PARP-1 in tumor complicated with depression—possible role and therapeutic perspective: a narrative review

Introduction

Psycho-oncology is a field that examines the psychological aspects of malignant tumor patients, aiming to help them cope with fear, anxiety, and depression during diagnosis, treatment, and rehabilitation (1). The prevalence of depression and anxiety comorbid with tumors is estimated to be 20%, which is much higher than that of the general population (2). Depression often co-occurs with tumor progression, and it can also exacerbate tumor deterioration. This not only increases the medical costs of patients but also impairs their quality of life, treatment adherence, and survival outcomes. Therefore, it is essential to enhance the awareness and management of depression comorbidity in tumor treatment.

Poly(ADP)-ribose polymerase (PARP) is a family of protein enzymes involved in deoxyribonucleic acid (DNA) damage repair, first identified by Chambon et al. in 1963 (3). The family consists of 17 subtypes, each exhibiting functional and pathological heterogeneity across various diseases and biological processes (4). PARP-1, the first discovered subtype, is overexpressed and activated in various tumors and contributes to tumor development (5-8). Furthermore, there are clinical cases indicating a strong correlation between PARP inhibitors and improvement in depression treatment (9). Mechanistically, PARP inhibitors and depression are associated with inflammation and oxidative stress (10-15). Thus, PARP-1 is a potential therapeutic target for patients with tumor comorbidity with depression. Based on the comorbidity mechanisms between tumors and depression, this article investigates the critical role of PARP-1 in modulating cell death, inflammatory response, and oxidative stress, and reviews the research advances of PARP-1 in patients with tumor comorbidity with depression, offering new perspectives for the treatment and drug development of related diseases. We present this article in accordance with the Narrative Review reporting checklist (available at https://tcr.amegroups.com/article/view/10.21037/tcr-2025-739/rc).

Methods

We systematically analyzed literature from PubMed, Web of Science, and Cochrane Library (01/01/1994-01/06/2025) using keywords: “PARP-1”, “cancer”, “depression”, “cancer-related depression”, “cancer and co-morbid depression”. Preclinical studies and clinical trials were prioritized for mechanistic and therapeutic evidence synthesis. The search strategy is detailed in Table 1.

The function of PARP-1

PARP-1 is the first and most extensively studied subtype of PARP, with multiple functions and accounting for over 90% of PARPs activity (4). PARP-1 operates mainly in the nucleus, where it regulates various cellular processes such as DNA repair, chromatin remodeling, gene expression, and cell death by synthesizing poly(ADP-ribose) (PAR) chains (Figure 1). A major function of PARP-1 is to participate in DNA damage response and repair. Upon single or double-strand DNA breaks in cells, PARP-1 rapidly recognizes and binds to the damaged site, using nicotinamide adenine dinucleotide (NAD⁺) as a substrate to transfer ADP-ribose units to itself or other target proteins, forming PAR chains (16). These PAR chains act as signaling molecules, recruiting and activating other enzymes involved in DNA repair, such as DNA ligase III (LigIII) (17), DNA polymerase β (polβ) (18), and scaffold protein X-ray repair cross-complementing gene 1 (XRCC1) (19). After repair is completed, the PAR chains are degraded, restoring the cell to its normal state. Moreover, PARP-1 can stabilize replication forks by interacting with them, thereby maintaining genome stability (16). Besides DNA repair, PARP-1 has other functions such as modulating chromatin structure, influencing gene expression and epigenetic modification (20-22). Furthermore, PARP-1 can facilitate the loading and retention of RNA polymerase II at active promoters by interacting with it and enhance the transcriptional activation of downstream genes (23,24). Since PARP-1 plays a crucial role in maintaining genome stability and regulating cell fate, its overactivation can result in cell death or mutation, making it closely associated with various diseases such as cancer, neurodegenerative diseases, and inflammation. Exploring the function and mechanism of PARP-1 is of great importance for understanding life phenomena and developing new therapeutic strategies for related diseases.

Figure 1 The function of PARP-1. PARP-1 regulates various cellular processes such as DNA repair, chromatin remodeling, gene expression, and cell death by synthesizing PAR chains. CTCF, CCCTC-binding factor; DNA, deoxyribonucleic acid; DNA LigIII, DNA ligase III; DNA polβ, DNA polymerase β; PAR, poly(ADP-ribose); PARP-1, poly(ADP-ribose) polymerase-1; RNA pol II, RNA polymerase II; ROS, reactive oxygen species; XRCC1, X-ray repair cross-complementing gene 1.

The potential role of PARP-1 in the mechanism of tumor comorbidity with depression

Tumors and depression have a complex comorbid relationship and are mutually associated with increased risk (25,26). The exact mechanisms underlying this comorbidity are not fully elucidated, but recent evidence suggests that PARP-1 may be a key mediator through its effects on downstream molecular pathways, such as inflammation, innate immunity, DNA damage repair, and oxidative stress etc. (Figure 2).

