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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Background
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Background
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Background
Chronic cisplatin treatment promotes enhanced damage repair and tumor progression in a mouse model of lung cancerPreprint
Oliver, T. G., Mercer, K. L., Sayles, L. C., Burke, J. R., Mendus, D., Lovejoy, K. S., Cheng, M.-H., Subramanian, A., Mu, D., Powers, S., et al. (2010) · Genes & Development · doi:10.1101/gad.1897010 · Cited by 213
Interaction of Sirt3 with OGG1 contributes to repair of mitochondrial DNA and protects from apoptotic cell death under oxidative stress
Cheng, Y., Ren, X., Gowda, A. S., Shan, Y., Zhang, L., Yuan, Y.-S., Patel, R., Wu, H., Huber-Keener, K., Yang, J. W., et al. (2013) · Cell Death & Disease · doi:10.1038/cddis.2013.254 · Cited by 205
Self-citation
DNA damage response – A double-edged sword in cancer prevention and cancer therapy
Tian, H., Gao, Z., Li, H., Zhang, B., Wang, G., Zhang, Q., Pei, D., & Zheng, J. (2014) · Cancer Letters · doi:10.1016/j.canlet.2014.12.038 · Cited by 189 · cited 1×
“DDR is a complex network that functions in different ways to target various DNA lesions, including signal transduction, transcriptional regulation, cell-cycle checkpoints, induction of apoptosis, damage tolerance processes, and multiple DNA repair pathways (Figure 1) (Giglia-Mari et al., 2011; Tian et al., 2015).”
Background
N6-Methylation of Adenosine of FZD10 mRNA Contributes to PARP Inhibitor Resistance
Fukumoto, T., Zhu, H., Nacarelli, T., Karakashev, S. V., Fatkhutdinov, N., Wu, S., Liu, P., Kossenkov, A. V., Showe, L. C., Jean, S., et al. (2019) · Cancer Research · doi:10.1158/0008-5472.can-18-3592 · Cited by 181
USP1 Is Required for Replication Fork Protection in BRCA1-Deficient Tumors
Lim, K. S., Li, H., Roberts, E. A., Gaudiano, E. F., Clairmont, C. S., Sambel, L. A., Ponnienselvan, K., Liu, J., Yang, C., Kozono, D., et al. (2018) · Molecular Cell · doi:10.1016/j.molcel.2018.10.045 · Cited by 174
Preclinical Evaluation of the WEE1 Inhibitor MK-1775 as Single-Agent Anticancer Therapy
Guertin, A. D., Li, J., Liu, Y., Hurd, M. S., Schuller, A., Long, B., Hirsch, H., Feldman, I., Benita, Y., Toniatti, C., et al. (2013) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-13-0025 · Cited by 171 · cited 1×
“Inhibition of WEE1 causes aberrant DNA replication and replication-dependent DNA damage in cells by suppressing CDK2 (Guertin et al., 2013).”
Background
Overall survival and updated progression-free survival outcomes in a randomized phase II study of combination cediranib and olaparib versus olaparib in relapsed platinum-sensitive ovarian cancer.
Liu, J. F., Barry, W., Birrer, M., Lee, J., Buckanovich, R. J., Fleming, G., Rimel, B., Buss, M., Nattam, S., Hurteau, J. A., et al. (2019) · Annals of Oncology · doi:10.1093/annonc/mdz018 · Cited by 165 · cited 1×
“PAPR1 inhibitors in combination with IR or with other different anticancer agents are currently undergoing clinical trials for treatment of patients with BRCA1/2 mutation or HRR-deficiency advanced solid tumors, which shown promising clinical activity (Bang et al., 2017; Wilson et al., 2017; Loibl et al., 2018; Colema…”
Background
Inhibition of Nuclear PTEN Tyrosine Phosphorylation Enhances Glioma Radiation Sensitivity through Attenuated DNA Repair
Ma, J., Benítez, J. A., Li, J., Miki, S., de Albuquerque, C. P., Galatro, T. F. D. A., Orellana, L., Zanca, C., Reed, R., Boyer, A. D., et al. (2019) · Cancer Cell · doi:10.1016/j.ccell.2019.01.020 · Cited by 162
DNA damage related crosstalk between the nucleus and mitochondria
Saki, M. R., & Prakash, A. (2016) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2016.11.050 · Cited by 153 · cited 1×
“…| Article 6292661 REVIEW published: 08 February 2021 doi: 10.3389/fphar.2020.629266 TLS and double-strand break repair (DSBR), can repair damaged DNA to maintain mitochondria genetic integrity, protect mtDNA against oxidative damage, and promote cell survival (Ohta, 2006; Saki and Prakash, 2017).”
