Cyclooxygenase-2 (COX-2) enzyme inhibitors as potential enhancers of tumor radioresponse.

Cyclooxygenase-2 (COX-2) enzyme inhibitors as potential enhancers of tumor radioresponse.
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环加氧酶-2 (COX-2) 酶抑制剂作为肿瘤放射反应的潜在增强剂。

DOI:
10.1053/srao.2001.26018
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发表时间:
2001
影响因子:
3.5
通讯作者:
Luka Milas
Luka Milas
中科院分区:
医学2区
文献类型:
--
作者:
Luka Milas

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环氧合酶-2 (COX-2) 是一种由多种因素诱导的酶,包括肿瘤促进剂、细胞因子、生长因子和缺氧。它参与花生四烯酸向前列腺素的代谢转化,主要在炎症状态和肿瘤中。在正常组织中,前列腺素由 COX-1 合成,发挥多种稳态生理功能。 COX-2 过度表达与癌发生、持续肿瘤生长和促进转移扩散有关。 COX-2 及其产品可以充当保护剂,防止电离辐射造成的细胞损伤。我描述的研究结果表明,通过选择性 COX-2 抑制剂或常用的非甾体抗炎药 (NSAID) 抑制 COX-2 或前列腺素类药物具有抗肿瘤活性,并且可以改善肿瘤对放射的反应,而不显着影响正常组织的放射反应。 COX-2 抑制剂和放射以多种复杂的方式相互作用,酶抑制剂直接或间接增强放射对肿瘤细胞的破坏。 COX-2 代表了改善癌症放射治疗的潜在分子靶点。
Cyclooxygenase-2 (COX-2) is an enzyme induced by a variety of factors including tumor promoters, cytokines, growth factors and hypoxia. It is involved in the metabolic conversion of arachidonic acid to prostanoids, primarily in inflammatory states and tumors. In normal tissues, prostanoids are synthesized by COX-1, and they exert numerous homeostatic physiologic functions. COX-2 overexpression is linked to carcinogenesis, maintenance of progressive tumor growth and facilitation of metastatic spread. COX-2 and its products may act as protectors against cell damage by ionizing radiation. I describe findings showing that inhibition of COX-2 or prostanoids by selective COX-2 inhibitors or commonly used nonsteroidal antiinflammatory drugs (NSAIDs) has antitumor activity and may improve tumor response to radiation without significantly affecting normal tissue radioresponse. COX-2 inhibitors and radiation interact in multiple complex ways, with the enzyme inhibitor directly or indirectly augmenting tumor cell destruction by radiation. COX-2 represents a potential molecular target for improvement of cancer radiotherapy.
DOI: --
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类二十烷酸和辐射。
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期刊: European journal of cancer (Oxford, England : 1990)
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