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Journal articles on the topic 'Radiation Induced Activation'

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Author: Grafiati

Published: 14 March 2023

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1

TAKAMASA, Tomoji, Koji OKAMOTO, Kaichiro MISHIMA, and Masahiro FURUYA. "Radiation Induced Surface Activation." Journal of the Atomic Energy Society of Japan / Atomic Energy Society of Japan 45, no. 2 (2003): 112–17. http://dx.doi.org/10.3327/jaesj.45.112.

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2

KIKUCHI, Takayoshi, Yoshinori HIROSE, Tatsuya HAZUKU, and Tomoji TAKAMASA. "ICONE15-10316 EFFECT OF RADIATION INDUCED SURFACE ACTIVATION ON SURFACE WETTABILITY IN HIGH-TEMPERATURE CONDITION." Proceedings of the International Conference on Nuclear Engineering (ICONE) 2007.15 (2007): _ICONE1510. http://dx.doi.org/10.1299/jsmeicone.2007.15._icone1510_160.

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3

Yang, Nong, Xican Gao, Xiaofei Qu, Ruiguang Zhang, Fan Tong, Qian Cai, Jihua Dong, Yu Hu, Gang Wu, and Xiaorong Dong. "PIDD Mediates Radiation-Induced Microglia Activation." Radiation Research 186, no. 4 (October 2016): 345–59. http://dx.doi.org/10.1667/rr14374.1.

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4

Dong, X., M. Luo, J. Dong, and G. Wu. "The Mechanism of Radiation-induced Microglia Activation." International Journal of Radiation Oncology*Biology*Physics 78, no. 3 (November 2010): S632—S633. http://dx.doi.org/10.1016/j.ijrobp.2010.07.1473.

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5

Redd, Priscilla S., Kankana Bardhan, May R. Chen, Amy V. Paschall, Chunwan Lu, Roni J. Bollag, Fengchong Kong, et al. "NF-κB acts as a molecular link between tumor cells and Th1/Tc1 T cells in the tumor microenvironment to exert radiation-mediated tumor suppression." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 213.3. http://dx.doi.org/10.4049/jimmunol.196.supp.213.3.

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Abstract Radiation is a local treatment for many types of solid cancers. About two thirds of cancer patients require radiation during the course of their disease treatment. Radiation modulates both tumor cells and immune cells in the tumor microenvironment to exert anti-tumor activity, but the molecular connection between tumor cells and immune cells that mediates radiation-exerted tumor suppression activity is largely unknown. We report here that radiation induces rapid activation of the p65/p50 and p50/p50 NF-κB complexes in human soft tissue sarcoma (STS) cells. Radiation-activated p65/p50 and p50/p50 bind to the TNFα promoter to activate its transcription in STS cells. Radiation-induced TNFα then induces tumor cell death in an autocrine manner. Smac mimetic BV6 induces cIAP1 and cIAP2 degradation to increase tumor cell sensitivity to radiation-induced cell death in vitro and to enhance radiation-mediated suppression of STS xenografts in vivo. Inhibition of caspases, RIP1, or RIP3 blocks radiation/TNFα-induced cell death, whereas inhibition of RIP1 blocks TNFα-induced caspase activation, suggesting that caspases and RIP1 act sequentially to mediate the non-compensatory cell death pathways. We determined in a syngeneic sarcoma mouse model that radiation up-regulates the NF-κB target genes IRF3, IFNβ, and the T cell chemokines CCL2 and CCL5 in the tumor microenvironment, which is associated with activation and increased infiltration of Th1/Tc1 T cells in the tumor microenvironment. Consequently, combined BV6 and radiation completely suppressed tumor growth in vivo. Radiation-induced NF-κB functions as a molecular link between tumor cells and immune cells in the tumor microenvironment for radiation mediated tumor suppression.

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Judge, J. L., K. M. Owens, S. J. Pollock, C. F. Woeller, T. H. Thatcher, J. P. Williams, R. P. Phipps, P. J. Sime, and R. M. Kottmann. "Ionizing radiation induces myofibroblast differentiation via lactate dehydrogenase." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 8 (October 15, 2015): L879—L887. http://dx.doi.org/10.1152/ajplung.00153.2015.

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Pulmonary fibrosis is a common and dose-limiting side-effect of ionizing radiation used to treat cancers of the thoracic region. Few effective therapies are available for this disease. Pulmonary fibrosis is characterized by an accumulation of myofibroblasts and excess deposition of extracellular matrix proteins. Although prior studies have reported that ionizing radiation induces fibroblast to myofibroblast differentiation and collagen production, the mechanism remains unclear. Transforming growth factor-β (TGF-β) is a key profibrotic cytokine that drives myofibroblast differentiation and extracellular matrix production. However, its activation and precise role in radiation-induced fibrosis are poorly understood. Recently, we reported that lactate activates latent TGF-β through a pH-dependent mechanism. Here, we wanted to test the hypothesis that ionizing radiation leads to excessive lactate production via expression of the enzyme lactate dehydrogenase-A (LDHA) to promote myofibroblast differentiation. We found that LDHA expression is increased in human and animal lung tissue exposed to ionizing radiation. We demonstrate that ionizing radiation induces LDHA, lactate production, and extracellular acidification in primary human lung fibroblasts in a dose-dependent manner. We also demonstrate that genetic and pharmacologic inhibition of LDHA protects against radiation-induced myofibroblast differentiation. Furthermore, LDHA inhibition protects from radiation-induced activation of TGF-β. We propose a profibrotic feed forward loop, in which radiation induces LDHA expression and lactate production, which can lead to further activation of TGF-β to drive the fibrotic process. These studies support the concept of LDHA as an important therapeutic target in radiation-induced pulmonary fibrosis.

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7

Yacoub, Adly, Anna Miller, Ruben W. Caron, Liang Qiao, David A. Curiel, Paul B. Fisher, Michael P. Hagan, Steven Grant, and Paul Dent. "Radiotherapy-induced signal transduction." Endocrine-Related Cancer 13, Supplement_1 (December 2006): S99—S114. http://dx.doi.org/10.1677/erc.1.01271.