BackgroundInfluential
DNA-PK inhibition by NU7441 sensitizes breast cancer cells to ionizing radiation and doxorubicin
Ciszewski, W. M., Tavecchio, M., Dastych, J., & Curtin, N. J. (2013) · Breast Cancer Research and Treatment · doi:10.1007/s10549-013-2785-6 · Cited by 153 · cited 1×
“They could inhibit DSBs repair pathway and enhance the sensitivity of cancer cells to ionizing radiation or/and chemo-potentiation such as doxorubicin (Ciszewski et al., 2014).”
Background
A Small Molecule Inhibitor of Human RAD51 Potentiates Breast Cancer Cell Killing by Therapeutic Agents in Mouse Xenografts
Huang, F., & Mazin, A. V. (2014) · PLoS ONE · doi:10.1371/journal.pone.0100993 · Cited by 143 · cited 1×
“…HR RAD51 Combination with radiation in glioma stem cells; combination with clinically approved anticancer agents in breast cancer cell Huang and Mazin (2014), King et al. (2017) AG-14361 BER PARP1 Combination with lestaurtinib in breast cancer cells Vazquez-Ortiz et al. (2014) A-966492 BER…”
Background
Abrogation of radioresistance in glioblastoma stem‐like cells by inhibition of ATM kinase
Carruthers, R., Ahmed, S. U., Strathdee, K. E., Gomez-Roman, N., Amoah-Buahin, E., Watts, C., & Chalmers, A. J. (2014) · Molecular Oncology · doi:10.1016/j.molonc.2014.08.003 · Cited by 139
Hypoxia-Induced Epigenetic Regulation and Silencing of the BRCA1 Promoter
Lü, Y., Chu, A., Turker, M. S., & Glazer, P. M. (2011) · Molecular and Cellular Biology · doi:10.1128/mcb.01121-10 · Cited by 138 · cited 1×
“induced by hypoxia, suggesting that the hypoxic tumor microenvironment can suppress the HRR pathway to cause genetic instability (Bindra et al., 2004; Lu et al., 2011).”
Background
Lomeguatrib, a Potent Inhibitor of O6-Alkylguanine-DNA-Alkyltransferase: Phase I Safety, Pharmacodynamic, and Pharmacokinetic Trial and Evaluation in Combination with Temozolomide in Patients with Advanced Solid Tumors
Ranson, M., Middleton, M., Bridgewater, J., Lee, S., Dawson, M., Jowle, D., Halbert, G., Waller, S., McGrath, H., Gumbrell, L., et al. (2006) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-05-2198 · Cited by 135 · cited 2×
“…as well as PaTrin-2), another pseudo-substrate tested in clinical trials, has been shown to increase the therapeutic index of methylating agent temozolomide in nude mice bearing A375M human melanoma xenografts and patients with advanced solid tumors (Middleton et al., 2002; Ranson et al., 2006).”
Background
Use of poly ADP-ribose polymerase [PARP] inhibitors in cancer cells bearing DDR defects: the rationale for their inclusion in the clinic
Cerrato, A., Morra, F., & Celetti, A. (2016) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-016-0456-2 · Cited by 132 · cited 1×
“Numerous studies have indicated that certain cancers are associated with the defect or mutation in the proteins of nuclear or mitochondrial DNA repair pathways (Pearl et al., 2015; Cerrato et al., 2016).”
Background
Combined Inhibition of STAT3 and DNA Repair in Palbociclib-Resistant ER-Positive Breast Cancer
Kettner, N. M., Vijayaraghavan, S., Durak, M. G., Bui, T. N., Kohansal, M., Ha, M. J., Liu, B., Rao, X., Wang, J., Yi, M., et al. (2019) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-18-3274 · Cited by 128 · cited 1×
“Abnormal DNA repair activity was found in CDK4/ 6 inhibitors palbociclib-resistant breast cancer cells, whereas PARP inhibitors, olaparib and niraparib treatment could significantly inhibit palbociclib-resistant cancer cell viability (Kettner et al., 2019).”