Figure 2 The potential role of PARP-1 in the mechanism of tumor comorbidity with depression. PARP-1 plays an important role in the comorbidity mechanisms of tumors and depression by influencing downstream molecular mechanisms. The main influencing factors include inflammatory factors, innate immune activation, DNA damage repair, oxidative stress, etc. HR, homologous recombination repair; IL-1, interleukin-1; IL-2, interleukin-2; IL-6, interleukin-6; MyD88, myeloid differentiation factor 88; NF-κB, nuclear factor kappa-B; PARP-1, poly(ADP-ribose) polymerase-1; TLR4, Toll-like receptor 4; TNF-α, tumor necrosis factor α.

Inflammatory factors

Up to 15% of malignant tumors worldwide are induced by infections, such as bacterial, viral, and parasitic infections, all of which can induce abnormal inflammatory responses in the body, leading to the occurrence of malignant tumors (27). Numerous basic studies have also confirmed the close relationship between inflammation and tumors (28,29). The tumor matrix and microenvironment contain a large number of inflammatory cells and mediators, which can affect the growth, metastasis, and angiogenesis of tumor cells (30). In this cellular environment, the imbalance between pro-inflammatory and anti-inflammatory mechanisms is often the trigger signal for abnormal proliferation of tumor cells. Common pro-inflammatory cytokines include interleukin (IL)-1, IL-2, IL-6, interferon γ (IFN-γ), and tumor necrosis factor α (TNF-α), whose elevated expression levels are closely related to the occurrence and development of various cancers (31-35). PARP-1 is also involved in pathological physiological processes such as inflammation. For example, PARP-1 can regulate the nuclear factor-kappa B (NF-κB) signaling pathway, enhance the transcriptional activity of NF-κB on pro-inflammatory factors such as TNF-α, IL-6, and inducible nitric oxide synthase, thereby stimulating the proliferation, invasion, and metastasis of tumor cells and inhibiting the immune system’s clearance of tumors (36). Dörsam et al. (37) used transgenic mouse models and human tissue specimens to analyze the role of PARP-1 in colorectal cancer and found that PARP-1 can promote inflammation-driven colorectal tumor growth. Other studies have shown that PARP-1 affects the occurrence and development of leukemia (38), breast cancer (39), and ovarian cancer (40) through the NF-κB signaling pathway. Similar to the inflammatory profile observed in cancer patients, researchers have identified activated inflammatory pathways in individuals with depression, evidenced by significantly elevated levels of pro-inflammatory cytokines [e.g., IL-6, TNF-α, C-reactive protein (CRP)] and related signaling molecules in serum and the central nervous system. These findings correlate closely with core pathophysiological mechanisms of depression, including dysregulated neurotransmitter metabolism (e.g., serotonin depletion), neuroendocrine dysfunction [e.g., hypothalamic-pituitary-adrenal axis (HPA) axis hyperactivation], impaired neuroplasticity (e.g., reduced hippocampal neurogenesis), and behavioral abnormalities. Chronic inflammation is considered a critical driver of depression’s onset and progression. In addition, research has shown that the inflammatory factor NF-κB is a key pathway affecting the occurrence and development of depression (41). On one hand, NF-κB can promote inflammation by increasing the expression of pro-inflammatory factors such as TNF-α, IL-1β, and IL-6, thereby affecting neurotransmitter synthesis and release, leading to neuronal dysfunction and neurodegenerative changes (42,43). On the other hand, NF-κB can also regulate processes such as neurogenesis, synaptic plasticity, and neuroprotection by regulating the expression of neurotrophic factors such as brain-derived neurotrophic factor (BDNF), thereby affecting emotional and cognitive functions (44). In addition, NF-κB can interact with other signaling pathways such as Notch and Wnt to further regulate the expression of depression-related genes (45). Therefore, the NF-κB pathway is a potential therapeutic target for depression. Ahmadimanesh et al. (46) showed that PARP-1 activity in peripheral blood mononuclear cells from untreated depressed patients was significantly higher than that in controls. Increased PARP-1 activity was accompanied by activation of NF-κB and release of downstream pro-inflammatory cytokines. This suggests that PARP-1 expression activity in depressed patients is closely related to inflammation. Currently, there are few direct studies on PARP-1 and depression. Based on the relevance between inflammation pathways and depression pathogenesis as well as PARP-1’s role in inflammation mechanisms whether PARP-1 can affect depression through inflammation pathways may be a future research hotspot.

