Cited by 176NF-κB Signaling PathwaysDNA Repair MechanismsEffects of Radiation Exposure

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The ATM protein is required for sustained activation of NF-κB following DNA damage

Piret, Bernard, Schoonbroodt, Sonia, Piette, Jacques·1999·Oncogene

DOI 10.1038/sj.onc.1202541

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Abstract

Cells lacking an intact ATM gene are hypersensitive to ionizing radiation and show multiple defects in the cell cycle-coupled checkpoints. DNA damage usually triggers cell cycle arrest through, among other things, the activation of p53. Another DNA-damage responsive factor is NF-kappaB. It is activated by various stress situations, including oxidative stress, and by DNA-damaging compounds such as topoisomerase poisons. We found that cells from Ataxia Telangiectasia patients exhibit a defect in NF-kappaB activation in response to treatment with camptothecin, a topoisomerase I poison. In AT cells, this activation is shortened or suppressed, compared to that observed in normal cells. Ectopic expression of the ATM protein in AT cells increases the activation of NF-kappaB in response to camptothecin. MO59J glioblastoma cells that do not express the DNA-PK catalytic subunit respond normally to camptothecin. These results support the hypothesis that NF-kappaB is a DNA damage-responsive transcription factor and that its activation pathway by DNA damage shares some components with the one leading to p53 activation.

