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Cited by 881DNA Repair MechanismsCell death mechanisms and regulationCancer-related Molecular Pathways

The DOI matches its Crossref record; 180 of the 187 references it cites were found in a registry or an index.

DNA damage-induced cell death: From specific DNA lesions to the DNA damage response and apoptosis

Roos, Wynand P., Kaina, Bernd·2013·Cancer Letters
DOI 10.1016/j.canlet.2012.01.007
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Abstract

DNA damaging agents are potent inducers of cell death triggered by apoptosis. Since these agents induce a plethora of different DNA lesions, it is firstly important to identify the specific lesions responsible for initiating apoptosis before the apoptotic executing pathways can be elucidated. Here, we describe specific DNA lesions that have been identified as apoptosis triggers, their repair and the signaling provoked by them. We discuss methylating agents such as temozolomide, ionizing radiation and cisplatin, all of them are important in cancer therapy. We show that the potentially lethal events for the cell are O(6)-methylguanine adducts that are converted by mismatch repair into DNA double-strand breaks (DSBs), non-repaired N-methylpurines and abasic sites as well as bulky adducts that block DNA replication leading to DSBs that are also directly induced following ionizing radiation. Transcriptional inhibition may also contribute to apoptosis. Cells are equipped with sensors that detect DNA damage and relay the signal via kinases to executors, who on their turn evoke a process that inhibits cell cycle progression and provokes DNA repair or, if this fails, activate the receptor and/or mitochondrial apoptotic cascade. The main DNA damage recognition factors MRN and the PI3 kinases ATM, ATR and DNA-PK, which phosphorylate a multitude of proteins and thus induce the DNA damage response (DDR), will be discussed as well as the downstream players p53, NF-κB, Akt and survivin. We review data and models describing the signaling from DNA damage to the apoptosis executing machinery and discuss the complex interplay between cell survival and death.

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Crossref · 10.1016/j.canlet.2012.01.007

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Research works printed but not linked: 2

  1. Peto, 1984, IARC Sci. Publ., 627
  2. Roos, 2007, Apoptosis in malignant glioma cells triggered by the temozolomide-induced DNA lesion O(6)-methylguanine, Oncogene, 26, 186, 10.1038/sj.onc.1209785 · DOI

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Metadata

Authors
Roos, W. P., & Kaina, B.
Affiliations
Johannes Gutenberg University Mainz (DE)
Corresponding author
Kaina, Bernd
ORCID
Venue
Cancer Letters
Publisher
Elsevier BV
Published
2013-05
Volume
332
Issue
2
Pages
237-248
ISSN
0304-3835 (ISSN-L)
DOI
10.1016/j.canlet.2012.01.007
OpenAlex
W2064488040
Cited by
879
References
187
Citations by year
2026: 40 · 2025: 37 · 2024: 52 · 2023: 77 · 2022: 77 · 2021: 76 · 2020: 79 · 2019: 63 · 2018: 89 · 2017: 55 · 2016: 64 · 2015: 67 · 2014: 58 · 2013: 32
FWCI
4.93
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Cancer Letters (publishedVersion)
  • PubMed (publishedVersion)
Funders
Universitätsmedizin der Johannes Gutenberg-Universität Mainz
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Keywords
DNA damage response, apoptosis, DNA lesions, DNA mismatch repair, DNA double-strand breaks, abasic sites, bulky DNA adducts, ionizing radiation, temozolomide, cisplatin, DNA repair, MRN complex, ATM, ATR, DNA-dependent protein kinase, p53, NF-κB, Akt, survivin, transcriptional inhibition, cell cycle arrest, cancer therapy
MeSH terms
Survivin, Animals, Antineoplastic Agents, Cell Cycle, DNA, DNA Damage, DNA Repair, Guanine, Humans, Neoplasms, Phosphorylation, Radiation, Ionizing, Signal Transduction, NF-kappa B, Cell Death, Apoptosis, DNA Adducts, Inhibitor of Apoptosis Proteins, Proto-Oncogene Proteins c-akt

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