BackgroundSelf-citation
Selective resistance to the PARP inhibitor olaparib in a mouse model for BRCA1-deficient metaplastic breast cancer
Henneman, L., van Miltenburg, M. H., Michalak, E. M., Braumuller, T. M., Jaspers, J. E., Drenth, A. P., de Korte‐Grimmerink, R., Gogola, E., Szuhai, K., Schlicker, A., et al. (2015) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1500223112 · Cited by 126
RAD51 Is a Selective DNA Repair Target to Radiosensitize Glioma Stem Cells
King, H., Brend, T., Payne, H. L., Wright, A., Ward, T., Patel, K., Egnuni, T., Stead, L. F., Patel, A., Wurdak, H., et al. (2017) · Stem Cell Reports · doi:10.1016/j.stemcr.2016.12.005 · Cited by 121
Improvement of chemotherapy efficacy by inactivation of a DNA-repair pathway.
Middleton, M., & Margison, G. (2003) · The Lancet Oncology · doi:10.1016/s1470-2045(03)00959-8 · Cited by 114 · cited 1×
“Thus, the protective effect of MGMT could diminish the cytotoxic effects of alkylating agents (Middleton and Margison, 2003), suggesting that MGMT activity is likely to be a useful marker of the sensitivity of cancer cells to alkylating agents.”
Background
Graphene Nanoribbons as a Drug Delivery Agent for Lucanthone Mediated Therapy of Glioblastoma Multiforme
Chowdhury, S., Surhland, C., Sanchez, Z., Chaudhary, P., Kumar, S., Lee, S., Peña, L., Waring, M., Sitharaman, B., & Naidu, M. (2014) · Nanomedicine: Nanotechnology, Biology and Medicine · doi:10.1016/j.nano.2014.08.001 · Cited by 103
Pharmacologic inhibition of ATR and ATM offers clinically important distinctions to enhancing platinum or radiation response in ovarian, endometrial, and cervical cancer cells
Teng, P.-N., Bateman, N. W., Darcy, K. M., Hamilton, C. A., Maxwell, G. L., Bakkenist, C. J., & Conrads, T. P. (2015) · Gynecologic Oncology · doi:10.1016/j.ygyno.2014.12.035 · Cited by 102
Conditional Targeting of the DNA Repair Enzyme hOGG1 into Mitochondria
Rachek, L. I., Grishko, V. I., Musiyenko, S. I., Kelley, M. R., LeDoux, S. P., & Wilson, G. L. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m208770200 · Cited by 95 · cited 2×
“8-OxoG-recognizing DNA glycosylase 1 (OGG1) is an important DNA glycosylase for repair of 8oxoguanine (8-oxoG), which is one of the major DNA lesions both of the nDNA and mtDNA, especially in mtDNA (Rachek et al., 2002).”
Background
The PARP Inhibitor AZD2461 Provides Insights into the Role of PARP3 Inhibition for Both Synthetic Lethality and Tolerability with Chemotherapy in Preclinical Models
O’Connor, L. O., Rulten, S. L., Cranston, A. N., Odedra, R., Brown, H., Jaspers, J. E., Jones, L., Knights, C., Evers, B., Ting, A. K. T., et al. (2016) · Cancer Research · doi:10.1158/0008-5472.can-15-3240 · Cited by 93
Inactivation of O6-alkylguanine DNA alkyltransferase as a means to enhance chemotherapy.
Rabik, C., Njoku, M., & Dolan, M. (2006) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2006.03.004 · Cited by 92 · cited 2×
“…high MGMT expression in tumor cell is associated with the resistance to 1,3- bis- (2-chloroethyl) -1- nitrosourea (BCNU) and temozolomide (TMZ) (Happold et al., 2018; Hsu et al., 2018), which target the O6-position of guanine, resulting in cytotoxic and mutagenic DNA adducts (Rabik et al., 2006).”