Oxidative stress

Oxidative stress is a physiological state caused by an excess of reactive oxygen species (ROS) and an imbalance in antioxidant defense, which can damage the cellular structure and function of biological organisms (47). Many studies have shown that cancer cells produce more ROS than normal cells, such as abnormally elevated levels of ROS found in B-cell tumors (48), gastric cancer (49), colorectal cancer (50), and uterine fibroids (51). Abnormally elevated levels of ROS can induce cancer by causing DNA damage and chromosomal instability, activating oncogenes or inactivating tumor suppressor genes (52). Moreover, ROS also has a signaling role in cancer, affecting the expression of some hub genes in signaling pathways as well as the expression of proteases and receptors, thereby promoting cell proliferation, invasion, and metastasis of tumors (53,54). The relationship between PARP-1 and oxidative stress has been a research hotspot. On one hand, PARP-1 can maintain the genome stability of tumor cells by repairing DNA damage, thereby promoting tumor survival and drug resistance (55). On the other hand, PARP-1 can also exacerbate or mediate cell damage caused by oxidative stress through pathways such as promoting lipid peroxidation, increasing ROS production, inducing ferroptosis, and regulating hypoxia-inducible factors, inducing tumor occurrence (56). Hocsak et al. (57) showed that inhibition of PARP-1 reduced ROS-induced cell death and mitochondrial ROS production under oxidative stress. Besides tumors, oxidative stress is considered to be one of the important factors in the pathogenesis of depression. Many studies have confirmed that ROS levels in depressed patients are higher than those in normal individuals, while antioxidant defense capacity is reduced, leading to increased oxidative stress (58-60). Increased oxidative stress can cause a series of adverse consequences, such as inflammation, neurodegeneration, and neuronal death, thereby affecting neurotransmitters, neurogenesis, and synaptic plasticity-related neurobiological processes associated with depression (47). In addition, some factors that cause excessive free radical production, such as smoking, alcohol consumption, overweight or excessive exercise, are also related to the occurrence of depression (61). As a key protein in the oxidative stress pathway, the role of PARP-1 in the pathogenesis of depression is gradually being revealed. Szebeni et al. (62) found that compared with normal controls, PARP-1 gene expression increased in the white matter of the prefrontal cortex in major depressive disorder (MDD) patients and was accompanied by increased brain donor oxidation levels and telomere shortening (63). Adaikalakoteswari et al. (64) also confirmed that under oxidative stress conditions, PARP-1 expression levels and activity were significantly upregulated. Therefore, PARP-1 may participate in the pathogenesis of depression through oxidative stress. This will be a new research direction worth exploring.

DNA damage

Tumors result from genome instability, which is mainly caused by DNA damage (65). DNA damage refers to any abnormal change in the structure or sequence of DNA molecules that affects their function and integrity (66). DNA damage can be induced by endogenous or exogenous factors such as free radicals, chemicals, ultraviolet radiation, viruses, and inflammation (67,68). Unrepaired DNA damage can lead to gene mutations that activate oncogenes or inactivate tumor suppressor genes, thereby promoting tumor initiation and progression. PARP-1 is a key protein involved in DNA damage repair. On one hand, it can inhibit homologous recombination repair (HRR) of double-strand DNA breaks, leading to genome instability and chromosomal aberrations (69,70). On the other hand, it can also modulate some tumor-related transcription factors through poly(ADP-ribosyl)ation modification, such as NF-κB, hypoxia-inducible factor-1alpha (HIF-1α), p53, AP-1 (71). Furthermore, PARP-1 can influence oncogene expression by binding to chromatin or interacting with other chromatin regulatory factors, enhancing tumor adaptability (72,73). Recently, researchers have discovered that DNA damage also plays a significant role in the pathogenesis of depression. 8-hydroxyguanine (8oxoG) is an oxidized DNA nucleoside and the most widely used DNA damage biomarker in depression (74,75). Several studies have found that 8-oxoG levels in urine, plasma and brain white matter of depressed patients are markedly elevated (62,76-78) and correlate with depression severity (79). Although few studies have examined PARP-1 in depression, as a key factor in DNA damage repair, PARP-1 may be a potential target for the mechanism of tumor comorbidity with depression.

Innate immune activation

Innate immune activation is a key factor in tumor pathogenesis, involving multiple signaling pathways and cytokines. On one hand, innate immune activation can detect DNA released by tumor cells through the cGAS-STING pathway, which induces the production of IFNs and other immune-stimulating factors. These factors promote tumor mutation and evolution, increasing tumor heterogeneity and drug resistance (80-82). On the other hand, it can also modulate the tumor microenvironment through signaling molecules such as Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), interleukin-1 receptor-associated kinase 4 (IRAK4), affecting the function and polarization state of innate immune cells such as tumor-associated macrophages, neutrophils, natural killer cells, dendritic cells (83). Recently, more research has revealed that PARP-1 can influence innate immune activation in various ways. PARP-1 can recognize and bind to DNA damage sites and produce a large amount of PAR. PAR can act as a danger signal to induce innate immune cells to secrete inflammatory factors or IFNs (84). Moreover, PARP-1 can regulate its function by interacting with other proteins through PAR (85). Lin et al. (86) reported that PARP-1 can bind to innate immune receptors or signaling molecules such as TLR4, MyD88, IRAK4, affecting their recognition and response to tumors or viruses. Kim et al. (87) showed that PARP-1 can also regulate gene expression through PAR to affect the differentiation and polarization of immune cells. Sobczak et al. (88) demonstrate that PARP-1 promotes macrophage polarization toward the M1 phenotype, enhancing bactericidal and pro-inflammatory functions. Similarly, in psychoneuroimmunology, research has elucidated the link between innate immune activation and depression (89,90). Such activation triggers microglia to release oxidative stress molecules, including ROS, nitric oxide, and reactive nitrogen species, which induce neuronal oxidative damage and apoptosis, contributing to depressive symptoms (91). Consequently, PARP-1 emerges as a pivotal link between innate immune activation and depression pathogenesis, positioning it as a promising focus for future studies on depression and related immune mechanisms.

