Department of Environmental and Occupational Health, Fay W. Boozman College of Public Health, University of Arkansas for Medical Sciences, Little Rock, Arkansas.
Radiat Res. 2018 Jul;190(1):5-11. doi: 10.1667/RR15027.1. Epub 2018 Apr 26.
Aside from the generally accepted potential to cause DNA damage, it is becoming increasingly recognized that ionizing radiation has the capability to target the cellular epigenome. Epigenetics unifies the chemical marks and molecules that collectively facilitate the proper reading of genetic material. Among the epigenetic mechanisms of regulation, methylation of DNA is known to be the key player in the postirradiation response by controlling the expression of genetic information and activity of transposable elements. Radiation-induced alterations to DNA methylation may lead to cellular epigenetic reprogramming that, in turn, can substantially compromise the genomic integrity and has been proposed as one of the mechanisms of radiation-induced carcinogenesis. DNA methylation is strongly dependent on the one-carbon metabolism. This metabolic pathway is central to the support of DNA methylation by means of providing the donor of methyl groups, as well as for the synthesis of amino acids. To better understand the mechanisms of radiation-induced health effects, we study how exposure to radiation affects DNA methylation and one-carbon metabolism. Also, a tight interaction that exists between DNA methylation and one-carbon metabolism allows us to simultaneously manipulate both cellular epigenetic and metabolic profiles to modulate the normal and cancerous tissue response to radiotherapy.
除了普遍被认可的可能导致 DNA 损伤的能力外,电离辐射靶向细胞表观基因组的能力正日益得到认可。表观遗传学将共同促进遗传物质正确读取的化学标记和分子统一起来。在调节的表观遗传机制中,已知 DNA 甲基化是通过控制遗传信息的表达和转座因子的活性来控制辐射后反应的关键因素。辐射诱导的 DNA 甲基化改变可能导致细胞表观遗传重编程,进而严重损害基因组完整性,并被提议作为辐射诱导致癌的机制之一。DNA 甲基化强烈依赖于一碳代谢。这种代谢途径是通过提供甲基供体来支持 DNA 甲基化以及合成氨基酸的核心。为了更好地了解辐射诱导健康影响的机制,我们研究了辐射暴露如何影响 DNA 甲基化和一碳代谢。此外,DNA 甲基化和一碳代谢之间存在紧密的相互作用,使我们能够同时操纵细胞表观遗传和代谢特征,以调节正常组织和癌变组织对放射治疗的反应。