Background
Defective homologous recombination DNA repair as therapeutic target in advanced chordoma
Gröschel, S., Hübschmann, D., Raimondi, F., Horak, P., Warsow, G., Fröhlich, M., Klink, B., Gieldon, L., Hutter, B., Kleinheinz, K., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-09633-9 · Cited by 92
Intrinsic Resistance to Immune Checkpoint Blockade in a Mismatch Repair–Deficient Colorectal Cancer
Gurjao, C., Liu, D., Hofree, M., AlDubayan, S. H., Wakiro, I., Su, M.-J., Felt, K. D., Gjini, E., Brais, L. K., Rotem, A., et al. (2019) · Cancer Immunology Research · doi:10.1158/2326-6066.cir-18-0683 · Cited by 92 · cited 1×
“On the contrary, researchers also found that colorectal cancer (CRC) patient with DNA mismatch repair deficiency (dMMR)/a high-level of microsatellite instability (MSI-H) exhibited intrinsic resistance to immune checkpoint immune checkpoint inhibitor (Gurjao et al., 2019).”
Background
MGMT-activated DUB3 stabilizes MCL1 and drives chemoresistance in ovarian cancer
Wu, X., Luo, Q., Zhao, P., Chang, W., Wang, Y., Shu, T., Ding, F., Li, B., & Liu, Z. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1814742116 · Cited by 89 · cited 1×
“Based on lines of pre-clinical Lomeguatrib (PaTrin-2) Direct repair MGMT Pancreatic cancer cells; combination with HDACis in ovarian cancer Wu et al. (2019), Shi et al. (2020) Lucanthone BER APE1 Glioblastoma multiforme (GBM) cell Chowdhury et al. (2015) CRT0044876 BER APE1 Colon cancer cell lines…”
Method
Targeting the DNA damage response for cancer therapy
Powell, S. N., & Bindra, R. S. (2009) · DNA repair · doi:10.1016/j.dnarep.2009.04.011 · Cited by 86 · cited 1×
“Many inhibitors aiming at both ATM and DNA-PK have been reported to have great potential as a chemo- and radiotherapy sensitizing agents in cancer therapy (Powell and Bindra, 2009).”
Background
Contribution of somatic mutations in the mitochondrial genome to the development of cancer and tolerance against anticancer drugs
Ohta, S. (2006) · Oncogene · doi:10.1038/sj.onc.1209602 · Cited by 83 · cited 1×
“…| Article 6292661 REVIEW published: 08 February 2021 doi: 10.3389/fphar.2020.629266 TLS and double-strand break repair (DSBR), can repair damaged DNA to maintain mitochondria genetic integrity, protect mtDNA against oxidative damage, and promote cell survival (Ohta, 2006; Saki and Prakash, 2017).”
BackgroundInfluential
Histone methyltransferases EHMT1 and EHMT2 (GLP/G9A) maintain PARP inhibitor resistance in high-grade serous ovarian carcinoma
Watson, Z. L., Yamamoto, T. M., McMellen, A., Kim, H., Hughes, C. J., Wheeler, L., Post, M., Behbakht, K., & Bitler, B. (2019) · Clinical Epigenetics · doi:10.1186/s13148-019-0758-2 · Cited by 80
The prognostic value of MGMT promoter status by pyrosequencing assay for glioblastoma patients’ survival: a meta-analysis
Zhao, H.-L., Wang, S., Song, C.-W., Zha, Y.-H., & Li, L. (2016) · World Journal of Surgical Oncology · doi:10.1186/s12957-016-1012-4 · Cited by 79 · cited 6×
“Lucanthone combination with radiation and TMZ in GBM patients was tested in phase Ⅱ clinical trial (NCT01587144).”
BackgroundInfluentialSelf-citation
A phase I study of intravenous and oral rucaparib in combination with chemotherapy in patients with advanced solid tumours
Wilson, R. H., Evans, T. J., Middleton, M. R., Molife, L. R., Spicer, J. F., Dieras, V. C., Roxburgh, P., Giordano, H., Jaw‐Tsai, S., Goble, S. M., et al. (2017) · British Journal of Cancer · doi:10.1038/bjc.2017.36 · Cited by 78 · cited 1×
“PAPR1 inhibitors in combination with IR or with other different anticancer agents are currently undergoing clinical trials for treatment of patients with BRCA1/2 mutation or HRR-deficiency advanced solid tumors, which shown promising clinical activity (Bang et al., 2017; Wilson et al., 2017; Loibl et al., 2018; Colema…”
Background
APC loss affects DNA damage repair causing doxorubicin resistance in breast cancer cells
Stefanski, C. D., Keffler, K., McClintock, S., Milac, L., & Prosperi, J. R. (2019) · Neoplasia · doi:10.1016/j.neo.2019.09.002 · Cited by 78 · cited 2×
“Inhibiting DNA repair kinases could also prevent doxorubicin (DOX) resistance in breast cancer cells (Stefanski et al., 2019).”
