Antonakopoulos Nikolaos, Karamanolis D G
Department of Gastroenterology, Tzaneio Hospital, Piraeus, Greece.
Hepatogastroenterology. 2007 Sep;54(78):1694-700.
Experiments in animals and population-based studies have shown the efficacy of nonsteroidal antiinflammatory drugs in colorectal cancer prevention. COX-2 is overexpressed in dysplastic and neoplastic epithelium. COX-2 is a key-enzyme in several tumorigenic pathways, such as promotion of tumor angiogenesis. Non-selective inhibition of COX enzyme demonstrates a protective effect as well, suggesting that more than one mechanism takes place in neoplastic transformation. Blockade of COX enzyme by NSAIDs down-regulates its metabolic product prostaglandin E2. Inhibition of PGE2 seems to have a negative effect in cancer occurrence. Induction of apoptosis is another mechanism that explains the protective effect of NSAIDs. The recently discovered PPARdelta factor, is also overexpressed in neoplastic tissue, and may be a mediator through which COX-2 exerts its oncogenic effect.
动物实验和基于人群的研究表明，非甾体抗炎药在预防结直肠癌方面具有疗效。COX - 2在发育异常和肿瘤性上皮中过度表达。COX - 2是多种致瘤途径中的关键酶，如促进肿瘤血管生成。对COX酶的非选择性抑制也显示出保护作用，这表明肿瘤转化过程中发生了不止一种机制。非甾体抗炎药对COX酶的阻断会下调其代谢产物前列腺素E2。对PGE2的抑制似乎对癌症发生有负面影响。诱导细胞凋亡是另一种解释非甾体抗炎药保护作用的机制。最近发现的PPARδ因子在肿瘤组织中也过度表达，可能是COX - 2发挥其致癌作用的一种介质。
