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  1. AU="Konishi, Teruaki"
  2. AU="Jiang, Haiyue"
  3. AU="Kuznetsov, N S"
  4. AU=Rimmer Abi AU=Rimmer Abi
  5. AU="Zhou, Qinyao"
  6. AU="Taniguchi, Ryou"
  7. AU="Krauss, Thomas F"
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  32. AU="Prettner, Klaus"
  33. AU="Ambrožová, I."
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  37. AU="Spracklen, D."
  38. AU="Lobo, Brian C"
  39. AU=Zhuang Jianjian AU=Zhuang Jianjian
  40. AU=Pathanki Adithya M
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  55. AU="Ramamurthy, Santosh"
  56. AU="Xueying Huang"
  57. AU="Cromwell, Howard C"
  58. AU="Spence, John C H"
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  1. Artikel ; Online: Stimulation of Nuclear Factor (Erythroid-Derived 2)-like 2 Signaling by Nucleus Targeted Irradiation with Proton Microbeam

    Wang, Jun / Oikawa, Masakazu / Konishi, Teruaki

    Biology (Basel). 2023 Mar. 09, v. 12, no. 3

    2023  

    Abstract: Nuclear factor (erythroid-derived 2)-like 2 (NRF2), well-known as a master antioxidative response regulator in mammalian cells, is considered as a potential target for radiation protection and cancer therapy sensitization. We examined the response of ... ...

    Abstract Nuclear factor (erythroid-derived 2)-like 2 (NRF2), well-known as a master antioxidative response regulator in mammalian cells, is considered as a potential target for radiation protection and cancer therapy sensitization. We examined the response of NRF2 signaling in normal human lung fibroblast WI-38 cells to nucleus targeted irradiation by 3.4 MeV proton microbeam. Nucleus targeted irradiation stimulated the nucleus accumulation of NRF2 and the expression of its target gene, heme oxygenase 1 (HO-1). The nucleus accumulation of NRF2 increased from 3 h to 12 h post 500 proton irradiation. In the 500 protons range, higher number of protons resulted in increased NRF2 nucleus accumulation. Activating NRF2 with tert-butylhydroquinone reduced DNA double-strand break (DSB) formation in nucleus targeted irradiation by 15%. Moreover, ATM phosphorylation was found in nucleus targeted irradiation. Inhibiting ATM with ku55933 prevented NRF2 nucleus accumulation. Furthermore, nucleus targeted irradiation activated ERK 1/2, and ROS-ERK 1/2 signaling regulated NRF2 nucleus accumulation. Taken together, NRF2 signaling was activated by nucleus targeted irradiation and mitigated DNA DSB. The discovery of ATM and ERK 1/2 as upstream regulators of NRF2 signaling in nucleus targeted cells revealed new information regarding radiation protection.
    Schlagwörter DNA ; cancer therapy ; fibroblasts ; genes ; heme oxygenase (biliverdin-producing) ; humans ; hydroquinone ; irradiation ; lungs ; phosphorylation
    Sprache Englisch
    Erscheinungsverlauf 2023-0309
    Erscheinungsort Multidisciplinary Digital Publishing Institute
    Dokumenttyp Artikel ; Online
    ZDB-ID 2661517-4
    ISSN 2079-7737
    ISSN 2079-7737
    DOI 10.3390/biology12030419
    Datenquelle NAL Katalog (AGRICOLA)

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  2. Artikel: Stimulation of Nuclear Factor (Erythroid-Derived 2)-like 2 Signaling by Nucleus Targeted Irradiation with Proton Microbeam.

    Wang, Jun / Oikawa, Masakazu / Konishi, Teruaki

    Biology

    2023  Band 12, Heft 3

    Abstract: Nuclear factor (erythroid-derived 2)-like 2 (NRF2), well-known as a master antioxidative response regulator in mammalian cells, is considered as a potential target for radiation protection and cancer therapy sensitization. We examined the response of ... ...

    Abstract Nuclear factor (erythroid-derived 2)-like 2 (NRF2), well-known as a master antioxidative response regulator in mammalian cells, is considered as a potential target for radiation protection and cancer therapy sensitization. We examined the response of NRF2 signaling in normal human lung fibroblast WI-38 cells to nucleus targeted irradiation by 3.4 MeV proton microbeam. Nucleus targeted irradiation stimulated the nucleus accumulation of NRF2 and the expression of its target gene, heme oxygenase 1 (HO-1). The nucleus accumulation of NRF2 increased from 3 h to 12 h post 500 proton irradiation. In the 500 protons range, higher number of protons resulted in increased NRF2 nucleus accumulation. Activating NRF2 with
    Sprache Englisch
    Erscheinungsdatum 2023-03-09
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2661517-4
    ISSN 2079-7737
    ISSN 2079-7737
    DOI 10.3390/biology12030419
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  3. Artikel: The COX-2/PGE2 Response Pathway Upregulates Radioresistance in A549 Human Lung Cancer Cells through Radiation-Induced Bystander Signaling.