Background
The F-Box Domain-Dependent Activity of EMI1 Regulates PARPi Sensitivity in Triple-Negative Breast Cancers
Marzio, A., Puccini, J., Kwon, Y., Maverakis, N., Arbini, A., Sung, P., Bar‐Sagi, D., & Pagano, M. (2018) · Molecular Cell · doi:10.1016/j.molcel.2018.11.003 · Cited by 74 · cited 1×
“Another mechanism leading to resistance may restoration of HRR function or reconstruction of replication fork stability by increasing RAD51 expression or re-expressing BRCA1/2 (Ter Brugge et al., 2016; Quigley et al., 2017; Clements et al., 2018; Lim et al., 2018; Marzio et al., 2019).”
Background
Berberine attenuates XRCC1‐mediated base excision repair and sensitizes breast cancer cells to the chemotherapeutic drugs
Gao, X., Wang, J., Li, M., Wang, J., Lv, J., Zhang, L., Sun, C., Ji, J., Yang, W., Zhao, Z., et al. (2019) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.14560 · Cited by 73 · cited 1×
“Base Excision Repair A number of investigations have shown that inhibition of BER pathway can enhance the sensitivity of cancer cells to alkylating agents and radiotherapy (Neijenhuis et al., 2005; Gao et al., 2019).”
Background
Targeting the kinase activities of ATR and ATM exhibits antitumoral activity in mouse models of MLL -rearranged AML
Morgado-Palacin, I., Day, A., Murga, M., Lafarga, V., Antón, M. E., Tubbs, A., Chen, H.-T., Ergen, A. V., Anderson, R., Bhandoola, A., et al. (2016) · Science Signaling · doi:10.1126/scisignal.aad8243 · Cited by 73 · cited 1×
“AZD0156, a newly discovered ATM inhibitor, has the potential to promote the survival of leukemia-bearing mice and now is under clinical trial (Morgado-Palacin et al., 2016).”
Background
DNA-Dependent Protein Kinase Is a Molecular Target for the Development of Noncytotoxic Radiation–Sensitizing Drugs
Shinohara, E., Geng, L., Tan, J., Chen, H., Shir, Y., Edwards, E., Halbrook, J., Kesicki, E., Kashishian, A., & Hallahan, D. (2005) · Cancer Research · doi:10.1158/0008-5472.can-04-4250 · Cited by 71
Loss of E2F7 confers resistance to poly-ADP-ribose polymerase (PARP) inhibitors in BRCA2-deficient cells
Clements, K. E., Thakar, T., Nicolae, C. M., Liang, X., Wang, H., & Moldovan, G. (2018) · Nucleic Acids Research · doi:10.1093/nar/gky657 · Cited by 71
Glutamine deficiency induces DNA alkylation damage and sensitizes cancer cells to alkylating agents through inhibition of ALKBH enzymes
Tran, T. Q., Gabra, M. B. I., Lowman, X. H., Yang, Y., Reid, M. A., Pan, M., O'Connor, T. R., & Kong, M. (2017) · PLoS Biology · doi:10.1371/journal.pbio.2002810 · Cited by 65 · cited 1×
“Lack of glutamine led to DNA alkylation damage by inhibiting ALKBH activity and increased the sensitivity of cancer cells to alkylating agents (Tran et al., 2017).”
Background
Temporal DNA-PK activation drives genomic instability and therapy resistance in glioma stem cells
Wang, Y., Xu, H., Liu, T., Huang, M., Butter, P.-P., Li, C., Zhang, L., Kao, G. D., Gong, Y., Maity, A. M., et al. (2018) · JCI Insight · doi:10.1172/jci.insight.98096 · Cited by 65
ALDH1A1 Contributes to PARP Inhibitor Resistance via Enhancing DNA Repair in BRCA2−/− Ovarian Cancer Cells
Liu, L., Cai, S., Han, C., Banerjee, A. T., Wu, D., Cui, T., Xie, G., Zhang, J., Zhang, X., McLaughlin, E. M., et al. (2019) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-19-0242 · Cited by 64
DNA repair capacity in peripheral lymphocytes predicts survival of patients with non-small-cell lung cancer treated with first-line platinum-based chemotherapy.
