Cell Senescence and the DNA Single-Strand Break Damage Repair Pathway
Cellular senescence is a response to endogenous and exogenous stresses, including telomere dysfunction, oncogene activation, and persistent DNA damage. In particular, radiation damage induces oxidative base damage and bond breaking in the DNA double-helix structure, which are treated by dedicated en...
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| Format: | Article |
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MDPI AG
2024-12-01
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| Series: | DNA |
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| Online Access: | https://www.mdpi.com/2673-8856/4/4/36 |
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| author | Parvathy A. Sarma Corinne Abbadie Yvan de Launoit Fabrizio Cleri |
| author_facet | Parvathy A. Sarma Corinne Abbadie Yvan de Launoit Fabrizio Cleri |
| author_sort | Parvathy A. Sarma |
| collection | DOAJ |
| description | Cellular senescence is a response to endogenous and exogenous stresses, including telomere dysfunction, oncogene activation, and persistent DNA damage. In particular, radiation damage induces oxidative base damage and bond breaking in the DNA double-helix structure, which are treated by dedicated enzymatic repair pathways. In this review, we discuss the correlation between senescence and the accumulation of non-repaired single-strand breaks, as can occur during radiation therapy treatments. Recent in vitro cell irradiation experiments using high-energy photons have shown that single-strand breaks may be preferentially produced at the borders of the irradiated region, inducing senescence in competition with the apoptosis end-point typically induced by double-strand breaks. Such a particular response to radiation damage has been proposed as a possible cause of radiation-induced second primary cancer, as cells with an accumulation of non-repaired single-strand breaks might evade the senescent state at much later times. In addition, we highlight the peculiarities of strand-break repair pathways in relation to the base-excision pathway that repairs several different DNA oxidation defects. |
| format | Article |
| id | doaj-art-5215fae2a9fc4e91a5c18360c82e65c4 |
| institution | OA Journals |
| issn | 2673-8856 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | DNA |
| spelling | doaj-art-5215fae2a9fc4e91a5c18360c82e65c42025-08-20T02:00:32ZengMDPI AGDNA2673-88562024-12-014453055210.3390/dna4040036Cell Senescence and the DNA Single-Strand Break Damage Repair PathwayParvathy A. Sarma0Corinne Abbadie1Yvan de Launoit2Fabrizio Cleri3Université de Lille, Institut d’Electronique Microelectronique et Nanotechnologie (IEMN CNRS, UMR 8520), F-59652 Villeneuve d’Ascq, FranceUniversité de Lille, CNRS, Inserm, Institut Pasteur de Lille, CHU Lille, UMR9020-U1277-CANTHER-Cancer Heterogeneity, Plasticity, and Resistance to Therapies, F-59000 Lille, FranceUniversité de Lille, CNRS, Inserm, Institut Pasteur de Lille, CHU Lille, UMR9020-U1277-CANTHER-Cancer Heterogeneity, Plasticity, and Resistance to Therapies, F-59000 Lille, FranceUniversité de Lille, Institut d’Electronique Microelectronique et Nanotechnologie (IEMN CNRS, UMR 8520), F-59652 Villeneuve d’Ascq, FranceCellular senescence is a response to endogenous and exogenous stresses, including telomere dysfunction, oncogene activation, and persistent DNA damage. In particular, radiation damage induces oxidative base damage and bond breaking in the DNA double-helix structure, which are treated by dedicated enzymatic repair pathways. In this review, we discuss the correlation between senescence and the accumulation of non-repaired single-strand breaks, as can occur during radiation therapy treatments. Recent in vitro cell irradiation experiments using high-energy photons have shown that single-strand breaks may be preferentially produced at the borders of the irradiated region, inducing senescence in competition with the apoptosis end-point typically induced by double-strand breaks. Such a particular response to radiation damage has been proposed as a possible cause of radiation-induced second primary cancer, as cells with an accumulation of non-repaired single-strand breaks might evade the senescent state at much later times. In addition, we highlight the peculiarities of strand-break repair pathways in relation to the base-excision pathway that repairs several different DNA oxidation defects.https://www.mdpi.com/2673-8856/4/4/36cell senescenceDNA damageradiotherapyDNA repair pathwaysbase-excision repairsingle-strand breaks |
| spellingShingle | Parvathy A. Sarma Corinne Abbadie Yvan de Launoit Fabrizio Cleri Cell Senescence and the DNA Single-Strand Break Damage Repair Pathway DNA cell senescence DNA damage radiotherapy DNA repair pathways base-excision repair single-strand breaks |
| title | Cell Senescence and the DNA Single-Strand Break Damage Repair Pathway |
| title_full | Cell Senescence and the DNA Single-Strand Break Damage Repair Pathway |
| title_fullStr | Cell Senescence and the DNA Single-Strand Break Damage Repair Pathway |
| title_full_unstemmed | Cell Senescence and the DNA Single-Strand Break Damage Repair Pathway |
| title_short | Cell Senescence and the DNA Single-Strand Break Damage Repair Pathway |
| title_sort | cell senescence and the dna single strand break damage repair pathway |
| topic | cell senescence DNA damage radiotherapy DNA repair pathways base-excision repair single-strand breaks |
| url | https://www.mdpi.com/2673-8856/4/4/36 |
| work_keys_str_mv | AT parvathyasarma cellsenescenceandthednasinglestrandbreakdamagerepairpathway AT corinneabbadie cellsenescenceandthednasinglestrandbreakdamagerepairpathway AT yvandelaunoit cellsenescenceandthednasinglestrandbreakdamagerepairpathway AT fabriziocleri cellsenescenceandthednasinglestrandbreakdamagerepairpathway |