Bioinformatic analysis of gene expression of human peripheral blood cells related to radiation injury

XU You-qin ZHANG Qing-fen ZHANG Chao*

doi:10.16098/j.issn.0529-1356.2017.01.007

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Acta Anatomica Sinica ›› 2017, Vol. 48 ›› Issue (1) : 37-42. DOI: 10.16098/j.issn.0529-1356.2017.01.007

Cell and Molecules Biology

Bioinformatic analysis of gene expression of human peripheral blood cells related to radiation injury

XU You-qin ZHANG Qing-fen ZHANG Chao*

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Abstract

Objective To investigate genes associated with radiation injury and to reveal human peripheral blood cells change during radiation. Methods The microarray data of radiation induced gene expression in human blood were downloaded from the Gene Expression Omnibus (GEO) database and Qlucore Omics Explorer 3.0 software was used to screen differentially expressed genes. Further analysis of differentially expressed genes was conducted by the on-line tools STRING and DAVID. Results Of 94 differentially expressed genes, 31 genes were of co-overexpression and 11 genes were co-underexpressed. These genes were involved in the biological process and molecular function of regulation of apoptosis, regulation of programmed cell death, regulation of cell death, intracellular signaling cascade, response to DNA damage stimulus and regulation of cell cycle. STRING analysis showed that ubiquitin C(UBC)，proliferating cell nuclear antigen(PCNA)，murine double minute-2(MDM2) had important roles in the protein-protein interaction network, which participates in p53 pathway. Conclusion UBC, PCNA and MDM2 may be potential therapeutic targets of ionizing radiation exposure through the bioinformatics analysis, which needs further study.

Key words

Radiation injury / Gene microarray / Bioinformatics / Differentially expressed genes / Data analysis / Human

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XU You-qin ZHANG Qing-fen ZHANG Chao. Bioinformatic analysis of gene expression of human peripheral blood cells related to radiation injury[J]. Acta Anatomica Sinica. 2017, 48(1): 37-42 https://doi.org/10.16098/j.issn.0529-1356.2017.01.007

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