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

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DNA Repair Pathways in Cancer Therapy and Resistance

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

DOI 10.3389/fphar.2020.629266PMC PMC7898236

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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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FIGURE 1 DNA damage response. DNA damage is caused by endogenous agent oxygen species (ROS) or exogenous agents such as UV light, ionizing radiation (IR) and chemotherapy agents. DNA damage response (DDR) is induced to deal with the lesions, including signal transduction, transcriptional regulation, cell-cycle checkpoints, induction of apoptosis, multiple DNA repair pathways as well as damage tolerance processes. DNA repair pathways include nuclear and mitochondrial DNA repair pathways. Direct repair, BER, MMR and recombinational repair (HR and NHEJ) are existence in both nuclear and mitochondrial repair systems. NER has been reported only appearance in nucleus, and the existence of TLS pathway in mitochondria is unknown. NDNA, nuclear DNA; MtDNA, mitochondrial DNA; BER, base excision repair; HR, homologous recombination repair; NHEJ, non-homologous end joining; MMR, mismatch repair; TLS, translesion synthesis; NER, nucleotide excision repair.CC BY · PubMed Central

FIGURE 2 Mechanism and function of PARP and PARP inhibitors. The catalytic function of PARP1 is activated through binding to the SSBs site cuased by alkylating agents. Activated PARP1 undergo PARylation and recruitment of a serials of key DNA repair effectors involved in BER to repair DNA lesion. Finally, PARP1 release from DNA and regain inactive state. PARP inhibitors binds the catalytic site of PARP and impaired of the enzymatic activity of PARP which “trap” PARP1 on DNA, results in suppression of the catalytic cycle of PARP1 and BER. Trapping PARP1 on DNA lesion also collapses DNA replication fork, therefore transforming SSBs into genotoxic DSBs. This type of DNA lesion would normally induce HR for repairing damaged DNA. However, if HR-defective exist in tumor cells, including BRCA1/2 deficiency or mutation, another less effective and error-prone DSBs repair pathway NHEJ or alt-NHEJ could be utilized, which causing genomic instability, chromosomal fusions/translocations and subsequently inducing cell death. SSBs, single-strand breaks; DSB, double-strand break; BER, base excision repair; alt-NHEJ, alternative nonhomologous end joining; NHEJ, non-homologous end joining; HR, homologous recombination repair.CC BY · PubMed Central

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Recent developments in photodynamic therapy and its application against multidrug resistant cancers
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Signaling pathway dysregulation in breast cancer
Ryspayeva, D., Seyhan, A. A., MacDonald, W., Purcell, C., Roady, T. J., Ghandali, M., Verovkina, N., El‐Deiry, W. S., Taylor, M. S., & Graff, S. L. (2025) · Oncotarget · doi:10.18632/oncotarget.28701 · Cited by 31
Transmembrane nuclease NUMEN/ENDOD1 regulates DNA repair pathway choice at the nuclear periphery
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“Since abnormal function of DNA repair pathways is associated with the initiation and progression of cancer [53], further research should be conducted on the influence of alternative splice variants of XP genes on cancer risk.”
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The Dysregulation of MicroRNAs in the Development of Cervical Pre-Cancer—An Update
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p53-Dependent Cytoprotective Mechanisms behind Resistance to Chemo-Radiotherapeutic Agents Used in Cancer Treatment
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“Most drugs targeted to DNA damage are in development for anti-cancer therapy, aiming to kill the cancerous cells (Li et al., 2021).”
HNRNPC regulates RhoA to induce DNA damage repair and cancer‐associated fibroblast activation causing radiation resistance in pancreatic cancer
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Lycopene Supplementation to Serum-Free Maturation Medium Improves In Vitro Bovine Embryo Development and Quality and Modulates Embryonic Transcriptomic Profile
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SARS-CoV-2 and the Nucleus
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“Since DNA damage response (DDR) may contribute to the hypersensitivity or resistance of cancer cells to genotoxic agents [51], and CPZ shows a synergy with TMZ [36], we investigated the effects of CPZ on DNA repair pathways.”
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Elevated PAF1-RAD52 axis confers chemoresistance to human cancers
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“Being tumor‐suppressor genes, their alterations lead to more aggressive disease, while a defective DNA repair mechanism can also theoretically sensitize to chemotherapy and radiation.(9,19,20) However, the impact of DDR‐associated alterations on treatment outcomes in the setting of mCRPC has been quite inconsistent.”
Background
CircRNA_001895 promotes sunitinib resistance of renal cell carcinoma through regulation of apoptosis and DNA damage repair
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Nanoparticulate drug combination inhibits DNA damage repair and PD-L1 expression in BRCA-mutant and wild type triple-negative breast cancer
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Chemotherapy and Physical Therapeutics Modulate Antigens on Cancer Cells
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Polyploid giant cancer cells induced by Docetaxel exhibit a senescence phenotype with the expression of stem cell markers in ovarian cancer cells
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Background

Authors: Li, L.-Y., Guan, Y.-D., Chen, X.-S., Yang, J.-M., & Cheng, Y.
Affiliations: Central South University (CN)
Corresponding author: Cheng, Yan
ORCID: Cheng, Yan
Venue: Frontiers in Pharmacology
Publisher: Frontiers Media SA
Published: 2021-02-08
Volume: 11
Pages: 629266-629266
ISSN: 1663-9812 (ISSN-L)
DOI: 10.3389/fphar.2020.629266
PMC: PMC7898236
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: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (vor)
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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DNA Repair Pathways in Cancer Therapy and Resistance

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