前列腺素类物质在胃肠道肿瘤发病机制中的作用  被引量:2

Role of prostaglandins in pathogenesis of gastrointestinal cancer

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作  者:丁岩冰[1] 肖炜明[1] 王学浩[2] 

机构地区:[1]扬州市第一人民医院消化科,江苏省扬州市225001 [2]南京医科大学第一附属医院肝脏外科,江苏省南京市210029

出  处:《世界华人消化杂志》2006年第35期3391-3396,共6页World Chinese Journal of Digestology

摘  要:环氧合酶(cyclooxygenase,COX)是催化花生四烯酸转化为前列腺素过程中的一个关键限速酶.哺乳动物的COX有两种形式,即COX-1和COX-2.COX-1在大多数组织中都有表达,其催化产生的前列腺素参与维持机体正常的生理机能.而COX-2是一种诱导酶,在细胞受到各种刺激时,如组织损伤、炎症或细胞恶性转化时表达增强.近年来大量研究表明,COX-2通过前列腺素途径除参与炎症反应外,还与胃肠道肿瘤发生、发展关系密切,COX-2在结直肠癌、胃癌和食管癌中的作用主要是通过PGE2等前列腺素来调节的,目前的研究认为前列腺素对肿瘤的促进作用主要牵涉下列分子机制:促进细胞增殖、抑制凋亡、促进侵袭和转移、刺激血管生成和诱导免疫抑制.本文就前列腺素类物质在胃肠道肿瘤发病机制中的研究进展作一综述.There are 2 cyclooxygenase (COX) isoforms commonly referred to COX-1 and COX-2 for the temporal order of their discovery. Although both COX-1 and COX-2 are up-regulated in a variety of circumstances, normally, COX-1 is constitutively expressed in a broad range of cells and tissues. COX-1 expression remains constant under most physiologic or pathologic conditions, and COX-l-derived prostaglandins are considered to play a role in many normal physiologic processes, COX-2, by contrast, is an immediate- early response gene normally absent from most cells but highly inducible in response to inflammatory stimuli, including endotoxin, cytokines, hormones, and tumor promoters, Prostaglandins derived from COX-1 and COX-2 are involved in a variety of physiologic and pathologic processes in the gastrointestinal tract. Recent efforts to identify the molecular mechanisms by which COX-2-derived prostanoids exert their proneoplastic effects have provided a rationale for the possible use of non-steroidal anti-inflammatory drugs alone or in combination with conventional or experimental anticancer agents for the treatment or prevention of gastrointestinal cancers.

关 键 词:前列腺素类物质 环氧化酶 胃肠道肿瘤 分子机制 

分 类 号:R735[医药卫生—肿瘤]

 

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