The application of PARP-1 inhibitors in tumor comorbidity

PARP-1 inhibitors are drugs that block the activity of PARP-1 and are mainly used to treat solid tumors with BRCA1/2 mutations. Evidence also indicates that PARP1 is linked to oxidative stress, inflammatory responses, and neurological disorders, suggesting its potential role in depression’s pathogenesis (4,92,93). Thus, PARP-1 inhibitors may alleviate depression symptoms by modulating neurobiological processes. Based on the comorbidity mechanism of tumors and depression and the key role of PARP-1 in it, PARP-1 inhibitors have the potential to be an effective intervention for patients with both conditions.

Application of PARP-1 inhibitors in tumors

PARP-1 is a DNA damage repair enzyme that can repair DNA single-strand breaks through PARylation. Tumor cells with homologous recombination repair defects (HRD) lose the function of PARP-1, which prevents them from effectively repairing DNA double-strand breaks, leading to genomic instability and cell death. This strategy is called ‘synthetic lethality’ (94,95). Currently, the National Medical Products Administration (NMPA) of China has approved 4 PARP inhibitors (olaparib, niraparib, rucaparib, and talazoparib) for clinical treatment, mainly for adult patients with platinum-sensitive recurrent epithelial ovarian cancer, fallopian tube cancer or primary peritoneal cancer who have achieved complete or partial remission with platinum-containing chemotherapy. A phase III clinical randomized controlled trial showed that olaparib maintenance treatment significantly improved the progression-free survival (PFS) of advanced ovarian cancer patients (96). A multicenter, double-blind, randomized, controlled phase III clinical trial supported the long-term safe use of niraparib for maintenance treatment of recurrent ovarian cancer (97). Another phase III clinical trial published in the New England Journal showed that olaparib maintenance treatment prolonged the PFS of patients with breast cancer susceptibility gene (BRCA)-mutated metastatic pancreatic cancer compared with placebo (98). A phase III double-blind randomized trial on breast cancer by Tutt et al. (99) showed that olaparib maintenance treatment after local treatment or neoadjuvant chemotherapy significantly increased the survival period without invasive or distant disease compared with placebo. Moreover, multiple clinical trials are actively investigating the efficacy and safety of new PARP inhibitors combined with other anti-cancer treatments in other types of cancer (100-102).

Application of PARP-1 inhibitors in depression

PARP-1 has been previously reported to be closely related to various pathogenic mechanisms of depression, and the application of PARP-1 inhibitors in depression has become a research hotspot. Studies have found elevated levels of inflammatory cytokines IL-1β and TNF-α in human patients with MDD, and PARP-1 inhibition can block this effect (46,62,103). 3-aminobenzamide (3-AB) (104) and 5-aminoisoxazole-4-carboxamide (5-AIQ) (105) are effective PARP-1 inhibitors. Ordway et al. (106) showed the antidepressant activity of 3-AB and 5-AIQ in rodent models, which may be related to the anti-inflammatory effect of PARP-1 inhibition, suggesting that PARP-1 is a potential molecular target for antidepressant treatment. Sriram et al. (107) also demonstrated that 3-AB can reverse lipopolysaccharide (LPS)-induced depressive symptoms in mice. Minocycline, a high-affinity PARP-1 inhibitor, has antidepressant effects in both human and rodent models (108-111). An open-label study by Soczynska et al. (112) reported that minocycline as an adjunctive medication for bipolar depression patients also has antidepressant effects, possibly by targeting inflammatory cytokines. Moreover, several other studies indicated that minocycline adjunctive treatment can improve the clinical symptoms of patients with treatment-resistant depression (113-115). These results suggest that PARP-1 inhibitors have potential value in the treatment of depression. Interestingly, recent studies have reported conflicting findings regarding the role of PARP-1 in depression. A study of medicated patients with depression found lower mRNA levels of PARP-1 in the whole blood of depressed individuals compared to healthy controls, with electroconvulsive therapy (ECT) exerting no significant effect on PARP-1 levels. However, higher baseline PARP-1 was weakly correlated with greater emotional improvement post-ECT. These findings challenge the notion of a straightforward causal relationship between elevated PARP-1 levels and depression, suggesting instead that PARP-1 may exert a bidirectional regulatory role in depression’s pathogenesis or that its function varies across different stages and physiological states. Such insights offer new avenues for investigating the relationship between PARP-1 and depression and for refining the use of PARP-1 inhibitors in antidepressant therapy (116).

