Cited by 383DNA Repair MechanismsPARP inhibition in cancer therapyCancer-related Molecular Pathways

DNA Repair Pathways in Cancer Therapy and Resistance

Open access
Li, Lan-ya, Guan, Yi-di, Chen, Xi-sha, Yang, Jin-ming, Cheng, Yan·2021·Frontiers in Pharmacology

Abstract

DNA repair pathways are triggered to maintain genetic stability and integrity when mammalian cells are exposed to endogenous or exogenous DNA-damaging agents. The deregulation of DNA repair pathways is associated with the initiation and progression of cancer. As the primary anti-cancer therapies, ionizing radiation and chemotherapeutic agents induce cell death by directly or indirectly causing DNA damage, dysregulation of the DNA damage response may contribute to hypersensitivity or resistance of cancer cells to genotoxic agents and targeting DNA repair pathway can increase the tumor sensitivity to cancer therapies. Therefore, targeting DNA repair pathways may be a potential therapeutic approach for cancer treatment. A better understanding of the biology and the regulatory mechanisms of DNA repair pathways has the potential to facilitate the development of inhibitors of nuclear and mitochondria DNA repair pathways for enhancing anticancer effect of DNA damage-based therapy.

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Registry

Crossref · 10.3389/fphar.2020.629266

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  • Cancer cells are often characterized by increased replication stress, altered DNA repair mechanisms or changes in chromatin structure.

    “One possible explanation for the observed difference between cSNVs and dbSNVs could be system-wide alterations in cancer cells, which are often characterized by increased replication stress, altered DNA repair mechanisms or changes in chromatin structure (85,86).”

    From G-quadruplex-mediated genomic instability drives SNVs in cancer (2024) · cites this paper as [86]

    The ‘Role of DNA Repair Pathways in Cancer Biology’ section (page unavailable) describes defects and downregulation of DNA repair pathways in cancers, supporting the altered-repair part of the claim. The passages found do not establish that cancer cells are often characterized by increased replication stress or changes in chromatin structure; searches for those terms did not find support for those parts. (LLM, conf=0.86)

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Cites

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4 of the 140 references couldn’t be matched to a known paper.

Research works printed but not linked: 3

  1. Anderson C. T. Friedberg E. C. (1980). The presence of nuclear and mitochondrial uracil-DNA glycosylase in extracts of human KB cells. Nucleic Acids Res. 4, 875. PMC327318 6253928
  2. Liu L. Yan L. Donze J. R. Gerson S. L. (2003). Blockage of abasic site repair enhances antitumor efficacy of 1,3-bis-(2-chloroethyl)-1-nitrosourea in colon tumor xenografts. Mol. Cancer Ther. 10, 1061 14578471
  3. Luo M. Kelley M. R. (2004). Inhibition of the human apurinic/apyrimidinic endonuclease (APE1) repair activity and sensitization of breast cancer cells to DNA alkylating agents with lucanthone. Anticancer Res. 4, 2127 15330152

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Authors
Li, L.-Y., Guan, Y.-D., Chen, X.-S., Yang, J.-M., & Cheng, Y.
Affiliations
Central South University (CN)
Corresponding author
Cheng, Yan
Venue
Frontiers in Pharmacology
Published
2021-02-08
Volume
11
Pages
629266-629266
ISSN
1663-9812 (ISSN-L)
OpenAlex
W3127551105
Cited by
383
References
140
Citations by year
2026: 40 · 2025: 81 · 2024: 86 · 2023: 93 · 2022: 69 · 2021: 14
FWCI
7.08
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Pharmacology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • UKnowledge (University of Kentucky) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
National Natural Science Foundation of China (81422051 81472593 31401208)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Keywords
DNA repair pathways, DNA damage response, cancer therapy, chemoresistance, ionizing radiation, DNA-damaging agents, DNA repair inhibitors, mitochondrial DNA repair, tumor sensitivity

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