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活性氧对癌基因的激活和/或抗癌基因的失活。

Activation of oncogenes and/or inactivation of anti-oncogenes by reactive oxygen species.

作者信息

Wei H

机构信息

Department of Environmental Health Sciences, University of Alabama, Birmingham 35294-0008.

出版信息

Med Hypotheses. 1992 Nov;39(3):267-70. doi: 10.1016/0306-9877(92)90120-2.

Abstract

Abundant evidence indicates that reactive oxygen species (ROS) are involved in mutagenesis and carcinogenesis. These chemical-generated or phagocyte-released ROS are known to cause a variety of genetic alterations which lie at the heart of the carcinogenic process. ROS have also been shown to cause malignant transformation of normal cells, and to increase expression of certain proto-oncogenes such as c-fos and c-jun. It is known that certain proto-oncogenes and anti-oncogenes may serve as the targets of carcinogens of various sorts. I hypothesize that ROS-mediated DNA damage may cause mutations and/or deletions in certain specific coding regions of tumor-related genes, and could be responsible for subsequent activation of oncogenes and/or inactivation of anti-oncogenes.

摘要

大量证据表明,活性氧(ROS)参与了诱变和致癌过程。已知这些化学产生的或吞噬细胞释放的ROS会导致多种基因改变,而这些改变正是致癌过程的核心所在。ROS还被证明可导致正常细胞发生恶性转化,并增加某些原癌基因如c-fos和c-jun的表达。已知某些原癌基因和抗癌基因可能成为各类致癌物的作用靶点。我推测,ROS介导的DNA损伤可能会导致肿瘤相关基因某些特定编码区域发生突变和/或缺失,并可能导致随后原癌基因的激活和/或抗癌基因的失活。

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