Application of PARP-1 inhibitors in tumors with depression

Although the role of PARP-1 in tumors and depression-related diseases has been widely reported, its application in patients with tumors complicated by depression is still limited. Benjamin et al. (9) reported the effect of a PARP inhibitor on the depressive state of a human subject. The patient was a 61-year-old woman with a 20-year history of mild depression who received niraparib maintenance treatment for recurrent ovarian cancer. During recurrence, the patient developed severe depression and generalized anxiety, which could not be relieved after treatment with multiple antidepressants. After using niraparib, the patient’s anxiety and depression symptoms quickly improved, and the effect lasted for 10–14 days. Due to the adverse reaction of bone marrow suppression, the patient had stopped using niraparib several times during the treatment, and each time after stopping the medication, depression and anxiety worsened significantly, and the symptoms improved after re-administration. This case, involving repeated use and discontinuation of the PARP inhibitor and its impact on different depressive outcomes, underscores the strong temporal correlation between PARP inhibitor use and depressive states. It also suggests the potential value of PARP inhibitors in treating patients with both cancer and depression. Future research should further investigate the pharmacological basis of niraparib’s antidepressant and anxiolytic effects, as well as its potential use in treating other mental health disorders. Additionally, the potential adverse effects and safety concerns associated with long-term niraparib use must be considered, with strategies such as adjusting dosing regimens or modifying niraparib or similar compounds’ structures to ensure rational use in mental health treatment. This case not only provides insights into a novel role for Niraparib but also highlights the unexpected benefits that drugs may offer during treatment, warranting further attention and investigation in clinical practice.

Conclusions

The occurrence and development of tumors with depression involve multiple comorbidity mechanisms, with PARP-1 playing a key role in several links. It is closely related to multiple pathways, including inflammatory response, oxidative stress, DNA damage, and innate immune activation. Currently, basic research on PARP-1 and the clinical application of PARP inhibitors are mainly focused on the field of tumors. However, the role of PARP-1 and PARP inhibitors in depression-related diseases remains underexplored. For instance, is there a connection between non-coding RNAs targeting PARP-1 and depression? Do first-line antidepressants affect PARP-1-related pathways? These questions warrant further investigation in both basic and clinical research. As research on the pathogenesis of tumor complicated by depression deepens, mechanism research centered on PARP-1 and drug research targeting PARP-1 are expected to make new progress in the treatment of tumor complicated by depression.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://tcr.amegroups.com/article/view/10.21037/tcr-2025-739/rc

Peer Review File: Available at https://tcr.amegroups.com/article/view/10.21037/tcr-2025-739/prf

Funding: This research was supported by the Guangxi Natural Science Foundation (No. 2024GXNSFBA010154) and the Youth Science Foundation of Guangxi Medical University (No. GXMUYSF202338).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tcr.amegroups.com/article/view/10.21037/tcr-2025-739/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