    Kobayashi, Alisa / Hiroyama, Yota / Mamiya, Taisei / Oikawa, Masakazu / Konishi, Teruaki

    Biology

    2023  Band 12, Heft 11

    Abstract: This study aimed to determine the mechanism underlying the modulation of radiosensitivity in cancer cells by the radiation-induced bystander effect (RIBE). We hypothesized that the RIBE mediates cyclooxygenase-2 (COX-2) and its metabolite prostaglandin ... ...

    Abstract This study aimed to determine the mechanism underlying the modulation of radiosensitivity in cancer cells by the radiation-induced bystander effect (RIBE). We hypothesized that the RIBE mediates cyclooxygenase-2 (COX-2) and its metabolite prostaglandin E2 (PGE2) in elevating radioresistance in unirradiated cells. In this study, we used the SPICE-QST microbeam irradiation system to target 0.07-0.7% cells by 3.4-MeV proton microbeam in the cell culture sample, such that most cells in the dish became bystander cells. Twenty-four hours after irradiation, we observed COX-2 protein upregulation in microbeam-irradiated cells compared to that of controls. Additionally, 0.29% of the microbeam-irradiated cells exhibited increased cell survival and a reduced micronucleus rate against X-ray irradiation compared to that of non-microbeam irradiated cells. The radioresistance response was diminished in both cell groups with the hemichannel inhibitor and in COX-2-knockout cells under cell-to-cell contact and sparsely distributed conditions. The results indicate that the RIBE upregulates the cell radioresistance through COX-2/PGE2 intercellular responses, thereby contributing to issues, such as the risk of cancer recurrence.
    Sprache Englisch
    Erscheinungsdatum 2023-10-25
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2661517-4
    ISSN 2079-7737
    ISSN 2079-7737
    DOI 10.3390/biology12111368
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Nuclear factor (erythroid-derived 2)-like 2 antioxidative response mitigates cytoplasmic radiation-induced DNA double-strand breaks.

    Wang, Jun / Konishi, Teruaki

    Cancer science

    2019  Band 110, Heft 2, Seite(n) 686–696

    Abstract: It has been reported that DNA double-strand breaks (DSB) can be induced by cytoplasm irradiation, and that both reactive free radicals and mitochondria are involved in DSB formation. However, the cellular antioxidative responses that are stimulated and ... ...

    Abstract It has been reported that DNA double-strand breaks (DSB) can be induced by cytoplasm irradiation, and that both reactive free radicals and mitochondria are involved in DSB formation. However, the cellular antioxidative responses that are stimulated and the biological consequences of cytoplasmic irradiation remain unknown. Using the Single Particle Irradiation system to Cell (SPICE) proton microbeam facility at the National Institute of Radiological Sciences ([NIRS] Japan), the response of nuclear factor (erythroid-derived 2)-like 2 (NRF2) antioxidative signaling to cytoplasmic irradiation was studied in normal human lung fibroblast WI-38 cells. Cytoplasmic irradiation stimulated the localization of NRF2 to the nucleus and the expression of its target protein, heme oxygenase 1. Activation of NRF2 by tert-butylhydroquinone mitigated the levels of DSB induced by cytoplasmic irradiation. Mitochondrial fragmentation was also promoted by cytoplasmic irradiation, and treatment with mitochondrial division inhibitor 1 (Mdivi-1) suppressed cytoplasmic irradiation-induced NRF2 activation and aggravated DSB formation. Furthermore, p53 contributed to the induction of mitochondrial fragmentation and activation of NRF2, although the expression of p53 was significantly downregulated by cytoplasmic irradiation. Finally, mitochondrial superoxide (MitoSOX) production was enhanced under cytoplasmic irradiation, and use of the MitoSOX scavenger mitoTEMPOL indicated that MitoSOX caused alterations in p53 expression, mitochondrial dynamics, and NRF2 activation. Overall, NRF2 antioxidative response is suggested to play a key role against genomic DNA damage under cytoplasmic irradiation. Additionally, the upstream regulators of NRF2 provide new clues on cytoplasmic irradiation-induced biological processes and prevention of radiation risks.
    Mesh-Begriff(e) Antioxidants/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Cell Nucleus/radiation effects ; Cytoplasm/metabolism ; Cytoplasm/radiation effects ; DNA Breaks, Double-Stranded/radiation effects ; DNA Damage/radiation effects ; Heme Oxygenase-1/metabolism ; Humans ; Mitochondria/metabolism ; Mitochondria/radiation effects ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress/physiology ; Oxidative Stress/radiation effects ; Reactive Oxygen Species/metabolism ; Signal Transduction/radiation effects ; Tumor Suppressor Protein p53/metabolism
    Chemische Substanzen Antioxidants ; NF-E2-Related Factor 2 ; NFE2L2 protein, human ; Reactive Oxygen Species ; Tumor Suppressor Protein p53 ; Heme Oxygenase-1 (EC 1.14.14.18)
    Sprache Englisch
    Erscheinungsdatum 2019-02-01
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2115647-5
    ISSN 1349-7006 ; 1347-9032
    ISSN (online) 1349-7006
    ISSN 1347-9032
    DOI 10.1111/cas.13916
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Induction of DNA strand breaks and oxidative base damages in plasmid DNA by ultra-high dose rate proton irradiation.