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Exposure of tumor cells to ionizing radiation causes compensatory activation of multiple intracellular survival signaling pathways to maintain viability. In human carcinoma cells, radiation exposure caused an initial rapid inhibition of protein tyrosine phosphatase function and the activation of ERBB receptors and downstream signaling pathways. Radiation-induced activation of extracellular regulated kinase (ERK)1/2 promoted the cleavage and release of paracrine ligands in carcinoma cells which caused re-activation of ERBB family receptors and intracellular signaling pathways. Blocking ERBB receptor phosphorylation or ERK1/2 pathway activity using small-molecule inhibitors of kinases for a short period of time following exposure (3 h) surprisingly protected tumor cells from the toxic effects of ionizing radiation. Prolonged exposure (48–72 h) of tumor cells to inhibition of ERBB receptor/ERK1/2 function enhanced radiosensitivity. In addition to ERBB receptor signaling, expression of activated forms of RAS family members and alterations in p53 mutational status are known to regulate radiosensitivity apparently independent of ERBB receptor function; however, changes in RAS or p53 mutational status, in isogenic HCT116 cells, were also noted to modulate the expression of ERBB receptors and ERBB receptor paracrine ligands. These alterations in receptor and ligand expression correlated with changes in the ability of HCT116 cells to activate ERK1/2 and AKT after irradiation, and to survive radiation exposure. Collectively, our data in multiple human carcinoma cell lines argues that tumor cells are dynamic and rapidly adapt to any single therapeutic challenge, for example, radiation and/or genetic manipulation e.g. loss of activated RAS function, to maintain tumor cell growth and viability.

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8

FURUYA, Masahiro, Tomoji TAKAMASA, Koji OKAMOTO, David T. YASUNAGA, and Susumu UEMATSU. "Corrosion Control Based on Radiation Induced Surface Activation." Journal of The Japan Institute of Marine Engineering 41, no. 2 (2006): 278–84. http://dx.doi.org/10.5988/jime.41.2_278.

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9

XUE, JUN, JI-HUA DONG, GUO-DONG HUANG, XIAO-FEI QU, GANG WU, and XIAO-RONG DONG. "NF-κB signaling modulates radiation-induced microglial activation." Oncology Reports 31, no. 6 (April 23, 2014): 2555–60. http://dx.doi.org/10.3892/or.2014.3144.

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10

HONJO, Yoshio, Masahiro FURUYA, Tomoji TAKAMASA, and Koji OKAMOTO. "Mechanism of Hydrophilicity by Radiation-Induced Surface Activation." Journal of Power and Energy Systems 3, no. 1 (2009): 216–27. http://dx.doi.org/10.1299/jpes.3.216.

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11

Huang, Shanshan, Yongbiao Huang, Wanling Lin, Lei Wang, Yang Yang, Piao Li, Lei Xiao, Yuan Chen, Qian Chu, and Xianglin Yuan. "Sitagliptin Alleviates Radiation-Induced Intestinal Injury by Activating NRF2-Antioxidant Axis, Mitigating NLRP3 Inf--lammasome Activation, and Reversing Gut Microbiota Disorder." Oxidative Medicine and Cellular Longevity 2022 (May 17, 2022): 1–17. http://dx.doi.org/10.1155/2022/2586305.

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Radiation-induced intestinal injury is a common and critical complication of radiotherapy for pelvic or abdominal tumors, with limited therapeutic strategies and effectiveness. Sitagliptin, a dipeptidyl peptidase IV (DPP4) inhibitor, has previously been reported to alleviate total body irradiation- (TBI-) induced damage of hematopoietic system in mice, but its effect on radiation-induced intestinal injury remains unclear. In this study, we confirmed that Sitagliptin could not only protect mice from death and weight loss caused by whole abdominal irradiation (WAI) but also improve the morphological structure of intestine and the regeneration ability of enterocytes. In addition, Sitagliptin significantly inhibited the production of radiation-induced proinflammatory cytokines and reduced the number of apoptotic intestinal epithelial cells and γ-H2AX expression. In vitro, we demonstrated that Sitagliptin protected HIEC-6 cells from ionizing radiation, resulting in increased cell viability and reduced DNA damage. Mechanistically, the radiation protection of Sitagliptin might be related to the upregulation of NRF2 level and the decrease of NLRP3 inflammasome activity. Importantly, Sitagliptin significantly restored radiation-induced changes in bacterial composition. In conclusion, our results suggested that Sitagliptin could reduce WAI-induced intestinal injury in mice, which may provide novel therapeutic strategy for radiation-induced intestinal injury.

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12

Xu, Ping, Wen-Bo Zhang, Xin-Hua Cai, Pei-Yong Qiu, Ming-Hua Hao, and Dan-Dan Lu. "Activating AKT to inhibit JNK by troxerutin antagonizes radiation-induced PTEN activation." European Journal of Pharmacology 795 (January 2017): 66–74. http://dx.doi.org/10.1016/j.ejphar.2016.11.052.

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13

Li, Yongfeng, and Francis A. Cucinotta. "Mathematical Model of ATM Activation and Chromatin Relaxation by Ionizing Radiation." International Journal of Molecular Sciences 21, no. 4 (February 12, 2020): 1214. http://dx.doi.org/10.3390/ijms21041214.

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We propose a comprehensive mathematical model to study the dynamics of ionizing radiation induced Ataxia-telangiectasia mutated (ATM) activation that consists of ATM activation through dual mechanisms: the initiative activation pathway triggered by the DNA damage-induced local chromatin relaxation and the primary activation pathway consisting of a self-activation loop by interplay with chromatin relaxation. The model is expressed as a series of biochemical reactions, governed by a system of differential equations and analyzed by dynamical systems techniques. Radiation induced double strand breaks (DSBs) cause rapid local chromatin relaxation, which is independent of ATM but initiates ATM activation at damage sites. Key to the model description is how chromatin relaxation follows when active ATM phosphorylates KAP-1, which subsequently spreads throughout the chromatin and induces global chromatin relaxation. Additionally, the model describes how oxidative stress activation of ATM triggers a self-activation loop in which PP2A and ATF2 are released so that ATM can undergo autophosphorylation and acetylation for full activation in relaxed chromatin. In contrast, oxidative stress alone can partially activate ATM because phosphorylated ATM remains as a dimer. The model leads to predictions on ATM mediated responses to DSBs, oxidative stress, or both that can be tested by experiments.

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14

Laurie, R. M., M. W. T. Chao, and C. A. Dow. "Radiation induced liver disease: is hereditary haemochromatosis a risk factor?" Journal of Radiotherapy in Practice 3, no. 2 (March 2003): 101–4. http://dx.doi.org/10.1017/s1460396903000086.

