COX-2和P53在炎症应激和肿瘤发生中相互作用的研究进展

COX-2在多种肿瘤组织中过量表达,COX-2活性和前列腺素合成的增加促进细胞增殖、血管新生、肿瘤细胞浸润及抑制细胞凋亡.许多应激和前炎症信号,如氧自由基和DNA损伤剂,可诱导COX-2和P53的表达,而P53作为一种转录因子在肿瘤中常因突变而失活.已有研究表明,P53和COX-2存在复杂的交叉作用,P53能上调或下调COX-2的表达,而COX-2也可以调控p53转录活性,但两者相互作用的分子依据一直存在着争论.本文综述了炎症应激和肿瘤发生中COX-2和P53相互作用及其机制的研究进展.

Advance in Research on Relations between Cyclooxygenase-2 and P53 during Inflammatory Stress and Carcinogenesis

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.