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References

1. Perna G, Pinto E, Spiti A, et al. Foundations for a Personalized Psycho-Oncology: The State of the Art. J Pers Med 2024;14:892. [Crossref] [PubMed]
2. Pitman A, Suleman S, Hyde N, et al. Depression and anxiety in patients with cancer. BMJ 2018;361:k1415. [Crossref] [PubMed]
3. CHAMBON P. WEILL JD, MANDEL P. Nicotinamide mononucleotide activation of new DNA-dependent polyadenylic acid synthesizing nuclear enzyme. Biochem Biophys Res Commun 1963;11:39-43. [Crossref] [PubMed]
4. Arruri VK, Gundu C, Khan I, et al. PARP overactivation in neurological disorders. Mol Biol Rep 2021;48:2833-41. [Crossref] [PubMed]
5. Amor-Guéret M. Loss of cytidine deaminase expression as a potential attempt to counteract the process of carcinogenesis by reducing basal PARP-1 activity and increasing tau levels. Biochim Biophys Acta Mol Basis Dis 2024;1870:167213. [Crossref] [PubMed]
6. Wu Y, Xu S, Cheng S, et al. Clinical application of PARP inhibitors in ovarian cancer: from molecular mechanisms to the current status. J Ovarian Res 2023;16:6. [Crossref] [PubMed]
7. Kupczyk P, Simiczyjew A, Marczuk J, et al. PARP1 as a Marker of an Aggressive Clinical Phenotype in Cutaneous Melanoma-A Clinical and an In Vitro Study. Cells 2021;10:286. [Crossref] [PubMed]
8. Schiewer MJ, Knudsen KE. Transcriptional roles of PARP1 in cancer. Mol Cancer Res 2014;12:1069-80. [Crossref] [PubMed]
9. Jewett BE, Miller MN, Ligon LA, et al. Rapid and temporary improvement of depression and anxiety observed following niraparib administration: a case report. BMC Psychiatry 2020;20:171. [Crossref] [PubMed]
10. Mukhopadhyay P, Horváth B, Rajesh M, et al. PARP inhibition protects against alcoholic and non-alcoholic steatohepatitis. J Hepatol 2017;66:589-600. [Crossref] [PubMed]
11. Kovacs K, Vaczy A, Fekete K, et al. PARP Inhibitor Protects Against Chronic Hypoxia/Reoxygenation-Induced Retinal Injury by Regulation of MAPKs, HIF1α, Nrf2, and NFκB. Invest Ophthalmol Vis Sci 2019;60:1478-90. [Crossref] [PubMed]
12. Kovács D, Vántus VB, Vámos E, et al. Olaparib: A Clinically Applied PARP Inhibitor Protects from Experimental Crohn's Disease and Maintains Barrier Integrity by Improving Bioenergetics through Rescuing Glycolysis in Colonic Epithelial Cells. Oxid Med Cell Longev 2021;2021:7308897. [Crossref] [PubMed]
13. Regdon Z, Demény MA, Kovács K, et al. High-content screening identifies inhibitors of oxidative stress-induced parthanatos: cytoprotective and anti-inflammatory effects of ciclopirox. Br J Pharmacol 2021;178:1095-113. [Crossref] [PubMed]
14. Lindqvist D, Dhabhar FS, James SJ, et al. Oxidative stress, inflammation and treatment response in major depression. Psychoneuroendocrinology 2017;76:197-205. [Crossref] [PubMed]
15. Rawdin BJ, Mellon SH, Dhabhar FS, et al. Dysregulated relationship of inflammation and oxidative stress in major depression. Brain Behav Immun 2013;31:143-52. [Crossref] [PubMed]
16. Bürkle A. Physiology and pathophysiology of poly(ADP-ribosyl)ation. Bioessays 2001;23:795-806. [Crossref] [PubMed]
17. Stankova K, Ivanova K, Mladenov E, et al. Conformational transitions of proteins engaged in DNA double-strand break repair, analysed by tryptophan fluorescence emission and FRET. Biochem J 2012;443:701-9. [Crossref] [PubMed]
18. Moor NA, Vasil'eva IA, Kuznetsov NA, et al. Human apurinic/apyrimidinic endonuclease 1 is modified in vitro by poly(ADP-ribose) polymerase 1 under control of the structure of damaged DNA. Biochimie 2020;168:144-55. [Crossref] [PubMed]
19. Zhao ML, Stefanick DF, Nadalutti CA, et al. Temporal recruitment of base excision DNA repair factors in living cells in response to different micro-irradiation DNA damage protocols. DNA Repair (Amst) 2023;126:103486. [Crossref] [PubMed]
20. Krishnakumar R, Kraus WL. PARP-1 regulates chromatin structure and transcription through a KDM5B-dependent pathway. Mol Cell 2010;39:736-49. [Crossref] [PubMed]
21. Merkuryev AV, Egorov VV. Role of PARP-1 structural and functional features in PARP-1 inhibitors development. Bioorg Chem 2025;156:108188. [Crossref] [PubMed]
22. Pinton G, Boumya S, Ciriolo MR, et al. Epigenetic Insights on PARP-1 Activity in Cancer Therapy. Cancers (Basel) 2022;15:6. [Crossref] [PubMed]
23. Matveeva EA, Dhahri H, Fondufe-Mittendorf Y. PARP1's Involvement in RNA Polymerase II Elongation: Pausing and Releasing Regulation through the Integrator and Super Elongation Complex. Cells 2022;11:3202. [Crossref] [PubMed]
24. Eleazer R, Fondufe-Mittendorf YN. The multifaceted role of PARP1 in RNA biogenesis. Wiley Interdiscip Rev RNA 2021;12:e1617. [Crossref] [PubMed]
25. Mitchell AJ, Chan M, Bhatti H, et al. Prevalence of depression, anxiety, and adjustment disorder in oncological, haematological, and palliative-care settings: a meta-analysis of 94 interview-based studies. Lancet Oncol 2011;12:160-74. [Crossref] [PubMed]