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A 71-year-old man with Stage II gastric cancer developed rapid onset radiation induced liver disease after ceasing adjuvant chemotherapy and radiotherapy. Autopsy revealed moderate hepatocellular iron overload. Posthumously, he was found to be a compound heterozygote for hereditary haemochromatosis. Since both radiation and iron overload may induce liver damage through the activation of hepatic stellate cells, it is possible that hepatocellular iron overload may potentiate the effects of irradiation and predispose the patient to radiation induced liver disease.

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15

Dent, Paul, Dean B. Reardon, Jong Sung Park, Geoffrey Bowers, Craig Logsdon, Kristoffer Valerie, and Rupert Schmidt-Ullrich. "Radiation-induced Release of Transforming Growth Factor α Activates the Epidermal Growth Factor Receptor and Mitogen-activated Protein Kinase Pathway in Carcinoma Cells, Leading to Increased Proliferation and Protection from Radiation-induced Cell Death." Molecular Biology of the Cell 10, no. 8 (August 1999): 2493–506. http://dx.doi.org/10.1091/mbc.10.8.2493.

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Exposure of A431 squamous and MDA-MB-231 mammary carcinoma cells to ionizing radiation has been associated with short transient increases in epidermal growth factor receptor (EGFR) tyrosine phosphorylation and activation of the mitogen-activated protein kinase (MAPK) and c-Jun NH2-terminal kinase (JNK) pathways. Irradiation (2 Gy) of A431 and MDA-MB-231 cells caused immediate primary activations (0–10 min) of the EGFR and the MAPK and JNK pathways, which were surprisingly followed by later prolonged secondary activations (90–240 min). Primary and secondary activation of the EGFR was abolished by molecular inhibition of EGFR function. The primary and secondary activation of the MAPK pathway was abolished by molecular inhibition of either EGFR or Ras function. In contrast, molecular inhibition of EGFR function abolished the secondary but not the primary activation of the JNK pathway. Inhibition of tumor necrosis factor α receptor function by use of neutralizing monoclonal antibodies blunted primary activation of the JNK pathway. Addition of a neutralizing monoclonal antibody versus transforming growth factor α (TGFα) had no effect on the primary activation of either the EGFR or the MAPK and JNK pathways after irradiation but abolished the secondary activation of EGFR, MAPK, and JNK. Irradiation of cells increased pro-TGFα cleavage 120–180 min after exposure. In agreement with radiation-induced release of a soluble factor, activation of the EGFR and the MAPK and JNK pathways could be induced in nonirradiated cells by the transfer of media from irradiated cells 120 min after irradiation. The ability of the transferred media to cause MAPK and JNK activation was blocked when media were incubated with a neutralizing antibody to TGFα. Thus radiation causes primary and secondary activation of the EGFR and the MAPK and JNK pathways in autocrine-regulated carcinoma cells. Secondary activation of the EGFR and the MAPK and JNK pathways is dependent on radiation-induced cleavage and autocrine action of TGFα. Neutralization of TGFα function by an anti-TGFα antibody or inhibition of MAPK function by MEK1/2 inhibitors (PD98059 and U0126) radiosensitized A431 and MDA-MB-231 cells after irradiation in apoptosis, 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT), and clonogenic assays. These data demonstrate that disruption of the TGFα–EGFR–MAPK signaling module represents a strategy to decrease carcinoma cell growth and survival after irradiation.

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16

Han, Chuanhui, Victoria Godfrey, Zhida Liu, Yanfei Han, Longchao Liu, Hua Peng, Ralph R. Weichselbaum, Hasan Zaki, and Yang-Xin Fu. "The AIM2 and NLRP3 inflammasomes trigger IL-1–mediated antitumor effects during radiation." Science Immunology 6, no. 59 (May 7, 2021): eabc6998. http://dx.doi.org/10.1126/sciimmunol.abc6998.

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The inflammasome promotes inflammation-associated diseases, including cancer, and contributes to the radiation-induced tissue damage. However, the role of inflammasome in radiation-induced antitumor effects is unclear. We observed that tumors transplanted in Casp1−/− mice were resistant to radiation treatment compared with tumors in wild-type (WT) mice. To map out which molecule in the inflammasome pathway contributed to this resistant, we investigated the antitumor effect of radiation in several inflammasome-deficient mice. Tumors grown in either Aim2−/− or Nlrp3−/− mice remained sensitive to radiation, like WT mice, whereas Aim2−/−Nlrp3−/− mice showed radioresistance. Mechanistically, extracellular vesicles (EVs) and EV-free supernatant derived from irradiated tumors activated both Aim2 and Nlrp3 inflammasomes in macrophages, leading to the production of interleukin-1β (IL-1β). IL-1β treatment helped overcome the radioresistance of tumors growing in Casp1−/− and Aim2−/−Nlrp3−/− mice. IL-1 signaling in dendritic cells (DCs) promoted radiation-induced antitumor immunity by enhancing the cross-priming activity of DCs. Overall, we demonstrated that radiation-induced activation of the AIM2 and NLRP3 inflammasomes coordinate to induce some of the antitumor effects of radiation by triggering IL-1 signaling in DCs, leading to their activation and cross-priming.

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17

Hsu, Fei-Ting, Yu-Chang Liu, Tsu-Te Liu, and Jeng-Jong Hwang. "Curcumin Sensitizes Hepatocellular Carcinoma Cells to Radiation via Suppression of Radiation-Induced NF-κB Activity." BioMed Research International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/363671.

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The effects and possible underlying mechanism of curcumin combined with radiation in human hepatocellular carcinoma (HCC) cellsin vitrowere evaluated. The effects of curcumin, radiation, and combination of both on cell viability, apoptosis, NF-κB activation, and expressions of NF-κB downstream effector proteins were investigated with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), NF-κB reporter gene, mitochondrial membrane potential (MMP), electrophoretic mobility shift (EMSA), and Western blot assays in Huh7-NF-κB-luc2, Hep3B, and HepG2 cells. Effect of I kappa B alpha mutant (IκBαM) vector, a specific inhibitor of NF-κB activation, on radiation-induced loss of MMP was also evaluated. Results show that curcumin not only significantly enhances radiation-induced cytotoxicity and depletion of MMP but inhibits radiation-induced NF-κB activity and expressions of NF-κB downstream proteins in HCC cells. IκBαM vector also shows similar effects. In conclusion, we suggest that curcumin augments anticancer effects of radiation via the suppression of NF-κB activation.

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18

Storozynsky, Quinn, and Mary M. Hitt. "The Impact of Radiation-Induced DNA Damage on cGAS-STING-Mediated Immune Responses to Cancer." International Journal of Molecular Sciences 21, no. 22 (November 23, 2020): 8877. http://dx.doi.org/10.3390/ijms21228877.

