期刊
EPIGENETICS
卷 8, 期 8, 页码 839-848出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/epi.25498
关键词
radiation; DNA methylation; epigenetics; profiling; gene ontology; 5-methylcytosine; DNA repair; cell cycle; apoptosis
资金
- NCI NIH HHS [P30 CA022453, R01 CA140314] Funding Source: Medline
- NIEHS NIH HHS [R01 ES012933, R21 ES021983, P30 ES020957] Funding Source: Medline
DNA methylation can regulate gene expression and has been shown to modulate cancer cell biology and chemotherapy resistance. Therapeutic radiation results in a biological response to counter the subsequent DNA damage and genomic stress in order to avoid cell death. In this study, we analyzed DNA methylation changes at >450,000 loci to determine a potential epigenetic response to ionizing radiation in MDA-MB-231 cells. Cells were irradiated at 2 and 6 Gy and analyzed at 7 time points from 1-72 h. Significantly differentially methylated genes were enriched in gene ontology categories relating to cell cycle, DNA repair, and apoptosis pathways. The degree of differential methylation of these pathways varied with radiation dose and time post-irradiation in a manner consistent with classical biological responses to radiation. A cell cycle arrest was observed 24 h post-irradiation and DNA damage, as measured by H2AX, resolved at 24 h. In addition, cells showed low levels of apoptosis 2-48 h post-6 Gy and cellular senescence became significant at 72 h post-irradiation. These DNA methylation changes suggest an epigenetic role in the cellular response to radiation.
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