癌变
血管生成
环氧合酶
癌症研究
转录因子
炎症
抄写(语言学)
DNA损伤
细胞凋亡
生物
癌症
化学
酶
免疫学
DNA
遗传学
基因
生物化学
哲学
语言学
出处
期刊:Int J Genet
日期:2009-10-15
卷期号:32 (05): 372-376
被引量:1
标识
DOI:10.3760/cma.j.issn.1673-4386.2009.05.013
摘要
Over expression of Cyclooxygenase-2 (COX-2) is observed in most tumor types.Increased COX-2 activity and synthesis of prostaglandins stimulates proliferation,angiogenesis,and invasion,and inhibits apoptosis.Many stress and proinfiammatory signals induce COX-2 and P53 expression,including oxyradicals or DNA-damaging agents.P53,a transcription factor,is often inactivated by mutation in cancer.Several studies have identified complex cross-talks between P53 and COX-2,whereby P53 can either up-regulate or down-regulate the expression of COX-2,which in turn controls p53 transcriptional activity.However,the molecular bases of these effects are open to debate.In this review,we summarize the relationship and molecular mechanisms between COX-2 and P53 during inflammatory stress and carcinogenesis.
Key words:
COX-2; P53; Cancer; Inflammation
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