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Radiotherapy is a major modality used to combat a wide range of cancers. Classical radiobiology principles categorize ionizing radiation (IR) as a direct cytocidal therapeutic agent against cancer; however, there is an emerging appreciation for additional antitumor immune responses generated by this modality. A more nuanced understanding of the immunological pathways induced by radiation could inform optimal therapeutic combinations to harness radiation-induced antitumor immunity and improve treatment outcomes of cancers refractory to current radiotherapy regimens. Here, we summarize how radiation-induced DNA damage leads to the activation of a cytosolic DNA sensing pathway mediated by cyclic GMP-AMP (cGAMP) synthase (cGAS) and stimulator of interferon genes (STING). The activation of cGAS–STING initiates innate immune signaling that facilitates adaptive immune responses to destroy cancer. In this way, cGAS–STING signaling bridges the DNA damaging capacity of IR with the activation of CD8+ cytotoxic T cell-mediated destruction of cancer—highlighting a molecular pathway radiotherapy can exploit to induce antitumor immune responses. In the context of radiotherapy, we further report on factors that enhance or inhibit cGAS–STING signaling, deleterious effects associated with cGAS–STING activation, and promising therapeutic candidates being investigated in combination with IR to bolster immune activation through engaging STING-signaling. A clearer understanding of how IR activates cGAS–STING signaling will inform immune-based treatment strategies to maximize the antitumor efficacy of radiotherapy, improving therapeutic outcomes.

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19

Kim, Lee, Seo, Kim, Kim, Kim, Kang, Seong, Youn, and Youn. "Cellular Stress Responses in Radiotherapy." Cells 8, no. 9 (September 18, 2019): 1105. http://dx.doi.org/10.3390/cells8091105.

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Radiotherapy is one of the major cancer treatment strategies. Exposure to penetrating radiation causes cellular stress, directly or indirectly, due to the generation of reactive oxygen species, DNA damage, and subcellular organelle damage and autophagy. These radiation-induced damage responses cooperatively contribute to cancer cell death, but paradoxically, radiotherapy also causes the activation of damage-repair and survival signaling to alleviate radiation-induced cytotoxic effects in a small percentage of cancer cells, and these activations are responsible for tumor radio-resistance. The present study describes the molecular mechanisms responsible for radiation-induced cellular stress response and radioresistance, and the therapeutic approaches used to overcome radioresistance.

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20

Wang, Xiaofei, Clare H. McGowan, Ming Zhao, Liusheng He, Jocelyn S. Downey, Colleen Fearns, Yibin Wang, Shi Huang, and Jiahuai Han. "Involvement of the MKK6-p38γ Cascade in γ-Radiation-Induced Cell Cycle Arrest." Molecular and Cellular Biology 20, no. 13 (July 1, 2000): 4543–52. http://dx.doi.org/10.1128/mcb.20.13.4543-4552.2000.

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ABSTRACT The p38 group of kinases belongs to the mitogen-activated protein (MAP) kinase superfamily with structural and functional characteristics distinguishable from those of the ERK, JNK (SAPK), and BMK (ERK5) kinases. Although there is a high degree of similarity among members of the p38 group in terms of structure and activation, each member appears to have a unique function. Here we show that activation of p38γ (also known as ERK6 or SAPK3), but not the other p38 isoforms, is required for γ-irradiation-induced G2arrest. Activation of the MKK6-p38γ cascade is sufficient to induce G2 arrest in cells, and expression of dominant negative alleles of MKK6 or p38γ allows cells to escape the DNA damage-induce G2 delay. Activation of p38γ is dependent on ATM and leads to activation of Cds1 (also known as Chk2). These data suggest a model in which activation of ATM by γ irradiation leads to the activation of MKK6, p38γ, and Cds1 and that activation of both MKK6 and p38γ is essential for the proper regulation of the G2checkpoint in mammalian cells.

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21

Kariyazaki, Makoto, Hiroaki Abe, Akio Sayano, Fumihisa Kano, Yoshio Katano, Takashi Onitsuka, and Naoto Sekimura. "Ray Type Dependence of Radiation Induced Surface Activation Phenomenon." Journal of the Japan Institute of Metals 71, no. 4 (2007): 423–26. http://dx.doi.org/10.2320/jinstmet.71.423.

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22

OKAMOTO, Koji, Yasuyuki IMAI, Masahiro FURUYA, and Tomoji TAKAMASA. "Boiling Enhancement and Visualization on Radiation Induced Surface Activation." Reference Collection of Annual Meeting 2004.8 (2004): 153–54. http://dx.doi.org/10.1299/jsmemecjsm.2004.8.0_153.

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23

Kr�mer, M., S. Stein, S. Mai, E. Kunz, H. K�nig, H. Loferer, H. H. Grunicke, H. Ponta, P. Herrlich, and H. J. Rahmsdorf. "Radiation-induced activation of transcription factors in mammalian cells." Radiation and Environmental Biophysics 29, no. 4 (December 1990): 303–13. http://dx.doi.org/10.1007/bf01210410.

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24

Suzuki, Keiji, Seiji Kodama, and Masami Watanabe. "Radiation-induced genomic instability and delayed activation of p53." International Congress Series 1236 (July 2002): 309–11. http://dx.doi.org/10.1016/s0531-5131(01)00880-9.

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25

Wang, Shizong, and Jianlong Wang. "Degradation of carbamazepine by radiation-induced activation of peroxymonosulfate." Chemical Engineering Journal 336 (March 2018): 595–601. http://dx.doi.org/10.1016/j.cej.2017.12.068.

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26

Takamasa, T., T. Hazuku, K. Okamoto, K. Mishima, and M. Furuya. "Radiation induced surface activation on Leidenfrost and quenching phenomena." Experimental Thermal and Fluid Science 29, no. 3 (March 2005): 267–74. http://dx.doi.org/10.1016/j.expthermflusci.2004.05.014.

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27

JAFFRÉZOU, JEAN-PIERRE, ALAIN P. BRUNO, ANDRÉ MOISAND, THIERRY LEVADE, and GUY LAURENT. "Activation of a nuclear sphingomyelinase in radiation induced apoptosis." FASEB Journal 15, no. 1 (January 2001): 123–33. http://dx.doi.org/10.1096/fj.00-0305com.