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“The “ up ” gene set was enriched especially for targets of MYC but also NFKB1 , the latter having been previously implicated in the regulation of senescence in response to DNA damage (Mercurio and Manning 1999; Piret et al. 1999; Chien et al. 2011; Kang et al. 2015; Voce et al. 2015).”
Background
KINK-1, a Novel Small-Molecule Inhibitor of IKKβ, and the Susceptibility of Melanoma Cells to Antitumoral Treatment
Schön, M., Wienrich, B. G., Kneitz, S., Sennefelder, H., Amschler, K., Voehringer, V., Weber, O., Stiewe, T., Ziegelbauer, K. B., & Schön, M. P. (2008) · JNCI Journal of the National Cancer Institute · doi:10.1093/jnci/djn174 · Cited by 63
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“An accumulation of ROS can severely damage cellular macromolecules, especially DNA, and induce cell cycle arrest [17].”
Background
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“Indeed, IκB-α [77,78] or NEMO [80] phosphorylation allows the nuclear translocation of NF-κB and the activation of its DNA binding activity.”
Background
Sam68/KHDRBS1 is critical for colon tumorigenesis by regulating genotoxic stress-induced NF-κB activation
Fu, K., Sun, X., Wier, E. M., Hodgson, A., Liu, Y., Sears, C. L., & Wan, F. (2016) · eLife · doi:10.7554/elife.15018 · Cited by 55
“(Li et al., 2001; Piret et al., 1999), poly (ADP-ribose) polymerase 1 (PARP1) was recently revealed”
BackgroundInfluential
Activation of Nuclear Factor κB by Different Agents
Hellweg, C. E., Arenz, A., Bogner, S., Schmitz, C., & Baumstark‐Khan, C. (2006) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1378.066 · Cited by 49
Genetic Evidence of a Role for ATM in Functional Interaction between Human T-Cell Leukemia Virus Type 1 Tax and p53
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DNA double-strand breaks: a potential therapeutic target for neurodegenerative diseases
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IκB kinase β phosphorylates Dok1 serines in response to TNF, IL-1, or γ radiation
Lee, S., Andrieu‐Soler, C., Saltel, F., Destaing, O., Auclair, J., Pouchkine, V., Michelon, J., Salaun, B., Kobayashi, R., Jurdic, P., et al. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0408061101 · Cited by 48
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“These cells also display a defect in NF-κB activation that could explain in part their enhanced apoptotic responses to DNA damaging agents [52].”
Background
PPM1G Binds 7SK RNA and Hexim1 To Block P-TEFb Assembly into the 7SK snRNP and Sustain Transcription Elongation
Gudipaty, S. A., McNamara, R. P., Morton, E. L., & D’Orso, I. (2015) · Molecular and Cellular Biology · doi:10.1128/mcb.00226-15 · Cited by 48
“Since inhibition of ATM blocks the PPM1G-7SK RNA interaction as well as the activation of NF- B transcription in response to DNA damage (48, 57, 62), it appears that both molecular events are intimately coupled and that the role of ATM in promoting the PPM1G-7SK RNA interaction relies on NF- B signaling.”
Background
Transcription Factors in the Cellular Response to Charged Particle Exposure
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Phosphorylation of p65(RelA) on Ser547 by ATM Represses NF-κB-Dependent Transcription of Specific Genes after Genotoxic Stress
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“The primordial role of ATM kinase in NF-kB activation by DSB was demonstrated some years ago [25,26], but the different molecular mechanisms by which it controls this signaling cascade are continuously uncovered.”
BackgroundSelf-citation
Signalling loops and linear pathways: NF- B activation in response to genotoxic stress
Brzóska, K., & Szumiel, I. (2008) · Mutagenesis · doi:10.1093/mutage/gen056 · Cited by 41
TSG101 associates with PARP1 and is essential for PARylation and DNA damage‐induced NF‐κB activation
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“Following activation, auto-modified PARP1 forms a transient nuclear complex with IKK c , PIASy, and ATM (Stilmann et al , 2009).”
Influential
Importance of PIKKs in NF-κB activation by genotoxic stress
Sabatel, H., Pirlot, C., Piette, J. G., & Habraken, Y. (2011) · Biochemical Pharmacology · doi:10.1016/j.bcp.2011.07.105 · Cited by 39
“AT cells\IR\20 Gy [10] AT cells\CPT\10 mM [113]”
BackgroundMethodSelf-citation
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“Also, ATM sustains NFkB activation following DNA damage.(20) As we have shown that inhibition of NFkB by chemotherapeutics sensitizes glioma cells to TNFa-induced apoptosis,(21,22) we investigated whether TNFa effects the responsiveness of glioma cell to NCS by fine tuning the”
Background
The Molecular Mechanisms in Senescent Cells Induced by Natural Aging and Ionizing Radiation
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Sustained elevation of NF‐ κ B DNA binding activity in radiation‐induced lung damage in rats
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“In a cell culture model, it has been found that ataxia telangiectasia mutated (ATM) plays a role in sustained activation of NF-kB after DNA damage (Piret et al. 1999).”
Background
Cellular Monitoring of the Nuclear Factor κB Pathway for Assessment of Space Environmental Radiation
Baumstark‐Khan, C., Hellweg, C. E., Arenz, A., & Meier, M. M. (2005) · Radiation Research · doi:10.1667/rr3397.1 · Cited by 35
“In a cell culture model, it has been found that ataxia telangiectasia mutated protein (ATM) plays a role in sustained activation of NF-kB in response to DNA double-strand breaks (12, 13), probably by its PI3 kinase-like activity (3).”
Background
ATM-dependent activation of the gene encoding MAP kinase phosphatase 5 by radiomimetic DNA damage
Bar‐Shira, A., Rashi‐Elkeles, S., Zlochover, L., Moyal, L., Smorodinsky, N. I., Seger, R., & Shiloh, Y. (2002) · Oncogene · doi:10.1038/sj.onc.1205127 · Cited by 34
“It appears that when the damage involves DSBs, this response is ATM-dependent with regard to both the NF-kB pathway (Lee et al., 1998; Li et al., 2000; Piret et al., 1999) and the MAP kinase system (Shafman et al., 1995; Wang et al., 2000).”
Background
Melatonin increases the chemosensitivity of diffuse large B-cell lymphoma cells to epirubicin by inhibiting P-glycoprotein expression via the NF-κB pathway
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“Similarly, a picture is also emerging in which certain genotoxic stress inducers mediate NF- B signaling by triggering IKK activation (31, 42, 52, 61, 65, 69).”
Background
c‐IAP2 is induced by ionizing radiation through NF‐κB binding sites
Ueda, T., Akiyama, N., Sai, H., Oya, N., Noda, M., Hiraoka, M., & Kizaka‐Kondoh, S. (2001) · FEBS Letters · doi:10.1016/s0014-5793(01)02145-7 · Cited by 30
Ataxia-Telangiectasia-Mutated (ATM) Protein Can Enhance Human Immunodeficiency Virus Type 1 Replication by Stimulating Rev Function
Ariumi, Y., & Trono, D. (2006) · Journal of Virology · doi:10.1128/jvi.80.5.2445-2452.2006 · Cited by 30
“Interestingly, the activation of NF- B following DNA damage is abrogated in ATM-deficient cells (29), indicating a link between NF- B and the ATM signaling pathway.”
Background
Differential involvement of the hMRE11/hRAD50/NBS1 complex, BRCA1 and MLH1 in NF-κB activation by camptothecin and X-ray
Habraken, Y., Jolois, O., & Piette, J. G. (2003) · Oncogene · doi:10.1038/sj.onc.1206893 · Cited by 29
“ATM is the only nuclear protein shown to be an intermediate in NF-kB activation by DSB, since NF-kB activation by CPT or IR is reduced in intensity and duration in AT-deficient cell lines (Piret et al., 1999; Li et al., 2001).”
BackgroundSelf-citation
Parp3 promotes astrocytic differentiation through a tight regulation of Nox4-induced ROS and mTorc2 activation
Rodríguez-Vargas, J. M., Martin-Hernandez, K., Wang, W., Kunath, N., Suganthan, R., Amé, J., Oliver, F. J., Ye, J., Bjørås, M., & Dantzer, F. (2020) · Cell Death and Disease · doi:10.1038/s41419-020-03167-5 · Cited by 28
The Function of SUMOylation and Its Role in the Development of Cancer Cells under Stress Conditions: A Systematic Review
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“PTM of NF-κB essential modulator (NEMO) is indispensable to link the cellular genotoxic response to NF-κB via the ATM kinase [69, 70].”
Background
Crosstalk between cGAS-STING pathway and autophagy in cancer immunity
Lu, Q., Chen, Y., Li, J., Zhu, F., & Zheng, Z. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1139595 · Cited by 28
Quantitative Proteomics Reveal ATM Kinase-dependent Exchange in DNA Damage Response Complexes
Choi, S., Srivas, R., Fu, K. Y., Hood, B. L., Dost, B., Gibson, G. A., Watkins, S. C., Houten, B. V., Bandeira, N., Conrads, T. P., et al. (2012) · Journal of Proteome Research · doi:10.1021/pr3005524 · Cited by 27