Wang, L.-E., Yin, M., Dong, Q., Stewart, D., Merriman, K., Amos, C., Spitz, M., & Wei, Q. (2011) · Journal of Clinical Oncology · doi:10.1200/jco.2010.34.3616 · Cited by 63 · cited 2×
“Cisplatin-resistant tumor cells exhibited higher level of DNA damage repair related genes and DRC, inhibition of NER pathway significantly enhanced the sensitivity of tumor cells to cisplatin (Oliver,Mercer, 2010;Wang et al., 2011).”
Background
MGMT gene promoter methylation as a potent prognostic factor in glioblastoma treated with temozolomide-based chemoradiotherapy: a single-institution study.
Kim, Y. S., Kim, S. H., Cho, J., Kim, J. W., Chang, J.-H., Kim, D. S., Lee, K. S., & Suh, C. (2012) · International Journal of Radiation Oncology, Biology, Physics · doi:10.1016/j.ijrobp.2011.12.086 · Cited by 61 · cited 6×
“Lucanthone combination with radiation and TMZ in GBM patients was tested in phase Ⅱ clinical trial (NCT01587144).”
BackgroundInfluential
Persistent DNA damage triggers activation of the integrated stress response to promote cell survival under nutrient restriction
Clementi, E., Inglin, L., Beebe, E., Gsell, C., Garajovà, Z., & Markkanen, E. (2020) · BMC Biology · doi:10.1186/s12915-020-00771-x · Cited by 60 · cited 1×
“DNA repair pathways play an important role in the maintenance of genome stability and integrity through correcting the impaired DNA that may contribute to carcinogenesis (Clementi et al., 2020).”
Background
BET bromodomain inhibitors synergize with ATR inhibitors to induce DNA damage, apoptosis, senescence-associated secretory pathway and ER stress in Myc-induced lymphoma cells
Muralidharan, S. V., Bhadury, J., Nilsson, L. M., Green, L. C., McLure, K. G., & Nilsson, J. A. (2016) · Oncogene · doi:10.1038/onc.2015.521 · Cited by 59
DNA Mismatch Repair Deficiency and Immune Checkpoint Inhibitors in Gastrointestinal Cancers
Bañobre, J. R., & Goel, A. (2018) · Gastroenterology · doi:10.1053/j.gastro.2018.11.071 · Cited by 58 · cited 2×
“Frontiers in Pharmacology | www.frontiersin.org February 2021 | Volume 11 | Article 6292668 Li et al. DNA Repair in Cancer Therapy and clinical evidence, the US Food and drug Administration (FDA) has approved anti-PD-1 antibodies for the treatment of patients with MMR-deficient (Ruiz-Bañobre and Goel, 2019).”
Background
The ATM and ATR inhibitors CGK733 and caffeine suppress cyclin D1 levels and inhibit cell proliferation
Alao, J. P., & Sunnerhagen, P. (2009) · Radiation Oncology · doi:10.1186/1748-717x-4-51 · Cited by 55 · cited 1×
“…cells Muralidharan et al. (2016) AZ20 HR ATR Colorectal adenocarcinoma tumor cells Foote et al. (2013) CGK733 HR ATM/ATR Human breast cancer cells Alao and Sunnerhagen (2009) NU7026 NHEJ DNA-PK Combination with carbon ion irradiation in non-small cell lung cancer cell Ma et al. (2015) NU7441…”
Background
mi RNA ‐106a and prostate cancer radioresistance: a novel role for LITAF in ATM regulation
Hoey, C., Ray, J., Jeon, J., Huang, X., Taeb, S., Ylanko, J., Andrews, D. W., Boutros, P. C., & Liu, S. K. (2018) · Molecular Oncology · doi:10.1002/1878-0261.12328 · Cited by 50
DNA‐PKcs Deficiency Inhibits Glioblastoma Cell‐Derived Angiogenesis After Ionizing Radiation
Liu, Y., Zhang, L., Liu, Y., Sun, C., Zhang, H., Miao, G., Di, C. X., Zhou, X. H., Zhou, R., & Wang, Z. (2014) · Journal of Cellular Physiology · doi:10.1002/jcp.24841 · Cited by 50 · cited 1×
“It has been reported that DNA-PK activity plays a role in chemo-radiotherapy resistance (Wang Y. et al., 2018; Stefanski et al., 2019; Alikarami et al., 2017; Liu et al., 2015).”