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28

Guo, Guozheng, Tieli Wang, Qian Gao, Daniel Tamae, Patty Wong, Tammy Chen, Wei-Chung Chen, John E. Shively, Jeffery YC Wong, and Jian Jian Li. "Expression of ErbB2 enhances radiation-induced NF-κB activation." Oncogene 23, no. 2 (January 2004): 535–45. http://dx.doi.org/10.1038/sj.onc.1207149.

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Hu, Liqiong, Hao Chen, Xingliang Zhang, Zhencheng Feng, Haifeng Zhang, and Qingqi Meng. "Rosiglitazone ameliorates radiation-induced intestinal inflammation in rats by inhibiting NLRP3 inflammasome and TNF-α production." Journal of Radiation Research 61, no. 6 (September 2, 2020): 842–50. http://dx.doi.org/10.1093/jrr/rraa062.

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Abstract Radiation-induced acute intestinal injury is a common and serious occurrence following abdominal and pelvic irradiation. The Nod-like receptor protein 3 (NLRP3)-dependant inflammasome and inflammation activation is crucial in this process. In a pre-experimental design of radiation-induced intestinal injury, we found that rosiglitazone inhibited caspase-1 which is a key marker of inflammasome activation. The purpose of the present study was to clarify the inhibitory effect of rosiglitazone on the NLRP3 inflammasome both in vivo and in vitro. Radiation-induced intestinal injury after rosiglitazone treatment, and the expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), caspase-1 and NLRP3 in a radiation-induced intestinal injury model in a rat and macrophages were observed. We found that rosiglitazone ameliorated radiation-induced intestinal injury in rats by suppressing the expression of caspase-1, NLRP3, IL-1β and TNF-α. Treatment with rosiglitazone in vitro reduced the expression of NLRP3, and the NLRP3 activator monosodium urate (MSU) reversed the inhibition of IL-1β and TNF-α by rosiglitazone in macrophages. MSU reversed the protective effect of rosiglitazone on radiation-induced intestinal injury in rats by reversing the rosiglitazone-induced inhibition of IL-1β and TNF-α. Taken together, these findings indicate that the peroxisome proliferator-activated receptor gamma (PPARγ) agonist, rosiglitazone, ameliorates radiation-induced intestine inflammation in rats via inhibiting the induction of the NLRP3-dependent inflammasome in macrophages.

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Zhao, Yi, Jae-Hyeok Kang, Ki-Chun Yoo, Seok-Gu Kang, Hae-June Lee, and Su-Jae Lee. "K-RAS Acts as a Critical Regulator of CD44 to Promote the Invasiveness and Stemness of GBM in Response to Ionizing Radiation." International Journal of Molecular Sciences 22, no. 20 (October 10, 2021): 10923. http://dx.doi.org/10.3390/ijms222010923.

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Radiation therapy is a current standard-of-care treatment and is used widely for GBM patients. However, radiation therapy still remains a significant barrier to getting a successful outcome due to the therapeutic resistance and tumor recurrence. Understanding the underlying mechanisms of this resistance and recurrence would provide an efficient approach for improving the therapy for GBM treatment. Here, we identified a regulatory mechanism of CD44 which induces infiltration and mesenchymal shift of GBM. Ionizing radiation (IR)-induced K-RAS/ERK signaling activation elevates CD44 expression through downregulation of miR-202 and miR-185 expression. High expression of CD44 promotes SRC activation to induce cancer stemness and EMT features of GBM cells. In this study, we demonstrate that the K-RAS/ERK/CD44 axis is a key mechanism in regulating mesenchymal shift of GBM cells after irradiation. These findings suggest that blocking the K-RAS activation or CD44 expression could provide an efficient way for GBM treatment.

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31

Xu, Meiling, Qiuhong Fan, Junjun Zhang, Yanfang Chen, Ruizhe Xu, Liesong Chen, Peifeng Zhao, and Ye Tian. "NFAT3/c4-mediated excitotoxicity in hippocampal apoptosis during radiation-induced brain injury." Journal of Radiation Research 58, no. 6 (August 10, 2017): 827–33. http://dx.doi.org/10.1093/jrr/rrx041.

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Abstract Whole brain irradiation (WBI) has become an indispensible tool in the treatment of head and neck cancer, and it has greatly improved patient survival rate and total survival time. In addition, prophylactic cranial irradiation (PCI) has dramatically decreased the incidence of brain metastatic carcinoma. However, WBI may induce temporary functional deficits or even progressive, irreversible cognitive dysfunction that compromises the quality of life for survivors. Unfortunately, the exact molecular mechanisms for cognitive damage remain elusive, and no treatment or preventative measures are available for use in the clinic. In the present study, the nuclear factor of activated T cells isoform 4 (NFAT3/c4) was found to play a vital role in excitotoxic hippocampus cell apoptosis induced by radiation. Sprague–Dawley (SD) rats received 20 Gy WBI, after which we detected NFAT3/c4-mediated excitotoxicity. We found that radiation caused hippocampus excitotoxicity, resulting from overactivation of the N-methyl-D-aspartate receptor (NMDAR) and always accompanied by subsequent elevation of the intracellular calcium level and activation of calcineurin (CaN). P-NFAT3/c4 was the principal downstream target of CaN, including regulation of its nuclear translocation as well as transcriptional activities. Radiation recruited NMDAR/NFAT3/c4 activation and subsequent Bax induction in hippocampus cells. Once treated with the NFAT3/c4 inhibitor 11R-VIVIT peptide pre-irradiation, hippocampal proliferation and neuron survival (dentate gyrus cells in particular) were protected from radiation-induced injury, resulting in inhibition of the apoptosis marker Bax. Our principal aim was to illuminate the role of NFAT3/c4-mediated excitotoxicity in hippocampal apoptosis during radiation-induced brain injury. This study is the first time that radiation-induced activation of NFAT3/c4 has been recorded, and our results suggest that NFAT3/c4 may be a novel target for prevention and treatment of radiation-induced brain injury.

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Kim, Kyoung M., Yin Zhang, Bo-Yeon Kim, Sook J. Jeong, Sung A. Lee, Gun-Do Kim, Anatoly Dritschilo, and Mira Jung. "The p65 subunit of nuclear factor-κB is a molecular target for radiation sensitization of human squamous carcinoma cells." Molecular Cancer Therapeutics 3, no. 6 (June 1, 2004): 693–98. http://dx.doi.org/10.1158/1535-7163.693.3.6.

