Abstract
In our study, we estimate an effect from chromosome aberrations and genome mutations on changes in microRNA expression profiles in cancer cell lines demonstrating different radiosensitivity. Here, cell viability and microRNA spectrum have been estimated 1, 4, and 24 h after irradiation. MiSeq high-throughput sequencing system (Illumina, San Diego, CA, USA) is employed to perform microRNA spectrum estimation. In the K562 cell line, the number of expressed microRNAs in chromosomes demonstrates a more pronounced variation. An analysis of microRNA effects on signaling pathway activity demonstrates differences in post-transcriptional regulation of the expression of genes included into 40 signaling pathways. In the K562 cell line, microRNA dynamics analyzed for their dependence on chromosome localization show a wider scattering of microRNA expression values for a pair of chromosomes compared to the HL-60 cell line. An analysis of microRNAs expression in the K562 and HL-60 cell lines after irradiation has shown that chromosome abnormalities can affect microRNA expression changes. A study of radiation-induced changes of microRNA expression profiles in the K562 and HL-60 cell lines has revealed a dependence of microRNA expression changes on the number of chromosome aberrations and genome mutations.
Highlights
Radiation therapy is widespread for cancer treatment [1]
The study of the dynamics of microRNA global expression has revealed that radiation exposure causes a significant change in the expression of microRNAs and, can have a significant effect on posttranscriptional regulation of gene expression
The dynamics of the number of expressed microRNAs changing with the chromosomal location after irradiation show that changes in the amount of microRNAs are typical for all chromosomes and are more pronounced in the radioresistant K562 cell line
Summary
Radiation therapy is widespread for cancer treatment [1]. In some cases, this therapy is inefficient due to radioresistance of cancer cells. Radioresistance is a complex phenomenon associated with the ability of cancer cells to maintain clonogenic potential under exposure to therapeutic doses of ionizing radiation [2]. Ionizing radiation induces cell death, mainly due to DNA damage. The inability to repair radiation-induced DNA damage triggers programmed cell death (PCD) and the cell dies [3]. The ability to trigger PCD can be reduced in response to radiation-induced DNA damage [4]. Another radioresistance mechanism of cancer cells is their ability to abnormally activate
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