Activation of oncogenes and/or inactivation of anti-oncogenes by reactive oxygen species.
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.
Wei
H
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Department of Environmental Health Sciences, University of Alabama, Birmingham 35294-0008.
D000818:Animals; D004249:DNA Damage; D005786:Gene Expression Regulation / Q000187:drug effects; D016147:Genes, Tumor Suppressor / Q000187:drug effects*; D006801:Humans; D008957:Models, Genetic; D009857:Oncogenes / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000633:toxicity*
D017382:Reactive Oxygen Species