    Konishi, Teruaki / Kusumoto, Tamon / Hiroyama, Yota / Kobayashi, Alisa / Mamiya, Taisei / Kodaira, Satoshi

    International journal of radiation biology

    2023  Band 99, Heft 9, Seite(n) 1405–1412

    Abstract: Purpose: Radiation cancer therapy with ultra-high dose rate (UHDR) exposure, so-called FLASH radiotherapy, appears to reduce normal tissue damage without compromising tumor response to therapy. The aim of this study was to clarify whether a 59.5 MeV ... ...

    Abstract Purpose: Radiation cancer therapy with ultra-high dose rate (UHDR) exposure, so-called FLASH radiotherapy, appears to reduce normal tissue damage without compromising tumor response to therapy. The aim of this study was to clarify whether a 59.5 MeV proton beam at an UHDR of 48.6 Gy/s could effectively reduce the DNA damage of pBR322 plasmid DNA in solution compared to the conventional dose rate (CONV) of 0.057 Gy/s.
    Materials and methods: A simple system, consisting of pBR322 plasmid DNA in 1× Tris-EDTA buffer, was initially employed for proton beam exposure. We then used formamidopyrimidine-DNA glycosylase (Fpg) enzymes. which convert oxidative base damages of oxidized purines to DNA strand breaks, to quantify DNA single strand breaks (SSBs) and double strand breaks (DSBs) by agarose gel electrophoresis.
    Results: Our findings showed that the SSB induction rate (SSB per plasmid DNA/Gy) at UHDR and the induction of Fpg enzyme sensitive sites (ESS) were significantly reduced in UHDR compared to CONV. However, there was no significant difference in DSB induction and non-DSB cluster damages.
    Conclusions: UHDR of a 59.5 MeV proton beam could reduce non-clustered, non-DSB damages, such as SSB and sparsely distributed ESS. However, this effect may not be significant in reducing lethal DNA damage that becomes apparent only in acute radiation effects of mammalian cells and in vivo studies.
    Mesh-Begriff(e) Animals ; Protons ; Dose-Response Relationship, Radiation ; DNA/radiation effects ; Plasmids/genetics ; DNA Damage ; Oxidative Stress ; Mammals/genetics
    Chemische Substanzen Protons ; DNA (9007-49-2)
    Sprache Englisch
    Erscheinungsdatum 2023-02-13
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3065-x
    ISSN 1362-3095 ; 0020-7616 ; 0955-3002
    ISSN (online) 1362-3095
    ISSN 0020-7616 ; 0955-3002
    DOI 10.1080/09553002.2023.2176562
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Radiation quality effects alteration in COX-2 pathway to trigger radiation-induced bystander response in A549 lung carcinoma cells.

    Kobayashi, Alisa / Konishi, Teruaki

    Journal of radiation research

    2018  Band 59, Heft 6, Seite(n) 754–759

    Abstract: This study aimed to determine whether the radiation-induced bystander effect (RIBE) is affected by radiation quality. To mimic the different radiation qualities of the direct action (D)/indirect action (ID) ratio, A549 cells were exposed to X-rays, with ... ...

