects both mitogenic and survival pathways by targeting phosphoinositide-dependent kinase-1/Akt, signal transducer and activator of transcription 3, and mitogen-activated protein kinase signaling (17,24,25). Figure 2.…”

Section: Discussionmentioning

confidence: 99%

Proteomic Profiling Identifies Cyclooxygenase-2-Independent Global Proteomic Changes by Celecoxib in Colorectal Cancer Cells

Lou

Xiao²,

Stauffer³

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Celecoxib, a selective inhibitor of the enzyme cyclooxygenase-2 (COX-2), has been shown to be a promising chemoprevention agent. The chemopreventive efficacy of celecoxib is believed to be a consequence of its COX-2-dependent and COX-2-independent effects on a variety of cellular processes including proliferation, apoptosis, angiogenesis, and immunosurveillance. In an attempt to identify proteomic markers modulated by celecoxib that are independent of its inhibitory effect on COX-2, the colorectal cancer cell line HCT-116, a nonexpresser of COX-2, was treated with celecoxib. We used the powerful, state-of-the-art two-dimensional difference gel electrophoresis technology coupled with mass spectrometric sequencing to compare global proteomic profiles of HCT-116 cells before and after treatment with celecoxib. Among the differentially expressed proteins identified following celecoxib treatment were proteins involved in diverse cellular functions including glycolysis, protein biosynthesis, DNA synthesis, mRNA processing, protein folding, phosphorylation, redox regulation, and molecular chaperon activities. Our study presents a comprehensive analysis of large-scale celecoxib-modulated proteomic alterations, at least some of which may be mechanistically related to the COX-2-independent chemopreventive effect of celecoxib. (Cancer Epidemiol Biomarkers Prev 2006;15(9):1598 -606)

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“…Information regarding the molecular pathways that regulate the anti-proliferative effects of individual NSAIDs is controversial at the present time [3][4][5]. Recent have identified a series of new molecular targets for NSAIDs that are mainly involved in signaling pathways; these include 15-lipoxygenase-1 [6], extracellular signalregulated kinase 1/2 signaling [7], nuclear factor kappaB (NF-_B) [8] and the Akt/PKB kinases [9].…”

Section: Introductionmentioning

confidence: 99%

The COX-2 Selective Inhibitor-Independent COX-2 Effect on Colon Carcinoma Cells is Associated with the Delta1/Notch1 Pathway

Zhang

Bai

et al. 2008

Dig Dis Sci

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Our results show that the selective COX-2 inhibitor may inhibit the proliferation and induce apoptosis in colon cancer cells through the COX-2-dependent pathway (HT-29) by decreasing the COX-2 mRNA/PGE2 levels and the activity of the COX-2-independent pathway (SW480). The Notch1 signal pathway mediates the effects of the COX-2 inhibitor on the proliferation and apoptosis of colon cancer cells. This may be a new target of the selective COX-2 inhibitor effect on colon cancer.

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Selective COX-2 inhibitor regulates the MAP kinase signaling pathway in human osteoarthritic chondrocytes after induction of nitric oxide

Cited by 11 publications

References 0 publications

Celecoxib Can Induce Vascular Endothelial Growth Factor Expression and Tumor Angiogenesis

Celecoxib Can Induce Vascular Endothelial Growth Factor Expression and Tumor Angiogenesis

Proteomic Profiling Identifies Cyclooxygenase-2-Independent Global Proteomic Changes by Celecoxib in Colorectal Cancer Cells

The COX-2 Selective Inhibitor-Independent COX-2 Effect on Colon Carcinoma Cells is Associated with the Delta1/Notch1 Pathway

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