Differential Protein Expression in the Epidermis of Wild-Type and COX-2 Transgenic Mice

Müller‐Decker, Karin; Fürstenberger, Gerhard; Neumann, Melanie; Schnölzer, Martina

doi:10.1159/000091975

Cited by 6 publications

(5 citation statements)

References 61 publications

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“…Genetic study of COX-2 knockout mice has revealed a strong correlation between COX-2 expression and cancer development, indicating that COX-2 contributes to carcinogenesis and oncogenesis [42, 43]. Our previous findings also suggest several cancer-related biological effects of COX-2, including anti-apoptotic effect, cell transformation, and cell cycle progression in different context [44].…”

Section: Discussionmentioning

confidence: 83%

p27 suppresses cyclooxygenase-2 expression by inhibiting p38β and p38δ-mediated CREB phosphorylation upon arsenite exposure

Che

Liu

Huang

et al. 2013

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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p27 is a cyclin-dependent kinase (CDK) inhibitor that suppresses a cell’s transition from G0 to S phase, therefore acting as a tumor suppressor. Our most recent studies demonstrate that upon arsenite exposure, p27 suppresses Hsp27 and Hsp70 expressions through the JNK2/c-Jun- and HSF-1-dependent pathways, suggesting a novel molecular mechanism underlying the tumor suppressive function of p27 in a CDK-independent manner. We found that p27-deficiency (p27−/−) resulted in the elevation of cyclooxygenase-2 (COX-2) expression at transcriptional level, whereas the introduction of p27 brought back COX-2 expression to a level similar to that of p27+/+ cells, suggesting that p27 exhibits an inhibitory effect on COX-2 expression. Further studies identified that p27 inhibition of COX-2 expression was specifically due to phosphorylation of transcription factor cAMP response element binding (CREB) phosphorylation mediated by p38β and p38δ. These results demonstrate a novel mechanism underlying tumor suppression effect of p27 and will contribute to understanding of the overall mechanism of p27 tumor suppression in a CDK-independent manner.

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Section: Discussionmentioning

confidence: 83%

p27 suppresses cyclooxygenase-2 expression by inhibiting p38β and p38δ-mediated CREB phosphorylation upon arsenite exposure

Che

Liu

Huang

et al. 2013

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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“…Several lines of evidence has accumulated suggesting that inducible form of COX‐2, a central enzyme in the prostaglandin (PG) biosynthetic pathway, plays an important role in tumorigenesis 28. Knockout and various transgenic approaches and pharmacologic studies show strong evidence for a cause‐and‐effect relationship between the aberrant COX‐2 expression and tumor formation in numerous animal models, including in mouse skin 29. In a multistage skin carcinogenesis experiment with a classical initiation/promotion using DMBA and TPA, COX‐2 deficiency led to a gene dosage‐dependent reduction of the papilloma yield and incidence compared with wild‐type mice 30.…”

Section: Discussionmentioning

confidence: 96%

6‐Shogaol is more effective than 6‐gingerol and curcumin in inhibiting 12‐O‐tetradecanoylphorbol 13‐acetate‐induced tumor promotion in mice

Hsieh

et al. 2010

Molecular Nutrition Food Res

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We previously reported that 6-shogaol strongly suppressed lipopolysaccharide-induced overexpression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in murine macrophages. In this study, we further compared curcumin, 6-gingerol, and 6-shogaol's molecular mechanism of action and their anti-tumor properties. We demonstrate that topical application of 6-shogaol more effectively inhibited 12-O-tetradecanoylphorbol 13-acetate (TPA)-stimulated transcription of iNOS and COX-2 mRNA expression in mouse skin than curcumin and 6-gingerol. Pretreatment with 6-shogaol has resulted in the reduction of TPA-induced nuclear translocation of the nuclear factor-kappaB subunits. 6-Shogaol also reduced TPA-induced phosphorylation of IkappaBalpha and p65, and caused subsequent degradation of IkappaBalpha. Moreover, 6-shogaol markedly suppressed TPA-induced activation of extracellular signal-regulate kinase1/2, p38 mitogen-activated protein kinase, JNK1/2, and phosphatidylinositol 3-kinase/Akt, which are upstream of nuclear factor-kappaB and AP-1. Furthermore, 6-shogaol significantly inhibited 7,12-dimethylbenz[a]anthracene/TPA-induced skin tumor formation measured by the tumor multiplicity of papillomas at 20 wk. Presented data reveal for the first time that 6-shogaol is an effective anti-tumor agent that functions by down-regulating inflammatory iNOS and COX-2 gene expression in mouse skin. It is suggested that 6-shogaol is a novel functional agent capable of preventing inflammation-associated tumorigenesis.

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“…COX-2 is known to promote cancer development. Using COX-2 knockout mice, a strong correlation between COX-2 expression and cancer development was revealed, indicating that COX-2 contributes to carcinogenesis and oncogenesis (Muller-Decker et al , 2006). In this study, we report that co-exposure to arsenic and ethanol induces high COX-2 expressions in a variety of colorectal cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Ethanol enhances arsenic-induced cyclooxygenase-2 expression via both NFAT and NF-κB signalings in colorectal cancer cells

Wang

Hitron

Wise

et al. 2015

Toxicology and Applied Pharmacology

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Arsenic is a known carcinogen to humans, and chronic exposure to environmental arsenic is a worldwide health concern. As a dietary factor, ethanol carries a well-established risk for malignancies, but the effects of co-exposure to arsenic and ethanol on tumor development are not well understood. In the present study, we hypothesized that ethanol would enhance the function of an environmental carcinogen such as arsenic through increase in COX-2 expression. Our in vitro results show that ethanol enhanced arsenic-induced COX-2 expression. We also show that the increased COX-2 expression associates with intracellular ROS generation, up-regulated AKT signaling, with activation of both NFAT and NF-κB pathways. We demonstrate that antioxidant enzymes have an inhibitory effect on arsenic/ethanol-induced COX-2 expression, indicating that the responsive signaling pathways from co-exposure to arsenic and ethanol relate to ROS generation. In vivo results also show that co-exposure to arsenic and ethanol increased COX-2 expression in mice. We conclude that ethanol enhances arsenic-induced COX-2 expression in colorectal cancer cells via both the NFAT and NF-κB pathways. These results imply that, as a common dietary factor, ethanol ingestion may be a compounding risk factor for arsenic-induced carcinogenesis/cancer development.

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Differential Protein Expression in the Epidermis of Wild-Type and COX-2 Transgenic Mice

Cited by 6 publications

References 61 publications

p27 suppresses cyclooxygenase-2 expression by inhibiting p38β and p38δ-mediated CREB phosphorylation upon arsenite exposure

p27 suppresses cyclooxygenase-2 expression by inhibiting p38β and p38δ-mediated CREB phosphorylation upon arsenite exposure

6‐Shogaol is more effective than 6‐gingerol and curcumin in inhibiting 12‐O‐tetradecanoylphorbol 13‐acetate‐induced tumor promotion in mice

Ethanol enhances arsenic-induced cyclooxygenase-2 expression via both NFAT and NF-κB signalings in colorectal cancer cells

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