Identification of radiation-specific responses from gene expression profile

Park, Woong-Yang; Hwang, Chang-Il; Im, Chang Nim; Kang, Min Ji; Woo, Jeong Soo; Kim, Ju Hoon; Kim, Yon Su; Kim, Ju Han; Kim, Ho; Kim, Kyung A.; Yu, Hyung Jin; Lee, Sue Jae; Lee, Yun Sil; Seo, Jeong Sun

doi:10.1038/sj.onc.1205977

Cited by 105 publications

(71 citation statements)

References 41 publications

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“…As p53 has been considered one of the major determinants of gene induction patterns following many types of stress, this finding suggests that the mechanism of action of a specific stress agent may be a stronger determinant of gene expression patterns than cellular genotype, or by extension, possibly even interindividual differences. Similar results were reported in a more restricted study comparing g-irradiation with UV radiation, adriamycin, and cisplatin, where no dependence on p53 status was found within the gene expression signatures (Park et al, 2002). This suggests that while p53 strongly regulates a subset of genes in response to specific stresses, the majority of stressregulated genes are p53-independent.…”

Section: Discussionsupporting

confidence: 71%

“…Initial steps in this direction include defining gene expression signatures for different classes of toxic agents. For example, a gene expression signature was identified discriminating between ionizing radiation and base-damaging agents, such as ultraviolet (UV) radiation and cisplatin (Park et al, 2002). Another profile identified cisplatin as distinct from nongenotoxic agents (Burczynski et al, 2000), while a study using rats treated in vivo identified a gene expression profile distinguishing between pheonbarbital and peroxisome proliferators (Hamadeh et al, 2002a, b).…”

Section: Introductionmentioning

confidence: 99%

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Stress-specific signatures: expression profiling of p53 wild-type and -null human cells

et al. 2005

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Gene expression responses of human cell lines exposed to a diverse set of stress agents were compared by cDNA microarray hybridization. The B-lymphoblastoid cell line TK6 (p53 wild-type) and its p53-null derivative, NH32, were treated in parallel to facilitate investigation of p53-dependent responses. RNA was extracted 4 h after the beginning of treatment when no notable decrease in cell viability was evident in the cultures. Gene expression signatures were defined that discriminated between four broad general mechanisms of stress agents: Non-DNAdamaging stresses (heat shock, osmotic shock, and 12-Otetradecanoylphorbol 13-acetate), agents causing mainly oxidative stress (arsenite and hydrogen peroxide), ionizing radiations (neutron and c-ray exposures), and other DNAdamaging agents (ultraviolet radiation, methyl methanesulfonate, adriamycin, camptothecin, and cis-Platinum(II)diammine dichloride (cisplatin)). Within this data set, non-DNA-damaging stresses could be discriminated from all DNA-damaging stresses, and profiles for individual agents were also defined. While DNA-damaging stresses showed a strong p53-dependent element in their responses, no discernible p53-dependent responses were triggered by the non-DNA-damaging stresses. A set of 16 genes did exhibit a robust p53-dependent pattern of induction in response to all nine DNA-damaging agents, however.

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Section: Discussionsupporting

confidence: 71%

Section: Introductionmentioning

confidence: 99%

Stress-specific signatures: expression profiling of p53 wild-type and -null human cells

et al. 2005

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“…We observed the induction of HIF-1 under hypoxic conditions in our experimental system, but a relation to apoptosis via interaction with p53 cannot be postulated, because all Jurkat cells are know to be p53 negative (Park et al, 2002). Therefore, the activation of mitochondrial apoptotic pathways under hypoxia occurs independently of p53 in this setting.…”

Section: Discussionmentioning

confidence: 74%

Molecular ordering of hypoxia-induced apoptosis: critical involvement of the mitochondrial death pathway in a FADD/caspase-8 independent manner

et al. 2004

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“…To elucidate the mechanism of radioresistance of cancer cells at the whole-genome or proteome level, several studies have reported profiled gene expression (Park et al, 2002;Amundson et al, 2005) or proteome information (An and Seong, 2006;Skvortsova et al, 2008) related to radioresistance. However, no previous study has reported on the global analysis of aberrant CpG methylation related to radioresistance in cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Global analysis of CpG methylation reveals epigenetic control of the radiosensitivity in lung cancer cell lines

et al. 2010

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Epigenetic regulation by CpG methylation has an important role in tumorigenesis as well as in the response to cancer therapy. To analyze the mechanism of epigenetic control of radiosensitivity, the CpG methylation profiles of radiosensitive H460 and radioresistant H1299 human non-small cell lung cancer (NSCLC) cell lines were analyzed using microarray profiling. These analyses revealed 1091 differentially methylated genes (DMG) (absolute difference of mean b-values, |Db % |40.5), including genes involved in cell adhesion, cell communication, signal transduction and transcriptional regulation. Among the 747 genes hypermethylated in radioresistant H1299 cells, CpG methylation of SERPINB5 and S100A6 in radioresistant H1299 cells was confirmed by methylationspecific PCR. Reverse transcriptase-PCR showed higher expression of these two genes in radiosensitive H460 cells compared with radioresistant H1299 cells. Downregulation of SERPINB5 or S100A6 by small interfering RNA in H460 cells increased the resistance of these cells to ionizing radiation. In contrast, promoter CpG sites of 344 genes, including CAT and BNC1, were hypomethylated in radioresistant H1299 cells. Suppression of CAT or BNC1 mRNA expression in H1299 cells also reduced the resistance of these cells to ionizing radiation. Thus, we identified DMGs by genome-wide CpG methylation profiling in two NSCLC cell lines with different responses to ionizing radiation, and our data indicated that these differences may be critical for epigenetic regulation of radiosensitivity in lung cancer cells.

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Identification of radiation-specific responses from gene expression profile

Cited by 105 publications

References 41 publications

Stress-specific signatures: expression profiling of p53 wild-type and -null human cells

Stress-specific signatures: expression profiling of p53 wild-type and -null human cells

Molecular ordering of hypoxia-induced apoptosis: critical involvement of the mitochondrial death pathway in a FADD/caspase-8 independent manner

Global analysis of CpG methylation reveals epigenetic control of the radiosensitivity in lung cancer cell lines

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