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Abstract The transcription factor nuclear factor-κB (NF-κB) is activated in response to various stimuli including ionizing radiation. Disruption of NF-κB activation by mutant forms of the NF-κB inhibitor IκB-α or by proteasome inhibitors enhances both sensitivity to radiation and radiation-induced apoptosis. Human squamous carcinoma SCC-35 cells stably expressing a fragment (residues 1 to 84) of human p65 have been shown to exhibit down-regulation of both endogenous p65 mRNA and its protein. The mutant protein also inhibited radiation-induced NF-κB activation by preventing the proteolysis of IκB-α. This resulted in enhancement of cellular radiosensitivity and radiation-induced apoptosis. The NH2-terminal region of p65 is thus a potential molecular target for disruption of NF-κB activation and sensitization of tumors to radiotherapy.

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33

Schieven, GL, JM Kirihara, DE Myers, JA Ledbetter, and FM Uckun. "Reactive oxygen intermediates activate NF-kappa B in a tyrosine kinase- dependent mechanism and in combination with vanadate activate the p56lck and p59fyn tyrosine kinases in human lymphocytes." Blood 82, no. 4 (August 15, 1993): 1212–20. http://dx.doi.org/10.1182/blood.v82.4.1212.1212.

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Abstract We have previously observed that ionizing radiation induces tyrosine phosphorylation in human B-lymphocyte precursors by stimulation of unidentified tyrosine kinases and this phosphorylation is substantially augmented by vanadate. Ionizing radiation generates reactive oxygen intermediates (ROI). Because H2O2 is a potent ROI generator that readily crosses the plasma membrane, we used H2O2 to examine the effects of ROI on signal transduction. We now provide evidence that the tyrosine kinase inhibitor herbimycin A and the free radical scavenger N- acetyl-cysteine inhibit both radiation-induced and H2O2-induced activation of NF-kappa B, indicating that activation triggered by ROI is dependent on tyrosine kinase activity. H2O2 was found to stimulate Ins-1,4,5-P3 production in a tyrosine kinase-dependent manner and to induce calcium signals that were greatly augmented by vanadate. The synergistic induction of tyrosine phosphorylation by H2O2 plus vanadate included physiologically relevant proteins such as PLC gamma 1. Although treatment of cells with H2O2 alone did not affect the activity of src family kinases, treatment with H2O2 plus vanadate led to activation of the p56lck and p59fyn tyrosine kinases. The combined inhibition of phosphatases and activation of kinases provides a potent mechanism for the synergistic effects of H2O2 plus vanadate. Induction of tyrosine phosphorylation by ROI may thus lead to many of the pleiotropic effects of ROI in lymphoid cells, including downstream activation of PLC gamma 1 and NF-kappa B.

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34

Schieven, GL, JM Kirihara, DE Myers, JA Ledbetter, and FM Uckun. "Reactive oxygen intermediates activate NF-kappa B in a tyrosine kinase- dependent mechanism and in combination with vanadate activate the p56lck and p59fyn tyrosine kinases in human lymphocytes." Blood 82, no. 4 (August 15, 1993): 1212–20. http://dx.doi.org/10.1182/blood.v82.4.1212.bloodjournal8241212.

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We have previously observed that ionizing radiation induces tyrosine phosphorylation in human B-lymphocyte precursors by stimulation of unidentified tyrosine kinases and this phosphorylation is substantially augmented by vanadate. Ionizing radiation generates reactive oxygen intermediates (ROI). Because H2O2 is a potent ROI generator that readily crosses the plasma membrane, we used H2O2 to examine the effects of ROI on signal transduction. We now provide evidence that the tyrosine kinase inhibitor herbimycin A and the free radical scavenger N- acetyl-cysteine inhibit both radiation-induced and H2O2-induced activation of NF-kappa B, indicating that activation triggered by ROI is dependent on tyrosine kinase activity. H2O2 was found to stimulate Ins-1,4,5-P3 production in a tyrosine kinase-dependent manner and to induce calcium signals that were greatly augmented by vanadate. The synergistic induction of tyrosine phosphorylation by H2O2 plus vanadate included physiologically relevant proteins such as PLC gamma 1. Although treatment of cells with H2O2 alone did not affect the activity of src family kinases, treatment with H2O2 plus vanadate led to activation of the p56lck and p59fyn tyrosine kinases. The combined inhibition of phosphatases and activation of kinases provides a potent mechanism for the synergistic effects of H2O2 plus vanadate. Induction of tyrosine phosphorylation by ROI may thus lead to many of the pleiotropic effects of ROI in lymphoid cells, including downstream activation of PLC gamma 1 and NF-kappa B.

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35

Jones, Dylan T., Kanagasabai Ganeshaguru, Robert J. Anderson, Trevor R. Jackson, K. Richard Bruckdorfer, Sylvia Y. Low, Lars Palmqvist, et al. "Albumin activates the AKT signaling pathway and protects B-chronic lymphocytic leukemia cells from chlorambucil- and radiation-induced apoptosis." Blood 101, no. 8 (April 15, 2003): 3174–80. http://dx.doi.org/10.1182/blood-2002-07-2143.

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Abstract Activation of the phosphatidylinositol 3- kinase/AKT pathway antagonizes apoptosis in diverse cellular systems. We previously showed that human plasma activated AKT and potently blocked the ability of chlorambucil or gamma radiation to induce apoptosis of B-chronic lymphocytic leukemia (CLL) cells. Here we report experiments that identify albumin as the major component of plasma that blocks CLL cell killing by chlorambucil or radiation. Intact plasma depleted of albumin by chromatography on Cibacron blue–Sepharose or plasma from a subject with analbuminemia failed either to activate AKT or to protect CLL cells from chlorambucil-induced apoptosis. Both functions were restored by re-addition of albumin. The protective action of albumin as well as AKT activation was compromised by the binding of lipids. Fluorescence-activated cell sorter (FACScan) analysis demonstrated the uptake of fluoresceinated albumin by CLL cells. Accumulation of albumin in intracellular vesicles was also shown by confocal microscopy. Indirect inhibition of AKT activation by the phosphatidylinositol 3-kinase inhibitor LY294002 reversed the blockade of chlorambucil-induced killing by plasma albumin. The data suggest that activation of AKT consequent to binding of albumin by CLL cells blocks chlorambucil- and radiation-induced apoptosis. Strategies designed to block albumin-induced antiapoptotic signaling may, therefore, be of value in enhancing cytotoxic drug action on CLL cells.