    Abstract This study aimed to determine whether the radiation-induced bystander effect (RIBE) is affected by radiation quality. To mimic the different radiation qualities of the direct action (D)/indirect action (ID) ratio, A549 cells were exposed to X-rays, with either 100 mM of the radical scavenger, thio-urea (TU+), or null (TU-). Biological responses in irradiated and bystander cells were compared at equal lethal effects of a 6% survival dose, which was estimated from the survival curves to be 8 Gy and 5 Gy for TU+ and TU-, respectively. Cyclooxygenase-2 (COX-2) expression in TU- irradiated cells increased up to 8 h post-irradiation, before decreasing towards 24 h. The concentration of prostaglandin E2 (PGE2), a primary product of COX-2 and known as a secreted inducible factor in RIBE, increased over 3-fold compared with that in the control at 8 h post-irradiation. Conversely, COX-2 expression and PGE2 production of TU+ irradiated cells were drastically suppressed. These results show that the larger D/ID suppressed COX-2 expression and PGE2 production in irradiated cells. However, in contrast to the case in the irradiated cells, COX-2 expression was equally observed in the TU- and TU+ co-cultured bystander cells, which showed the highest expression levels at 24 h post-irradiation. Taken together, these findings demonstrate that radiation quality, such as the D/ID ratio, may be an important factor in the alteration of signalling pathways involved in RIBE.
    Mesh-Begriff(e) A549 Cells ; Bystander Effect/radiation effects ; Cyclooxygenase 2/metabolism ; Dinoprostone/metabolism ; Humans ; Lung Neoplasms/enzymology ; Lung Neoplasms/pathology ; Reactive Oxygen Species/metabolism ; Signal Transduction/radiation effects ; Thiourea/pharmacology ; X-Rays
    Chemische Substanzen Reactive Oxygen Species ; Cyclooxygenase 2 (EC 1.14.99.1) ; Thiourea (GYV9AM2QAG) ; Dinoprostone (K7Q1JQR04M)
    Sprache Englisch
    Erscheinungsdatum 2018-08-01
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 603983-2
    ISSN 1349-9157 ; 0449-3060
    ISSN (online) 1349-9157
    ISSN 0449-3060
    DOI 10.1093/jrr/rry065
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel: Primary and Secondary Bystander Effects of Proton Microbeam Irradiation on Human Lung Cancer Cells under Hypoxic Conditions.

    Autsavapromporn, Narongchai / Kobayashi, Alisa / Liu, Cuihua / Duangya, Aphidet / Oikawa, Masakazu / Tengku Ahmad, Tengku Ahbrizal / Konishi, Teruaki

    Biology

    2023  Band 12, Heft 12

    Abstract: Tumor hypoxia is the most common feature of radioresistance to the radiotherapy (RT) of lung cancer and results in poor clinical outcomes. High-linear energy transfer (LET) radiation is a novel RT technique to overcome this problem. However, a limited ... ...

    Abstract Tumor hypoxia is the most common feature of radioresistance to the radiotherapy (RT) of lung cancer and results in poor clinical outcomes. High-linear energy transfer (LET) radiation is a novel RT technique to overcome this problem. However, a limited number of studies have been elucidated on the underlying mechanism(s) of RIBE and RISBE in cancer cells exposed to high-LET radiation under hypoxia. Here, we developed a new method to investigate the RIBE and RISBE under hypoxia using the SPICE-QST proton microbeams and a layered tissue co-culture system. Normal lung fibroblast (WI-38) and lung cancer (A549) cells were exposed in the range of 06 Gy of proton microbeams, wherein only ~0.04-0.15% of the cells were traversed by protons. Subsequently, primary bystander A549 cells were co-cultured with secondary bystander A549 cells in the presence or absence of a GJIC and NO inhibitor using co-culture systems. Studies show that there are differences in RIBE in A549 and WI-38 primary bystander cells under normoxia and hypoxia. Interestingly, treatment with a GJIC inhibitor showed an increase in the toxicity of primary bystander WI-38 cells but a decrease in A549 cells under hypoxia. Our results also show the induction of RISBE in secondary bystander A549 cells under hypoxia, where GJIC and NO inhibitors reduced the stressful effects on secondary bystander A549 cells. Together, these preliminary results, for the first time, represented the involvement of intercellular communications through GJIC in propagation of RIBE and RISBE in hypoxic cancer cells.
    Sprache Englisch
    Erscheinungsdatum 2023-12-03
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2661517-4
    ISSN 2079-7737
    ISSN 2079-7737
    DOI 10.3390/biology12121485
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  8. Artikel ; Online: Dose Rate Effects on Hydrated Electrons, Hydrogen Peroxide, and a OH Radical Molecular Probe Under Clinical Energy Protons.