26. Pinquart M, Duberstein PR. Depression and cancer mortality: a meta-analysis. Psychol Med 2010;40:1797-810. [Crossref] [PubMed]
27. Kuper H, Adami HO, Trichopoulos D. Infections as a major preventable cause of human cancer. J Intern Med 2000;248:171-83. [Crossref] [PubMed]
28. Greten FR, Grivennikov SI. Inflammation and Cancer: Triggers, Mechanisms, and Consequences. Immunity 2019;51:27-41. [Crossref] [PubMed]
29. Zhao H, Wu L, Yan G, et al. Inflammation and tumor progression: signaling pathways and targeted intervention. Signal Transduct Target Ther 2021;6:263. [Crossref] [PubMed]
30. Currier MB, Nemeroff CB. Depression as a risk factor for cancer: from pathophysiological advances to treatment implications. Annu Rev Med 2014;65:203-21. [Crossref] [PubMed]
31. Liu C, Wu K, Li C, et al. SPP1+ macrophages promote head and neck squamous cell carcinoma progression by secreting TNF-α and IL-1β. J Exp Clin Cancer Res 2024;43:332. [Crossref] [PubMed]
32. Liu X. The paradoxical role of IFN-gamma in cancer: Balancing immune activation and immune evasion. Pathol Res Pract 2025;272:156046. [Crossref] [PubMed]
33. Kumari N, Dwarakanath BS, Das A, et al. Role of interleukin-6 in cancer progression and therapeutic resistance. Tumour Biol 2016;37:11553-72. [Crossref] [PubMed]
34. Park MD, Le Berichel J, Hamon P, et al. Hematopoietic aging promotes cancer by fueling IL-1⍺-driven emergency myelopoiesis. Science 2024;386:eadn0327. [Crossref] [PubMed]
35. Tanigawa K, Redmond WL. Current landscape and future prospects of interleukin-2 receptor (IL-2R) agonists in cancer immunotherapy. Oncoimmunology 2025;14:2452654. [Crossref] [PubMed]
36. Pazzaglia S, Pioli C. Multifaceted Role of PARP-1 in DNA Repair and Inflammation: Pathological and Therapeutic Implications in Cancer and Non-Cancer Diseases. Cells 2019;9:41. [Crossref] [PubMed]
37. Dörsam B, Seiwert N, Foersch S, et al. PARP-1 protects against colorectal tumor induction, but promotes inflammation-driven colorectal tumor progression. Proc Natl Acad Sci U S A 2018;115:E4061-70. [Crossref] [PubMed]
38. Hleihel R, Skayneh H, de Thé H, et al. Primary cells from patients with adult T cell leukemia/lymphoma depend on HTLV-1 Tax expression for NF-κB activation and survival. Blood Cancer J 2023;13:67. [Crossref] [PubMed]
39. Pavitra E, Kancharla J, Gupta VK, et al. The role of NF-κB in breast cancer initiation, growth, metastasis, and resistance to chemotherapy. Biomed Pharmacother 2023;163:114822. [Crossref] [PubMed]
40. Hu Z, Cang R, Zhang H, et al. The expression levels of NF-κB and IKKβ in epithelial ovarian cancer and their correlation with drug resistance-related genes MDR1, TOPOII, and ERCC1. Acta Biochim Pol 2023;70:23-9. [Crossref] [PubMed]
41. Torres MA, Pace TW, Liu T, et al. Predictors of depression in breast cancer patients treated with radiation: role of prior chemotherapy and nuclear factor kappa B. Cancer 2013;119:1951-9. [Crossref] [PubMed]
42. Wang X, Lin C, Jin S, et al. Cannabidiol alleviates neuroinflammation and attenuates neuropathic pain via targeting FKBP5. Brain Behav Immun 2023;111:365-75. [Crossref] [PubMed]
43. Li Y, Xia Y, Yin S, et al. Targeting Microglial α-Synuclein/TLRs/NF-kappaB/NLRP3 Inflammasome Axis in Parkinson's Disease. Front Immunol 2021;12:719807. [Crossref] [PubMed]
44. Caviedes A, Lafourcade C, Soto C, et al. BDNF/NF-κB Signaling in the Neurobiology of Depression. Curr Pharm Des 2017;23:3154-63. [Crossref] [PubMed]
45. Liao J, Zeng G, Fang W, et al. Increased Notch2/NF-κB Signaling May Mediate the Depression Susceptibility: Evidence from Chronic Social Defeat Stress Mice and WKY Rats. Physiol Behav 2021;228:113197. [Crossref] [PubMed]
46. Ahmadimanesh M, Abbaszadegan MR, Morshedi Rad D, et al. Effects of selective serotonin reuptake inhibitors on DNA damage in patients with depression. J Psychopharmacol 2019;33:1364-76. [Crossref] [PubMed]
47. Correia AS, Cardoso A, Vale N. Oxidative Stress in Depression: The Link with the Stress Response, Neuroinflammation, Serotonin, Neurogenesis and Synaptic Plasticity. Antioxidants (Basel) 2023;12:470. [Crossref] [PubMed]
48. Sousa-Pimenta M, Estevinho MM, Sousa Dias M, et al. Oxidative Stress and Inflammation in B-Cell Lymphomas. Antioxidants (Basel) 2023;12:936. [Crossref] [PubMed]
49. Liu Y, Shi Y, Han R, et al. Signaling pathways of oxidative stress response: the potential therapeutic targets in gastric cancer. Front Immunol 2023;14:1139589. [Crossref] [PubMed]
50. Bardelčíková A, Šoltys J, Mojžiš J. Oxidative Stress, Inflammation and Colorectal Cancer: An Overview. Antioxidants (Basel) 2023;12:901. [Crossref] [PubMed]
51. AlAshqar A, Lulseged B, Mason-Otey A, et al. Oxidative Stress and Antioxidants in Uterine Fibroids: Pathophysiology and Clinical Implications. Antioxidants (Basel) 2023;12:807. [Crossref] [PubMed]
