The mechanisms by which folate depletion enhances colorectal carcinogenesis: a unified scheme.
The mechanisms by which folate depletion enhances colorectal carcinogenesis: a unified scheme.
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叶酸消耗增强结直肠癌发生的机制：统一方案。
DOI：
10.1159/000061830
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发表时间：
2000
期刊：
影响因子：
--
通讯作者：
Choi,SW
中科院分区：
文献类型：
--
作者：
Mason,JB;Choi,SW
越来越多的流行病学、动物和人类研究表明，叶酸状态调节几种组织发生癌症的风险。叶酸消耗似乎会增强致癌作用[1]，叶酸补充剂具有保护作用[2]。虽然叶酸是DNA甲基化和合成的关键因素，而且DNA的畸变被广泛认为是大多数致癌过程的起源，但迄今为止的机制研究还没有完全确定这种作用的机制，大多数研究都集中在这些作用上。有趣的是，DNA甲基化的改变，尿嘧啶错误掺入或DNA链断裂增加引起的DNA完整性破坏，以及DNA修复的破坏都是相关的现象，每种现象都可以由叶酸消耗引起。它们被认为通过改变关键基因的表达来增强致癌作用。
An expanding body of epidemiologic, animal, and human studies suggests that folate status modulates the risk of developing cancers in several tissues. Folate depletion appears to enhance carcinogenesis [1], and folate supplementation has a protective effect [2]. The mechanistic studies performed to date have not fully defined the mechanisms that are responsible for mediating this effect, although rapid progress is being made.As folate is a critical element for both DNA methylation and synthesis, and because aberrations in DNA are widely held to be the origin of the majority of carcinogenic processes, most studies have focused on these effects. Interestingly, alterations in DNA methylation, disruption of DNA integrity caused by increased uracil misincorporation or DNA strand breaks, and disruption of DNA repair are related phenomena that can each be induced by folate depletion. They are believed to enhance carcinogenesis by altering the expression of critical genes.