摘要
氧化应激不但可导致基因遗传变化,还可诱发表观遗传变化。氧化应激引起的遗传变化主要是活性氧(ROS)攻击DNA,造成DNA链断裂、碱基修饰、DNA-DNA交联和DNA-蛋白质交联等多种形式的DNA损伤,这些损伤在肿瘤发生起始阶段发挥重要作用。氧化应激引起的表观遗传变化中,一个重要的机制是DNA甲基化水平改变,主要表现在高甲基化引起基因转录抑制(如抑癌基因)和低甲基化诱导基因转录激活(如癌基因),DNA甲基化水平变化与肿瘤发生息息相关。本工作介绍了ROS诱导的氧化应激引起的遗传改变和DNA甲基化水平变化在肿瘤发生中的作用,并展望了肿瘤治疗的发展趋势。
Oxidative stress changes mainly involve that ROS can initiate genetic and epigenetic alterations. Oxidative stress-induced genetic attacks DNA, inducing various DNA changes like strand breaks, base modifications, DNA-DNA and DNA-protein cross linkages which are all strongly implicated in the initiation stage of tumorigenesis. In oxidative stress-induced epigenetic changes, one of the most important mechanisms is the change of DNA metbylation levels： hypermethylation-induced transcriptional repression （in the case of tumor suppressor genes） or hypomethylation-induced activation （in the case of oncogenes）, which is closely associated with tumorigenesis. In this paper, the current status of knowledge on the role of ROS-induced oxidative stress in altering the genetic and DNA methylation during tumorigenesis was introduced, and the developing tendency of tumor therapy was prospected.
出处
《辐射研究与辐射工艺学报》
CAS
CSCD
2013年第6期1-8,共8页
Journal of Radiation Research and Radiation Processing
基金
国家重点基础研究发展规划项目(973计划
2010CB834203)
国家自然科学基金重点项目(10835011)
国家自然科学基金项目(10905080
11075191)
中国科学院"西部之光"项目(Y162100XB0
Y1621130SJ0)资助
