Cross‐talks between cyclooxygenase‐2 and tumor suppressor protein p53: Balancing life and death during inflammatory stress and carcinogenesis
Overexpression of Cyclooxygenase‐2 (COX‐2) is observed in most tumor types. Increased COX‐2 activity and synthesis of prostaglandins stimulates proliferation, angiogenesis, invasiveness and inhibits apoptosis. Many stress and proinflammatory signals induce COX‐2 expression, including oxyradicals or...
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Published in | International journal of cancer Vol. 121; no. 5; pp. 929 - 937 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
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Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.09.2007
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Abstract | Overexpression of Cyclooxygenase‐2 (COX‐2) is observed in most tumor types. Increased COX‐2 activity and synthesis of prostaglandins stimulates proliferation, angiogenesis, invasiveness and inhibits apoptosis. Many stress and proinflammatory signals induce COX‐2 expression, including oxyradicals or DNA‐damaging agents. The latter also induces p53, a transcription factor often inactivated by mutation in cancer. Several studies have identified complex cross‐talks between p53 and COX‐2, whereby p53 can either up‐ or down‐regulate COX‐2, which in turn controls p53 transcriptional activity. However, the molecular basis of these effects are open to debate, in particular since no p53 binding sequences have been identified in COX‐2 regulatory regions. In this review, we summarize the molecular mechanisms by which COX‐2 contributes to carcinogenesis and discuss the experimental set‐up, results and conclusions of studies analyzing cross‐talks between p53 and COX‐2. We propose 2 scenarios accounting for overexpression of COX‐2 in precursor and cancer lesions. In the “inflammatory” scenario, p53, activated by DNA damage induced by oxygen and nitrogen species, recruits NF‐kappaB to activate COX‐2, resulting in antiapoptotic effects that contribute to cell expansion in inflammatory precursor lesions. In the “constitutive proliferation” scenario, oncogenic stress due to activation of growth signaling cascades may upregulate COX‐2 promoter independently of NF‐kappaB and p53, synergizing with TP53 mutation to promote cancer progression. These 2 scenarios, although not mutually exclusive, may account for the diversity of the correlations between COX‐2 expression and TP53 mutation, which vary according to cancer types and biological contexts, and have implications for the use of COX‐2 inhibitors in cancer prevention and therapy. © 2007 Wiley‐Liss, Inc. |
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AbstractList | Overexpression of Cyclooxygenase-2 (COX-2) is observed in most tumor types. Increased COX-2 activity and synthesis of prostaglandins stimulates proliferation, angiogenesis, invasiveness and inhibits apoptosis. Many stress and proinflammatory signals induce COX-2 expression, including oxyradicals or DNA-damaging agents. The latter also induces p53, a transcription factor often inactivated by mutation in cancer. Several studies have identified complex cross-talks between p53 and COX-2, whereby p53 can either up- or down-regulate COX-2, which in turn controls p53 transcriptional activity. However, the molecular basis of these effects are open to debate, in particular since no p53 binding sequences have been identified in COX-2 regulatory regions. In this review, we summarize the molecular mechanisms by which COX-2 contributes to carcinogenesis and discuss the experimental set-up, results and conclusions of studies analyzing cross-talks between p53 and COX-2. We propose 2 scenarios accounting for overexpression of COX-2 in precursor and cancer lesions. In the inflammatory scenario, p53, activated by DNA damage induced by oxygen and nitrogen species, recruits NF-kappaB to activate COX-2, resulting in antiapoptotic effects that contribute to cell expansion in inflammatory precursor lesions. In the constitutive proliferation scenario, oncogenic stress due to activation of growth signaling cascades may upregulate COX-2 promoter independently of NF-kappaB and p53, synergizing with TP53 mutation to promote cancer progression. These 2 scenarios, although not mutually exclusive, may account for the diversity of the correlations between COX-2 expression and TP53 mutation, which vary according to cancer types and biological contexts, and have implications for the use of COX-2 inhibitors in cancer prevention and therapy. Overexpression of Cyclooxygenase‐2 (COX‐2) is observed in most tumor types. Increased COX‐2 activity and synthesis of prostaglandins stimulates proliferation, angiogenesis, invasiveness and inhibits apoptosis. Many stress and proinflammatory signals induce COX‐2 expression, including oxyradicals or DNA‐damaging agents. The latter