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Organ-Specific Gene Expressions in C57BL/6 Mice after Exposure to Low-Dose Radiation
Lee, Woo-Jung,Majumder, Zahidur Rahman,Jeoung, Doo-Il,Lee, Hae-June,Kim, Sung-Ho,Bae, Sangwoo,Lee, Yun-Sil BioOne (Radiation Research Society) 2006 Radiation research Vol.165 No.5
<P>The possibility that radiation-induced alterations in gene expression are tissue specific and are related to apoptosis was examined using samples from brain, heart, lung, spleen and intestine from female C57BL6 mice after exposure to 0.2 Gy radiation. Apoptosis was the highest in spleen and intestine, moderate in lung, and absent in brain and heart. However, the mRNA expression of Trp53 and Cdkn1a (p21) after irradiation was not different among the organ types, and immunohistochemistry revealed that all the organs expressed these two proteins after irradiation. When expression patterns of 23 genes in the organs were examined by RT-PCR, neogenine, Apo1, nuclease sensitive element binding protein 1, syntaxin, cyclin G1, hNOP56, paraoxonase and glutathione peroxidase were overexpressed after irradiation in all the organs sampled, suggesting them as universal exposure markers for low-dose radiation. Sialyltransferase may be a candidate for radiation detection in spleen and intestine, which are radiosensitive organs. Because Sod1 (Cu/ZnSOD) and alphaB crystalline were expressed only in spleen, and protein tyrosine kinase and platelet membrane glycoprotein lib were expressed in both spleen and lung, these genes may also be potential markers for detection of radiation exposure, especially low-dose radiation, in these tissues. These data suggested possible tissue-specific markers of low-dose radiation exposure and suggested potential novel genetic modifiers of radiation response.</P>
Suzuki, Minoru,Amano, Morikazu,Choi, Jihyung,Park, Heon Joo,Williams, Brent W.,Ono, Koji,Song, Chang W. BioOne (Radiation Research Society) 2006 Radiation research Vol.165 No.5
<P>It has been reported that beta-lapachone (beta-lap), a bioreductive anti-cancer drug, synergistically interacts with ionizing radiation and that the sensitivity of cells to beta-lap is closely related to the activity of NAD(P)H:quinone oxidoreductase 1 (NQO1). Here we report the results of our studies of mechanisms underlying the synergistic interaction of beta-lap and radiation in killing cancer cells using the DU-145 human prostate cancer cell line. The clonogenic cell death caused by the combination of radiation and beta-lap was synergistic when beta-lap was administered 0-10 h after irradiation but not when it was given before irradiation. The expression and activity of NQO1 increased significantly and remained elevated for longer than 12 h after 4 Gy irradiation, suggesting that the long-lasting elevation of NQO1 sensitized the cells to beta-lap. Studies with split-dose irradiation demonstrated that beta-lap given immediately after irradiation effectively inhibited sublethal radiation damage (SLD) repair. Taken together, these results lead us to conclude that the synergistic interaction between beta-lap and radiation in killing cells is the result of two distinct mechanisms: First, radiation sensitizes cells to beta-lap by up-regulating NQO1, and second, beta-lap sensitizes cells to radiation by inhibiting SLD repair. The combination of beta-lap and radiotherapy is potentially promising modality for the treatment of cancer in humans.</P>
Kim, Young-Mee,Shin, You Keun,Jun, Hyun Jung,Rha, Sun Young,Pyo, Hongryull Japan Radiation Research Society [etc.] 2011 JOURNAL OF RADIATION RESEARCH Vol.52 No.6
<P>To investigate genes regulated by COX-2 or a COX-2 specific inhibitor, celecoxib, in irradiated cancer cells, we analyzed changes in gene expression using complementary DNA microarray following celecoxib or combined celecoxib and ionizing radiation (IR) treatment in a stable COX-2 knockdown A549 (AS) and a mock cell line (AN). Thirty-six genes were differentially expressed by COX-2 knockdown. Celecoxib changed the expressions of 40 and 69 genes in AN and AS cells, respectively. Twenty-seven genes were synchronously regulated by COX-2 and celecoxib. Among these, celecoxib regulated ras homolog gene family B and mitosin protein expression in a COX-2 dependent manner, especially in irradiated cells. In addition, we identified 11 genes that changed by more than 1.5 times the expected additive values after celecoxib and IR treatment. The current study may provide evidence that COX-2 or celecoxib regulates various intracellular functions in addition to their enzymatic activity regulation. We also identified candidate molecules that may be responsible for COX-2-dependent radiosensitization by celecoxib.</P>