Background
A multikinase and DNA-PK inhibitor combination immunomodulates melanomas, suppresses tumor progression, and enhances immunotherapies
Tsai, A. K., Khan, A. Y., Worgo, C. E., Wang, L., Liang, Y.-Y., & Davila, E. (2017) · Cancer immunology research · doi:10.1158/2326-6066.cir-17-0009 · Cited by 47 · cited 1×
“recently found that NU7441 combination with a multikinase inhibitor regorafenib altered immune microenvironment of melanomas and enhanced the efficacy of various immunotherapies (Tsai et al., 2017).”
Background
Essential Role of DNA Base Excision Repair on Survival in an Acidic Tumor Microenvironment
Seo, Y., & Kinsella, T. J. (2009) · Cancer Research · doi:10.1158/0008-5472.can-09-0624 · Cited by 46
Activity of M3814, an Oral DNA-PK Inhibitor, In Combination with Topoisomerase II Inhibitors in Ovarian Cancer Models
Wise, H. C., Iyer, G., Moore, K., Temkin, S., Gordon, S., Aghajanian, C., & Grisham, R. (2019) · Scientific Reports · doi:10.1038/s41598-019-54796-6 · Cited by 45 · cited 2×
“Frontiers in Pharmacology | www.frontiersin.org February 2021 | Volume 11 | Article 6292666 Li et al. DNA Repair in Cancer Therapy topoisomerase inhibitors in ovarian cancer xenografts (Wise et al., 2019).”
Background
Mitochondrial DNA repair through OGG1 activity attenuates breast cancer progression and metastasis
Yuzefovych, L. V., Kahn, A. G., Schuler, M. A., Eide, L., Arora, R., Wilson, G., Tan, M., & Rachek, L. (2015) · Cancer Research · doi:10.1158/0008-5472.can-15-0692 · Cited by 45 · cited 2×
“Recently, researchers also proved that overexpression of mitochondrial OGG1 decreased breast cancer progression and metastasis (Yuzefovych et al., 2016).”
Background
MGMT Expression Predicts PARP-Mediated Resistance to Temozolomide
Erice, O., Smith, M. P., White, R., Goicoechea, I., Barriuso, J., Jones, C., Margison, G. P., Acosta, J. C., Wellbrock, C., & Arozarena, I. (2015) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-14-0810 · Cited by 44 · cited 1×
“Combination of temozolomide with PARP inhibitors (PARPi) in MGMT-positive cancer cells enhanced the anticancer effects (Erice et al., 2015; Jue et al., 2017).”
Background
Veliparib in combination with radiotherapy for the treatment of MGMT unmethylated glioblastoma
Jue, T. R., Nozue, K., Lester, A., Joshi, S. M., Schröder, L. B. W., Whittaker, S. P., Nixdorf, S., Rapkins, R. W., Khasraw, M., & McDonald, K. L. (2017) · Journal of Translational Medicine · doi:10.1186/s12967-017-1164-1 · Cited by 44
Effect of O6‐(4‐bromothenyl)guanine on different temozolomide schedules in a human melanoma xenograft model
Middleton, M., Thatcher, N., McMurry, T., McElhinney, R. S., Donnelly, D., & Margison, G. (2002) · International Journal of Cancer · doi:10.1002/ijc.10532 · Cited by 43 · cited 1×
“…as well as PaTrin-2), another pseudo-substrate tested in clinical trials, has been shown to increase the therapeutic index of methylating agent temozolomide in nude mice bearing A375M human melanoma xenografts and patients with advanced solid tumors (Middleton et al., 2002; Ranson et al., 2006).”
