环氧化酶-2调节细胞生长并促进肿瘤发生。
Cyclooxygenase-2 modulates cellular growth and promotes tumorigenesis.
作者信息
Trifan O C, Hla T
机构信息
University of Connecticut Health Center, Center for Vascular Biology, Farmigton, CT 03032, USA.
出版信息
J Cell Mol Med. 2003 Jul-Sep;7(3):207-22. doi: 10.1111/j.1582-4934.2003.tb00222.x.
Cyclooxygenase (COX)-2 and the prostaglandins resulting from its enzymatic activity have been shown to play a role in modulating cell growth and development of human neoplasia. Evidence includes a direct relationship between COX-2 expression and cancer incidence in humans and animal models, increased tumorigenesis after genetic manipulation of COX-2, and significant anti-tumor properties of non-steroidal anti-inflammatory drugs in animal models and in some human cancers. Recent data showed that COX-2 and the derived prostaglandins are involved in control of cellular growth, apoptosis, and signal through a group of nuclear receptors named peroxisome proliferator-activated receptors (PPARs). In this article we will review some of the findings suggesting that COX-2 is involved in multiple cellular mechanisms that lead to tumorigenesis.
环氧合酶（COX）-2及其酶活性产生的前列腺素已被证明在调节人类肿瘤的细胞生长和发展中发挥作用。证据包括COX-2表达与人类和动物模型中癌症发病率之间的直接关系、COX-2基因操作后肿瘤发生增加，以及非甾体抗炎药在动物模型和某些人类癌症中的显著抗肿瘤特性。最近的数据表明，COX-2和衍生的前列腺素通过一组名为过氧化物酶体增殖物激活受体（PPARs）的核受体参与细胞生长、凋亡和信号传导的控制。在本文中，我们将回顾一些表明COX-2参与导致肿瘤发生的多种细胞机制的研究结果。
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