DNA damage-related gene expression as biomarkers to assess cellular response after gamma irradiation of a human lymphoblastoid cell line

Bishay, Karine; Ory, Kathy; Lebeau, J.; Levalois, Céline; Olivier, Marie-Françoise; Chevillard, Sylvie

doi:10.1038/sj.onc.1203405

Cited by 38 publications

(16 citation statements)

References 37 publications

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“…Also the over-expression of HIP1 has been related to the induction of apoptosis, probably through its interaction with APAF-1 [28], a downstream effector of p53-mediated apoptosis [29]. These findings are in line with those from previous studies on gene expression in response to ionizing radiation [30][31][32], confirming the overall reliability of our experimental approach. Thus the data set was further inspected in order to identify those genes differently expressed in individuals with family history of gastric cancer (cases).…”

Section: Pbx3supporting

confidence: 93%

Gene expression in response to ionizing radiation and family history of gastric cancer

et al. 2010

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Genes and molecular pathways involved in familial clustering of gastric cancer have not yet been identified. The purpose of the present study was to investigate gene expression changes in response to a cellular stress, and its link with a positive family history for this neoplasia. To this aim leukocytes of healthy first-degree relatives of gastric cancer patients and controls were challenged in vitro with ionizing radiation and gene expression evaluated 4 h later on microarrays with 1,800 cancer-related genes. Eight genes, mainly involved in signal transduction and cell cycle regulation, were differentially expressed in healthy relatives of gastric cancer cases. Functional class scoring by Gene Ontology classification highlighted two G-protein related pathways, implicated in the proliferation of neoplastic tissue, which were differentially expressed in healthy subjects with positive family history of gastric cancer. The relative expression of 84 genes related to these pathways was examined using the SYBR green-based quantitative real-time PCR. The results confirmed the indication of an involvement of G-protein coupled receptor pathways in GC familiarity provided by microarray analysis. This study indicates a possible association between familiarity for gastric cancer and altered transcriptional response to ionizing radiation.

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Section: Pbx3supporting

confidence: 93%

Gene expression in response to ionizing radiation and family history of gastric cancer

et al. 2010

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“…35,36 Studies employing microarray technology have also found that repair genes are not upregulated after ionizing radiation exposure. 24,37 It is interesting to consider that if the adaptive response to ionizing radiation requires transcriptional activation, induction of BER genes may not be involved in radioadaptation.…”

Section: Discussionmentioning

confidence: 99%

Radiation‐induced gene expression profile of human cells deficient in 8‐hydroxy‐2′‐deoxyguanine glycosylase

Chaudhry

2005

Intl Journal of Cancer

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The human OGG1 gene encodes a DNA glycosylase that is involved in the base excision repair of 8-hydroxy-2 0 -deoxyguanine (8-OH-dG) from oxidatively damaged DNA. Cellular 8-OH-dG levels accumulate in the absence of this activity and could be deleterious for the cell. To assess the role of 8-oxoguanine glycosylase (OGG1) in the cellular defense mechanism in a specific DNA repair defect background, we set out to determine the expression pattern of base excision repair genes and other cellular genes not involved in the base excision pathway in OGG1-deficient human KG-1 cells after ionizing radiation exposure. KG-1 cells have lost OGG1 activity due to a homozygous mutation of Arg229Gln. Gene expression alterations were monitored at 4, 8, 12 and 24 hr in 2 Gy irradiated cells. Large-scale gene expression profiling was assessed with DNA microarray technology. Gene expression analysis identified a number of ionizing radiation-responsive genes, including several novel genes. There were 2 peaks of radiationinduced gene induction or repression: one at 8 hr and the other at 24 hr. Overall the number of downregulated genes was higher than the number of upregulated genes. The highest number of downregulated genes was at 8 hr postirradiation. Genes corresponding to cellular, physiologic, developmental and extracellular processes were identified. The highest number of radiationinduced genes belonged to the signal transduction category, followed by genes involved in transcription and response to stress. Microarray gene expression data were independently validated by relative quantitative RT-PCR. Surprisingly, none of the genes involved in the base excision repair of radiation-induced DNA damage showed altered expression. ' 2005 Wiley-Liss, Inc.

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“…Altered homologous recombination-related protein expression might indirectly lead to altered nonhomologous end-joining activity given the interplay between the two pathways during DNA double-strand break repair (32,33). Maintenance of survival in malignant cells, despite high levels of DNA double-strand breaks and chromosomal aberrations after DNA damage, is probably secondary to loss of potentially deleterious accentric fragments or other chromosomal abnormalities within micronuclei at 48 to 72 hours after irradiation (34,35).…”

Section: Discussionmentioning

confidence: 99%

Defective DNA Strand Break Repair after DNA Damage in Prostate Cancer Cells

et al. 2004

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Together with cell cycle checkpoint control, DNA repair plays a pivotal role in protecting the genome from endogenous and exogenous DNA damage. Although increased genetic instability has been associated with prostate cancer progression, the relative role of DNA double-strand break repair in malignant versus normal prostate epithelial cells is not known. In this study, we determined the RNA and protein expression of a series of DNA double-strand break repair genes in both normal (PrEC-epithelial and PrSC-stromal) and malignant (LNCaP, DU-145, and PC-3) prostate cultures. Expression of genes downstream of ATM after ionizing radiation-induced DNA damage reflected the p53 status of the cell lines. In the malignant prostate cell lines, mRNA and protein levels of the Rad51, Xrcc3, Rad52, and Rad54 genes involved in homologous recombination were elevated ϳ2-to 5-fold in comparison to normal PrEC cells. The XRCC1, DNA polymerase-␤ and -␦ proteins were also elevated. There were no consistent differences in gene expression relating to the nonhomologous end-joining pathway. Despite increased expression of DNA repair genes, malignant prostate cancer cells had defective repair of DNA breaks, alkali-labile sites, and oxidative base damage. Furthermore, after ionizing radiation and mitomycin C treatment, chromosomal aberration assays confirmed that malignant prostate cells had defective DNA repair. This discordance between expression and function of DNA repair genes in malignant prostate cancer cells supports the hypothesis that prostate tumor progression may reflect aberrant DNA repair. Our findings support the development of novel treatment strategies designed to reinstate normal DNA repair in prostate cancer cells.

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DNA damage-related gene expression as biomarkers to assess cellular response after gamma irradiation of a human lymphoblastoid cell line

Cited by 38 publications

References 37 publications

Gene expression in response to ionizing radiation and family history of gastric cancer

Gene expression in response to ionizing radiation and family history of gastric cancer

Radiation‐induced gene expression profile of human cells deficient in 8‐hydroxy‐2′‐deoxyguanine glycosylase

Defective DNA Strand Break Repair after DNA Damage in Prostate Cancer Cells

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