Background
Methoxyamine sensitizes the resistant glioblastoma T98G cell line to the alkylating agent temozolomide
Montaldi, A. P., & Sakamoto-Hojo, E. (2013) · Clinical and Experimental Medicine (Testo stampato) · doi:10.1007/s10238-012-0201-x · Cited by 42 · cited 1×
“Combined treatment with chemotherapeutic alkylating agent such as TMZ and BCNU could reinforce the cytotoxicity of alkylating agent by targeting BER pathway (Liu et al., 2003; Montaldi and Sakamoto-Hojo, 2013).”
Background
Contribution of Mitochondrial DNA Repair to Cell Resistance from Oxidative Stress*
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The expression of Exonuclease III from E. coli in mitochondria of breast cancer cells diminishes mitochondrial DNA repair capacity and cell survival after oxidative stress.
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Optimizing Glioblastoma Temozolomide Chemotherapy Employing Lentiviral-based Anti-MGMT shRNA Technology
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“Several studies in animal models have suggested that the therapy of MGMT gene silence was able to overcome TMZ resistance and increase tumor cell death (Viel et al., 2013).”
Background
Nontoxic concentration of DNA ‐ PK inhibitor NU7441 radio‐sensitizes lung tumor cells with little effect on double strand break repair
Sunada, S., Kanai, H., Lee, Y., Yasuda, T., Hirakawa, H., Liu, C., Fujimori, A., Uesaka, M., & Okayasu, R. (2016) · Cancer Science · doi:10.1111/cas.12998 · Cited by 38
Anti-tumor activity and mechanistic characterization of APE1/Ref-1 inhibitors in bladder cancer
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Combining carbon ion irradiation and non-homologous end-joining repair inhibitor NU7026 efficiently kills cancer cells
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“…Human breast cancer cells Alao and Sunnerhagen (2009) NU7026 NHEJ DNA-PK Combination with carbon ion irradiation in non-small cell lung cancer cell Ma et al. (2015) NU7441 NHEJ DNA-PK Combination with radiotherapy in non-small cell lung cancer cell Sunada et al. (2016) Abbreviations: MGMT,…”
Method
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Background
NU7441 Enhances the Radiosensitivity of Liver Cancer Cells
Yang, C., Wang, Q., Liu, X., Cheng, X., Jiang, X., Zhang, Y., Feng, Z., & Zhou, P. (2016) · Cellular Physiology and Biochemistry · doi:10.1159/000445551 · Cited by 35 · cited 4×
“Alexander K. Tsai et al. recently found that NU7441 combination with a multikinase inhibitor regorafenib altered immune microenvironment of melanomas and enhanced the efficacy of various immunotherapies (Tsai et al., 2017).”
Influential
Transcriptional control of O6‐methylguanine DNA methyltransferase expression and temozolomide resistance in glioblastoma
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Inhibition of Rad51 sensitizes breast cancer cells with wild-type PTEN to olaparib.
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Background
MGMT expression affects the gemcitabine resistance of pancreatic cancer cells
Shi, Y., Wang, Y., Qian, J., Yan, X., Han, Y. K., Yao, N., & Ma, J. (2020) · Life Sciences · doi:10.1016/j.lfs.2020.118148 · Cited by 26
Glucose starvation impairs DNA repair in tumour cells selectively by blocking histone acetylation.
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“Based on the concept of “synthetic lethality”-targeting either gene alone in a synthetic lethal pair is tolerated, but simultaneous targeting both genes is lethal, researchers applied PARPi to BRCA mutation tumors (Dhillon et al., 2016).”
Background
BET bromodomain inhibitors synergize with ATR inhibitors in melanoma
Muralidharan, S. V., Einarsdottir, B. O., Bhadury, J., Lindberg, M. F., Wu, J., Campeau, E., Bagge, R. O., Stierner, U. K., Ny, L., Nilsson, L. M., et al. (2017) · Cell Death and Disease · doi:10.1038/cddis.2017.383 · Cited by 21
Drug repurposing screen identifies lestaurtinib amplifies the ability of the poly (ADP-ribose) polymerase 1 inhibitor AG14361 to kill breast cancer associated gene-1 mutant and wild type breast cancer cells
Vázquez-Ortíz, G., Chisholm, C. L., Xu, X., Lahusen, T. J., Li, C., Sakamuru, S., Huang, R., Thomas, C. J., Xia, M., & Deng, C. (2014) · Breast Cancer Research · doi:10.1186/bcr3682 · Cited by 21
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See all 383

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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