Abstract
Ionizing radiation may be of both artificial and natural origin and causes cellular damage in living organisms. Radioactive isotopes have been used significantly in cancer therapy for many years. The formation of DNA double-strand breaks (DSBs) is the most dangerous effect of ionizing radiation on the cellular level. After irradiation, cells activate a DNA damage response, the molecular path that determines the fate of the cell. As an important element of this, homologous recombination repair is a crucial pathway for the error-free repair of DNA lesions. All components of DNA damage response are regulated by specific microRNAs. MicroRNAs are single-stranded short noncoding RNAs of 20–25 nt in length. They are directly involved in the regulation of gene expression by repressing translation or by cleaving target mRNA. In the present review, we analyze the biological mechanisms by which miRNAs regulate cell response to ionizing radiation-induced double-stranded breaks with an emphasis on DNA repair by homologous recombination, and its main component, the RAD51 recombinase. On the other hand, we discuss the ability of DNA damage response proteins to launch particular miRNA expression and modulate the course of this process. A full understanding of cell response processes to radiation-induced DNA damage will allow us to develop new and more effective methods of ionizing radiation therapy for cancers, and may help to develop methods for preventing the harmful effects of ionizing radiation on healthy organisms.
Highlights
Ionizing radiation (IR) consists of alpha, beta and neutron particles, as well as X and gamma rays.As a result of ionization, chemical reactions are initiated and they lead to major disorders of a number of cell molecules, including DNA [1,2,3]
Upregulated DNA damage repair genes are assigned as black arrows pointing up, while suppressed genes are presented as black arrows pointing down
Short non-coding RNAs, miRNAs, regulate many cellular factors, which participate in DNA damage response (DDR) and homologous recombination (HR) repair mechanisms after irradiation
Summary
Ionizing radiation (IR) consists of alpha, beta and neutron particles, as well as X and gamma rays. Radiation therapy has been in use for a long time, it is one of the most effective techniques applied in the eradication of cancerous lesions in humans [6,7,8]. Taking into account different DNA template requirements and the available set of proteins associated with the changing of the cell cycle phase, there are two distinct DSBs repair pathways, known as canonical non-homologous end joining (C-NHEJ) and homologous recombination (HR). Each of these repair mechanisms is designed for distinct tasks and brings different results for cells [13,14].
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