Authors: Piret, B., Schoonbroodt, S., & Piette, J.
Affiliations: University of Liège (BE)
ORCID: Schoonbroodt, Sonia
Piette, Jacques
Venue: Oncogene
Publisher: Springer Science and Business Media LLC
Published: 1999-04-01
Volume: 18
Issue: 13
Pages: 2261-2271
ISSN: 0950-9232 (ISSN-L)
1476-5594
DOI: 10.1038/sj.onc.1202541
OpenAlex: W2316716290
Cited by: 176
References: 96
Citations by year: 2025: 4 · 2024: 5 · 2023: 2 · 2022: 6 · 2021: 4 · 2020: 5 · 2019: 2 · 2018: 4 · 2017: 4 · 2016: 10 · 2015: 11 · 2014: 2 · 2013: 5 · 2012: 9
FWCI: 3.21
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Oncogene (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
Keywords: ATM protein, NF-κB activation, DNA damage response, camptothecin, topoisomerase I poisons, ataxia telangiectasia, p53, cell cycle checkpoints, radiosensitivity, DNA-dependent protein kinase, transcription factors
MeSH terms: NF-KappaB Inhibitor alpha, Adolescent, Age Factors, Antineoplastic Agents, Phytogenic, Ataxia Telangiectasia, Brain Neoplasms, Camptothecin, Cells, Cultured, Child, Child, Preschool, DNA Damage, DNA-Binding Proteins, Enzyme Inhibitors, Fibroblasts, Gene Expression Regulation, Glioblastoma, Humans, Leupeptins, Nuclear Proteins, Phosphoric Monoester Hydrolases, Protease Inhibitors, Proteins, Radiation Tolerance, Recombinant Fusion Proteins, Transcription, Genetic, Tumor Cells, Cultured, Tumor Necrosis Factor-alpha, Tumor Suppressor Protein p53, NF-kappa B, Protein Serine-Threonine Kinases, Cell Cycle Proteins, I-kappa B Proteins, Tumor Suppressor Proteins, DNA-Activated Protein Kinase, Topoisomerase I Inhibitors, Ataxia Telangiectasia Mutated Proteins

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The ATM protein is required for sustained activation of NF-κB following DNA damage

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