國家衛生研究院 NHRI:Item 3990099045/1267
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    题名: Differential cyclooxygenase-2 transcriptional control in proliferating versus quiescent fibroblasts
    作者: Wu, KK
    贡献者: Center for Cardiovascular and Blood Research
    摘要: Cyclooxygenase-2 (COX-2) overexpression is associated with cancer. One potential mechanism is DNA damage caused by COX-2 derived oxidants. Since DNA in proliferating cells is highly vulnerable to oxidative damage and mutation, we propose that COX-2 transactivation by exogenous stimuli is suppressed in proliferating cells compared to quiescent cells. In this review, we provide evidence for reduced COX-2 transcriptional expression in response to phorbol esters (PMA), lipopolysaccharide (LPS), interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF alpha). Our results show that COX-2 transcription in proliferating fibroblasts is suppressed by a small molecular weight compound produced by proliferating cells. By contrast, COX-2 expression in response to exogenous stimuli is robust in quiescent cells. The quiescent cells in human body may play a primary role in mounting response to exogenous stimuli. Salicylate inhibits COX-2 transcriptional activation in quiescent cells but not in serum-driven proliferating cells by blocking C/EBP beta DNA binding. These studies suggest that COX-2 expressions in quiescent and proliferating cells are regulated by different mechanisms. Further investigations into their transcriptional control mechanisms will have great impact on the fundamental understanding of the division of cell functions between quiescent and proliferating cells and the design of novel therapeutic strategies. (C) 2007 Elsevier Inc. All rights reserved.
    关键词: Biochemistry & Molecular Biology;Cell Biology
    日期: 2007-05
    關聯: Prostaglandins and Other Lipid Mediators. 2007 May;83(3):175-181.
    Link to: http://dx.doi.org/10.1016/j.prostaglandins.2007.01.002
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1098-8823&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000247048900003
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=34247634122
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