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36

Williams, Scott, Simon P. Keam, Heloise Halse, Thu Nguyen, Catherine Mitchell, Franco Caramia, David Byrne, et al. "Predicting radiation-induced immune trafficking and activation in localized prostate cancer." Journal of Clinical Oncology 38, no. 6_suppl (February 20, 2020): 340. http://dx.doi.org/10.1200/jco.2020.38.6_suppl.340.

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340 Background: Prostate cancer is frequently cured with high-dose rate brachytherapy as a front-line treatment. However, a significant number unfortunately develop intrinsic resistance. Although considered to be an immune-excluded tissue, immune responses are implicated in driving tumour-eradication in prostate cancer. This has not been proven, and yet is used as the rationale for numerous clinical trials combining radiation and immunotherapies. We hypothesise that there is a predictable but differential relationship between radiation and the immune responses in prostate cancer that could be used to fulfil a clinical need - identifying patients that would benefit from immune intervention in conjunction with radiation. Methods: We present here the results of comprehensive immunological profiling of a cohort of world-unique pre- and post-radiation tissues from 24 patients (RadBank cohort). These were assessed using pathological classification, tissue segmentation (cancer/surrounding stroma), multiplex IHC, gene expression profiling, T-cell receptor sequencing, and spatial computational analysis. Results: Our data resolved three classes of prostate cancer tissue based on immune infiltrate level, immune-activation and -checkpoint gene signatures, spatial clustering and T cell clone sequencing: We have begun to resolve clear patient and clinical classifiers based on immune responses to radiation, and identified patients groups likely to benefit from immune therapy alongside radiation. Conclusions: Importantly, these classifications are associated with baseline gene expression profiles that may be used for pre-clinical stratification and more sophisticated treatment paradigms.

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Pang, Qingsong, Ningbo Liu, Fengting Liu, Samir Agrawal, and Ping Wang. "Drp1 Activation Overcomes Diffuse Large B-Cell Lymphoma Cells Radioresistance." Blood 120, no. 21 (November 16, 2012): 5121. http://dx.doi.org/10.1182/blood.v120.21.5121.5121.

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Abstract Abstract 5121 Mitochondria undergo fusion and fission in response to physiological or pathological changes. Mitochondrial fusion is regulated by mitofusin-1 and 2 (MFN-1/2) and optic atrophy 1(OPA-1), whereas, mitochondrial fission (or fragmentation) is controlled by a Dynamin-related protein 1 (Drp1). Drp1 activation is triggered by dephosphorylation of Drp1 on its serine 637 site. Recent studies demonstrated that Drp1 activation plays an important role in mitochondrial fragmentation-induced cell death. The phosphorylation of Drp1 by serine kinase inhibits its GTPase activity and prevents mitochondrial fragmentation. Inhibition of Drp1 activation or loss of Drp1 function leads to slow down apoptosis and necrosis. Recent reports showed that patients who received consolidative radiotherapy (RT) combine R-CHOP had significant better 5-year event-free and overall survival rates than patients with diffuse large B-cell lymphoma who did not receive RT combination therapy. Although RT combination therapy significant increased survival of DLBCL, the mechanisms of RT induced cell death are reminded unclear. In this study, we investigated the roles of Drp1 activation in the sensitivity of DLBCL cells to radiotherapy. Radiation causes damage in both nuclear and mitochondrial DNAs and generation of reactive oxygen species (ROS) followed by caspase activation. In the radio-resistant DLBCL cells, radiation induced activation of Drp1, and led to mitochondrial fragmentation, caspase-3 activation and cell death. However, the sensitive DLBCL cells underwent cytochrome c release, caspase-3 activation and PARP cleavage but not the activation of Drip1. To confirm the role of Drp1 activation in radiation-induced cell death on radio-resistant cells, Drp1 was dephosphorylated by a serine kinase inhibitor STS. Co-treatment of radio-resistant DLBCL cells with STS and radiation greatly enhanced mitochondrial fragmentation and significantly increased the sensitivity of radio-resistant DLBCL cells to radiation-induced caspase-3 activation, PARP cleavage and apoptotic cell death. However, co-treatment with STS did not further increase the sensitivity of radio-sensitive cells to caspsase-3 activation and cell death. Our data indicate that radiation-induced cell death in radio-resistant DLBCL cells is regulated by Drp1. We therefore propose that Drp1 could be a potential target for overcoming radio-resistance. Disclosures: No relevant conflicts of interest to declare.

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38

Uddin, M. S., M. Baba, M. Hagiwara, F. Tarkanyi, F. Ditroi, S. Takacs, and A. Hermanne. "Experimental studies of the deuteron-induced activation cross-sections on natAg." Applied Radiation and Isotopes 64, no. 9 (September 2006): 1013–19. http://dx.doi.org/10.1016/j.apradiso.2006.04.001.

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39

Piao, Mei Jing, Kyoung Ah Kang, and Jin Won Hyun. "Protective effect of dieckol on γ-ray radiation-induced V79-4 lung fibroblast cell damage involved in modulation of reactive oxygen species." Journal of Medicine and Life Science 6, no. 5 (December 1, 2009): 368–72. http://dx.doi.org/10.22730/jmls.2009.6.5.368.

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lonizing radiation can induce oxidative stress through generation of reactive oxygen species (ROS) resulting in cell damage and cell death. We have investigated the radioprotective effect of dieckol, which was isolated from Ecklonia cava, against oxidative stress induced cell damage in Chinese hamster lung fibroblast (V79-4) cells. Dieckol was found to reduce the intracellular ROS generated by γ-ray radiation. Moreover, dieckol also protected the cell viability damaged by the radiation through inhibition of apoptosis. Irradiated cells with dieckol treatment reduced. the expression of phospho histone H2A.X (a marker for DNA strand breakage) and the activation of caspase 9, which were induced by radiation. These results suggest that dieckol protected γ-ray radiation induced apoptosis of V79-4 lung fibroblast cells by inhibiting ROS generation.

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40

Zhang, Tian, Lei Shi, Yan Li, Wei Mu, HaoMeng Zhang, Yang Li, XiaoYan Wang, WeiHe Zhao, YuHong Qi, and Linna Liu. "Polysaccharides extracted from Rheum tanguticum ameliorate radiation-induced enteritis via activation of Nrf2/HO-1." Journal of Radiation Research 62, no. 1 (November 3, 2020): 46–57. http://dx.doi.org/10.1093/jrr/rraa093.

