ACTIVATION OF ONCOGENES AND OR INACTIVATION OF ANTIONCOGENES BY REACTIVE OXYGEN SPECIES
ACTIVATION OF ONCOGENES AND OR INACTIVATION OF ANTIONCOGENES BY REACTIVE OXYGEN SPECIES
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DOI：
10.1016/0306-9877(92)90120-2
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发表时间：
1992-11-01
影响因子：
4.7
通讯作者：
WEI, H
中科院分区：
文献类型：
--
作者：
WEI, H
大量证据表明活性氧（reactive oxygen species， ROS）参与了肿瘤的诱变和癌变。这些化学物质产生的或吞噬细胞释放的活性氧已知会引起各种基因改变，而这些改变是致癌过程的核心。ROS也被证明能引起正常细胞的恶性转化，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种致癌物质的靶点。我推测ros介导的DNA损伤可能导致肿瘤相关基因特定编码区域的突变和/或缺失，并可能导致随后致癌基因的激活和/或抗癌基因的失活。
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.