    Kusumoto, Tamon / Danvin, Antoine / Mamiya, Taisei / Arnone, Aurelia / Chefson, Severine / Galindo, Catherine / Peaupardin, Philippe / Raffy, Quentin / Kamiguchi, Nagaaki / Amano, Daizo / Sasai, Kenzo / Konishi, Teruaki / Kodaira, Satoshi

    Radiation research

    2024  Band 201, Heft 4, Seite(n) 287–293

    Abstract: We report the dose rate dependence of radiation chemical yields (G value) of water radiolysis products under clinical energy protons (230 MeV) to understand mechanisms of the FLASH radiotherapy performed at ultra-high dose rate (>40 Gy/s). The G value of ...

    Abstract We report the dose rate dependence of radiation chemical yields (G value) of water radiolysis products under clinical energy protons (230 MeV) to understand mechanisms of the FLASH radiotherapy performed at ultra-high dose rate (>40 Gy/s). The G value of 7-hydoroxy-coumarin-3-carboxylic acid (7OH-C3CA) produced by reactions of coumarin-3-carboxylic acid (C3CA) with OH radicals and oxygen is evaluated by fluorescence method. Also, those of hydrated electrons and hydrogen peroxide are derived by absorption method using Saltzman and Ghomley techniques, respectively. Both G values of 7OH-C3CA and hydrated electrons decrease with increasing dose rate. The relative evolution of 7OH-C3CA is -39 ± 2% between 0.1 and 50 Gy/s. This value is higher than that of hydrated electrons, measured at -21 ± 4%. The G value of hydrogen peroxide in ultra-pure water also decreases with increasing dose rate. In comparison to these findings, we represent the increase of the G value of hydrogen peroxide with increasing dose rate in the mixture solution of MeOH and NaNO3, which act as scavengers of OH radicals and hydrated electrons, respectively, that decompose hydrogen peroxide. This finding indicates that a complex track structure can be expected with increasing dose rate and the reduction of OH radicals by forming hydrogen peroxide would be related to the sparing effect of healthy tissues.
    Mesh-Begriff(e) Protons ; Hydrogen Peroxide ; Electrons ; Water/chemistry
    Chemische Substanzen Protons ; Hydrogen Peroxide (BBX060AN9V) ; Water (059QF0KO0R)
    Sprache Englisch
    Erscheinungsdatum 2024-03-14
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 80322-4
    ISSN 1938-5404 ; 0033-7587
    ISSN (online) 1938-5404
    ISSN 0033-7587
    DOI 10.1667/RADE-23-00244.1
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Significant changes in yields of 7-hydroxy-coumarin-3-carboxylic acid produced under FLASH radiotherapy conditions.

    Kusumoto, Tamon / Kitamura, Hisashi / Hojo, Satoru / Konishi, Teruaki / Kodaira, Satoshi

    RSC advances

    2020  Band 10, Heft 63, Seite(n) 38709–38714

    Abstract: FLASH radiotherapy appears to kill off tumor cells while sparing healthy tissues, by irradiation at ultra high dose rate (>40 Gy ... ...

    Abstract FLASH radiotherapy appears to kill off tumor cells while sparing healthy tissues, by irradiation at ultra high dose rate (>40 Gy s
    Sprache Englisch
    Erscheinungsdatum 2020-10-27
    Erscheinungsland England
    Dokumenttyp Journal Article
    ISSN 2046-2069
    ISSN (online) 2046-2069
    DOI 10.1039/d0ra07999e
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel: Biologic Impact of Different Ultra-Low-Fluence Irradiations in Human Fibroblasts.

    Suzuki, Masao / Uchihori, Yukio / Kitamura, Hisashi / Oikawa, Masakazu / Konishi, Teruaki

    Life (Basel, Switzerland)

    2020  Band 10, Heft 8

    Abstract: In this study, we aimed to evaluate the cellular response of healthy human fibroblasts induced by different types of ultra-low-fluence radiations, including gamma rays, neutrons and high linear energy transfer (LET) heavy ions. NB1RGB cells were ... ...

    Abstract In this study, we aimed to evaluate the cellular response of healthy human fibroblasts induced by different types of ultra-low-fluence radiations, including gamma rays, neutrons and high linear energy transfer (LET) heavy ions. NB1RGB cells were pretreated with ultra-low-fluence radiations (~0.1 cGy/7-8 h) of
    Sprache Englisch
    Erscheinungsdatum 2020-08-18
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2662250-6
    ISSN 2075-1729
    ISSN 2075-1729
    DOI 10.3390/life10080154
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