also induces p53, a transcription factor often inactivated by mutation in cancer. Several studies have identified complex cross‐talks between p53 and COX‐2, whereby p53 can either up‐ or down‐regulate COX‐2, which in turn controls p53 transcriptional activity. However, the molecular basis of these effects are open to debate, in particular since no p53 binding sequences have been identified in COX‐2 regulatory regions. In this review, we summarize the molecular mechanisms by which COX‐2 contributes to carcinogenesis and discuss the experimental set‐up, results and conclusions of studies analyzing cross‐talks between p53 and COX‐2. We propose 2 scenarios accounting for overexpression of COX‐2 in precursor and cancer lesions. In the “inflammatory” scenario, p53, activated by DNA damage induced by oxygen and nitrogen species, recruits NF‐kappaB to activate COX‐2, resulting in antiapoptotic effects that contribute to cell expansion in inflammatory precursor lesions. In the “constitutive proliferation” scenario, oncogenic stress due to activation of growth signaling cascades may upregulate COX‐2 promoter independently of NF‐kappaB and p53, synergizing with TP53 mutation to promote cancer progression. These 2 scenarios, although not mutually exclusive, may account for the diversity of the correlations between COX‐2 expression and TP53 mutation, which vary according to cancer types and biological contexts, and have implications for the use of COX‐2 inhibitors in cancer prevention and therapy. © 2007 Wiley‐Liss, Inc. Abstract Overexpression of Cyclooxygenase‐2 (COX‐2) is observed in most tumor types. Increased COX‐2 activity and synthesis of prostaglandins stimulates proliferation, angiogenesis, invasiveness and inhibits apoptosis. Many stress and proinflammatory signals induce COX‐2 expression, including oxyradicals or DNA‐damaging agents. The latter also induces p53, a transcription factor often inactivated by mutation in cancer. Several studies have identified complex cross‐talks between p53 and COX‐2, whereby p53 can either up‐ or down‐regulate COX‐2, which in turn controls p53 transcriptional activity. However, the molecular basis of these effects are open to debate, in particular since no p53 binding sequences have been identified in COX‐2 regulatory regions. In this review, we summarize the molecular mechanisms by which COX‐2 contributes to carcinogenesis and discuss the experimental set‐up, results and conclusions of studies analyzing cross‐talks between p53 and COX‐2. We propose 2 scenarios accounting for overexpression of COX‐2 in precursor and cancer lesions. In the “inflammatory” scenario, p53, activated by DNA damage induced by oxygen and nitrogen species, recruits NF‐kappaB to activate COX‐2, resulting in antiapoptotic effects that contribute to cell expansion in inflammatory precursor lesions. In the “constitutive proliferation” scenario, oncogenic stress due to activation of growth signaling cascades may upregulate COX‐2 promoter independently of NF‐kappaB and p53, synergizing with TP53 mutation to promote cancer progression. These 2 scenarios, although not mutually exclusive, may account for the diversity of the correlations between COX‐2 expression and TP53 mutation, which vary according to cancer types and biological contexts, and have implications for the use of COX‐2 inhibitors in cancer prevention and therapy. © 2007 Wiley‐Liss, Inc. |
Author | Dar, Nazir Ahmad de Moraes, Emanuela de Moura Gallo, Claudia Vitoria Hainaut, Pierre |
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Keywords | COX-2 inhibitors COX-2 Enzyme Cyclooxygenase 2 Mortality p53 Protein DNA damage Inflammation Cyclooxygenase 2 inhibitor Malignant tumor Carcinogenesis Stress p53 Cancerology TP53 Gene Cell death Oxidoreductases Lesion Apoptosis Tumor suppressor gene Cancer |
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Snippet | Overexpression of Cyclooxygenase‐2 (COX‐2) is observed in most tumor types. Increased COX‐2 activity and synthesis of prostaglandins stimulates proliferation,... Overexpression of Cyclooxygenase-2 (COX-2) is observed in most tumor types. Increased COX-2 activity and synthesis of prostaglandins stimulates proliferation,... Abstract Overexpression of Cyclooxygenase‐2 (COX‐2) is observed in most tumor types. Increased COX‐2 activity and synthesis of prostaglandins stimulates... |
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SubjectTerms | Animals apoptosis Biological and medical sciences cancer Cell Transformation, Neoplastic COX‐2 COX‐2 inhibitors Cyclooxygenase 2 - metabolism DNA damage Humans inflammation Inflammation - metabolism Medical sciences p53 Tumor Suppressor Protein p53 - metabolism Tumors |
Title | Cross‐talks between cyclooxygenase‐2 and tumor suppressor protein p53: Balancing life and death during inflammatory stress and carcinogenesis |
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