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자료유형
학술저널
저자정보
Lee, Su-Yeon (Seoul National University Bioinformatics) Choi, Moon-Kyung (Department of Biochemistry and Molecular Biology, Seoul National University College of Medicine) Lim, Jung-Min (Department of Biochemistry and Molecular Biology, Seoul National University College of Medicine) Wu, Hong-Gyun (Department of Biochemistry, Radiation Oncology, Seoul National University College of Medicine) Kim, Ju-Han (Seoul National University Bioinformatics) Park, Woong-Yang (Department of Biochemistry and Molecular Biology, Seoul National University College of Medicine)
저널정보
한국유전체학회 Genomics & informatics Genomics & informatics 제6권 제1호
발행연도
2008.1
수록면
36 - 43 (8page)

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Radiotherapy would be the choice of treatment for human cancers, because of high cost-effectiveness. However, a certain population of patients shows a resistance to radiotherapy and recurrence. In an effort to increase the efficacy of radiotherapy, many efforts were driven to find the genes causing the unresponsiveness to ionizing radiation. In this paper, we compared the gene expression profiles of two lung cancer cell lines, H460 and H1299, which showed differential responses to ionizing radiations. Each cell were irradiated at 2 Gy, and harvested after 0, 2, 4, 8, 12 and 24 hours to examine the expressions. Two-way ANOVA analysis on time-series experiments of two cells could select 2863 genes differentially expressed upon ionizing radiation among 32,321 genes in microarray (p<0.05). We classified these genes into 21 clusters by SOM clustering according to the interaction between cell types and time. Two SOM clusters were enriched with apoptosis-related genes in pathway analysis. One cluster contained higher levels of phosphatidyl inositol 3-phosphate kinase (PI3K) subunits in H1299, radio-resistant cells than H460, radiosensitive cells. TRAIL receptors were expressed in H460 cells while the decoy receptor for TRAIL was expressed in H1299 cells. From these results, we could characterize the differential responsiveness to ionizing radiation according to their differential expressions of apoptosis-related genes, which might be the candidates to increase the power of radiotherapy.

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