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ABSTRACT Radiation-induced enteritis is a major side effect in cancer patients undergoing abdominopelvic radiotherapy. The Nrf2/HO-1 pathway is a critical endogenous antioxidant stress pathway, but its precise role in radiation-induced enteritis remains to be clarified. Polysaccharides extracted from Rheum tanguticum (RTP) can protect the intestinal cells from radiation-induced damage, but the underlying mechanism is unknown. SD rats and IEC-6 cells were exposed to 12 or 10 Gy X-ray radiation. Rat survival, and histopathological and immunohistochemical profiles were analyzed at different time points. Indicators of oxidative stress and inflammatory response were also assessed. Cell viability, apoptosis and Nrf2/HO-1 expression were evaluated at multiple time points. Significant changes were observed in the physiological and biochemical indexes of rats after radiation, accompanied by significant oxidative stress response. The mRNA and protein expression of Nrf2 peaked at 12 h after irradiation, and HO-1 expression peaked at 48 h after irradiation. RTP administration reduced radiation-induced intestinal damage, upregulated Nrf2/HO-1, improved physiological indexes, significantly decreased apoptosis and inflammatory factors, and upregulated HO-1, particularly at 48 h after irradiation. In conclusion, Nrf2 is activated in the early stage of radiation-induced intestinal injury and plays a protective role. RTP significantly ameliorates radiation-induced intestinal injury via the regulation of Nrf2 and its downstream protein HO-1.

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41

Dong, Guang-Zhi, Eun-Taex Oh, Hyemi Lee, Moon-Taek Park, Chang Won Song, and Heon Joo Park. "β-Lapachone suppresses radiation-induced activation of nuclear factor-κB." Experimental and Molecular Medicine 42, no. 5 (2010): 327. http://dx.doi.org/10.3858/emm.2010.42.5.034.

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42

Li, Hui-Fang, Jung-Sik Kim, and Todd Waldman. "Radiation-induced Akt activation modulates radioresistance in human glioblastoma cells." Radiation Oncology 4, no. 1 (2009): 43. http://dx.doi.org/10.1186/1748-717x-4-43.

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43

Waterhouse, Nigel J., Debra M. Finucane, Douglas R. Green, John S. Elce, Sharad Kumar, Emad S. Alnemri, Gerald Litwack, KumKum Khanna, Martin F. Lavin, and Dianne J. Watters. "Calpain activation is upstream of caspases in radiation-induced apoptosis." Cell Death & Differentiation 5, no. 12 (December 1998): 1051–61. http://dx.doi.org/10.1038/sj.cdd.4400425.

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44

TOMOZAWA, Hidemasa, Tomoji TAKAMASA, Hiroyuki DATE, Norio TSUJIMURA, and Koji OKAMOTO. "Electric Conduction and Radioactive Measurement by Radiation Induced Surface Activation." Reference Collection of Annual Meeting 2004.8 (2004): 157–58. http://dx.doi.org/10.1299/jsmemecjsm.2004.8.0_157.

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45

Dent, Paul, Adly Yacoub, Joseph Contessa, Ruben Caron, George Amorino, Kristoffer Valerie, Michael P. Hagan, Steven Grant, and Rupert Schmidt-Ullrich. "Stress and Radiation-Induced Activation of Multiple Intracellular Signaling Pathways1." Radiation Research 159, no. 3 (March 2003): 283–300. http://dx.doi.org/10.1667/0033-7587(2003)159[0283:sariao]2.0.co;2.

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46

Raju, G. J. Gumin, P. J. Tofilon, U. "Radiation-induced transcription factor activation in the rat cerebral cortex." International Journal of Radiation Biology 76, no. 8 (January 2000): 1045–53. http://dx.doi.org/10.1080/09553000050111514.

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47

Glover, D., J. B. Little, M. F. Lavin, and N. Gueven. "Low dose ionizing radiation‐induced activation of connexin 43 expression." International Journal of Radiation Biology 79, no. 12 (December 2003): 955–64. http://dx.doi.org/10.1080/09553000310001632895.

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48

Hagan, Michael P., Adly Yacoub, and Paul Dent. "Radiation-induced PARP activation is enhanced through EGFR-ERK signaling." Journal of Cellular Biochemistry 101, no. 6 (2007): 1384–93. http://dx.doi.org/10.1002/jcb.21253.

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49

Zhivotovsky, B., P. Nicotera, G. Bellomo, K. Hanson, and S. Orrenius. "Ca2+ and Endonuclease Activation in Radiation-Induced Lymphoid Cell Death." Experimental Cell Research 207, no. 1 (July 1993): 163–70. http://dx.doi.org/10.1006/excr.1993.1176.

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50

Brown, Charles O., Kelley Salem, Brett A. Wagner, Soumen Bera, Neeraj Singh, Ajit Tiwari, Amit Choudhury, Garry R. Buettner, and Apollina Goel. "Interleukin-6 counteracts therapy-induced cellular oxidative stress in multiple myeloma by up-regulating manganese superoxide dismutase." Biochemical Journal 444, no. 3 (May 29, 2012): 515–27. http://dx.doi.org/10.1042/bj20112019.

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IL (interleukin)-6, an established growth factor for multiple myeloma cells, induces myeloma therapy resistance, but the resistance mechanisms remain unclear. The present study determines the role of IL-6 in re-establishing intracellular redox homoeostasis in the context of myeloma therapy. IL-6 treatment increased myeloma cell resistance to agents that induce oxidative stress, including IR (ionizing radiation) and Dex (dexamethasone). Relative to IR alone, myeloma cells treated with IL-6 plus IR demonstrated reduced annexin/propidium iodide staining, caspase 3 activation, PARP [poly(ADP-ribose) polymerase] cleavage and mitochondrial membrane depolarization with increased clonogenic survival. IL-6 combined with IR or Dex increased early intracellular pro-oxidant levels that were causally related to activation of NF-κB (nuclear factor κB) as determined by the ability of N-acetylcysteine to suppress both pro-oxidant levels and NF-κB activation. In myeloma cells, upon combination with hydrogen peroxide treatment, relative to TNF (tumour necrosis factor)-α, IL-6 induced an early perturbation in reduced glutathione level and increased NF-κB-dependent MnSOD (manganese superoxide dismutase) expression. Furthermore, knockdown of MnSOD suppressed the IL-6-induced myeloma cell resistance to radiation. MitoSOX Red staining showed that IL-6 treatment attenuated late mitochondrial oxidant production in irradiated myeloma cells. The present study provides evidence that increases in MnSOD expression mediate IL-6-induced resistance to Dex and radiation in myeloma cells. The results of the present study indicate that inhibition of antioxidant pathways could enhance myeloma cell responses to radiotherapy and/or chemotherapy.

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