52. Srinivas US, Tan BWQ, Vellayappan BA, et al. ROS and the DNA damage response in cancer. Redox Biol 2019;25:101084. [Crossref] [PubMed]
53. Glorieux C, Liu S, Trachootham D, et al. Targeting ROS in cancer: rationale and strategies. Nat Rev Drug Discov 2024;23:583-606. [Crossref] [PubMed]
54. Moloney JN, Cotter TG. ROS signalling in the biology of cancer. Semin Cell Dev Biol 2018;80:50-64. [Crossref] [PubMed]
55. Kim DS, Camacho CV, Kraus WL. Alternate therapeutic pathways for PARP inhibitors and potential mechanisms of resistance. Exp Mol Med 2021;53:42-51. [Crossref] [PubMed]
56. Wen W, Jin K, Che Y, et al. Arnicolide D Inhibits Oxidative Stress-induced Breast Cancer Cell Growth and Invasion through Apoptosis, Ferroptosis, and Parthanatos. Anticancer Agents Med Chem 2024;24:836-44. [Crossref] [PubMed]
57. Hocsak E, Szabo V, Kalman N, et al. PARP inhibition protects mitochondria and reduces ROS production via PARP-1-ATF4-MKP-1-MAPK retrograde pathway. Free Radic Biol Med 2017;108:770-84. [Crossref] [PubMed]
58. Leonard B, Maes M. Mechanistic explanations how cell-mediated immune activation, inflammation and oxidative and nitrosative stress pathways and their sequels and concomitants play a role in the pathophysiology of unipolar depression. Neurosci Biobehav Rev 2012;36:764-85. [Crossref] [PubMed]
59. Scapagnini G, Davinelli S, Drago F, et al. Antioxidants as antidepressants: fact or fiction? CNS Drugs 2012;26:477-90. [Crossref] [PubMed]
60. Hovatta I, Juhila J, Donner J. Oxidative stress in anxiety and comorbid disorders. Neurosci Res 2010;68:261-75. [Crossref] [PubMed]
61. Bhatt S, Nagappa AN, Patil CR. Role of oxidative stress in depression. Drug Discov Today 2020;25:1270-6. [Crossref] [PubMed]
62. Szebeni A, Szebeni K, DiPeri TP, et al. Elevated DNA Oxidation and DNA Repair Enzyme Expression in Brain White Matter in Major Depressive Disorder. Int J Neuropsychopharmacol 2017;20:363-73. [PubMed]
63. Szebeni A, Szebeni K, DiPeri T, et al. Shortened telomere length in white matter oligodendrocytes in major depression: potential role of oxidative stress. Int J Neuropsychopharmacol 2014;17:1579-89. [Crossref] [PubMed]
64. Adaikalakoteswari A, Rema M, Mohan V, et al. Oxidative DNA damage and augmentation of poly(ADP-ribose) polymerase/nuclear factor-kappa B signaling in patients with type 2 diabetes and microangiopathy. Int J Biochem Cell Biol 2007;39:1673-84. [Crossref] [PubMed]
65. O'Connor MJ. Targeting the DNA Damage Response in Cancer. Mol Cell 2015;60:547-60. [Crossref] [PubMed]
66. Huang R, Zhou PK. DNA damage repair: historical perspectives, mechanistic pathways and clinical translation for targeted cancer therapy. Signal Transduct Target Ther 2021;6:254. [Crossref] [PubMed]
67. Groelly FJ, Fawkes M, Dagg RA, et al. Targeting DNA damage response pathways in cancer. Nat Rev Cancer 2023;23:78-94. [Crossref] [PubMed]
68. Kay J, Thadhani E, Samson L, et al. Inflammation-induced DNA damage, mutations and cancer. DNA Repair (Amst) 2019;83:102673. [Crossref] [PubMed]
69. Chapman JR, Taylor MR, Boulton SJ. Playing the end game: DNA double-strand break repair pathway choice. Mol Cell 2012;47:497-510. [Crossref] [PubMed]
70. Price BD, D'Andrea AD. Chromatin remodeling at DNA double-strand breaks. Cell 2013;152:1344-54. [Crossref] [PubMed]
71. Nagele A. Poly(ADP-ribosyl)ation as a fail-safe, transcription-independent, suicide mechanism in acutely DNA-damaged cells: a hypothesis. Radiat Environ Biophys 1995;34:251-4. [Crossref] [PubMed]
72. Messner S, Altmeyer M, Zhao H, et al. PARP1 ADP-ribosylates lysine residues of the core histone tails. Nucleic Acids Res 2010;38:6350-62. [Crossref] [PubMed]
73. Poirier GG, de Murcia G, Jongstra-Bilen J, et al. Poly(ADP-ribosyl)ation of polynucleosomes causes relaxation of chromatin structure. Proc Natl Acad Sci U S A 1982;79:3423-7. [Crossref] [PubMed]
74. Hazra TK, Hill JW, Izumi T, et al. Multiple DNA glycosylases for repair of 8-oxoguanine and their potential in vivo functions. Prog Nucleic Acid Res Mol Biol 2001;68:193-205. [Crossref] [PubMed]
75. Black CN, Bot M, Révész D, et al. The association between three major physiological stress systems and oxidative DNA and lipid damage. Psychoneuroendocrinology 2017;80:56-66. [Crossref] [PubMed]
76. Irie M, Asami S, Ikeda M, et al. Depressive state relates to female oxidative DNA damage via neutrophil activation. Biochem Biophys Res Commun 2003;311:1014-8. [Crossref] [PubMed]
77. Forlenza MJ, Miller GE. Increased serum levels of 8-hydroxy-2'-deoxyguanosine in clinical depression. Psychosom Med 2006;68:1-7. [Crossref] [PubMed]
78. Maes M, Mihaylova I, Kubera M, et al. Increased 8-hydroxy-deoxyguanosine, a marker of oxidative damage to DNA, in major depression and myalgic encephalomyelitis / chronic fatigue syndrome. Neuro Endocrinol Lett 2009;30:715-22. [PubMed]
79. Yi S, Nanri A, Matsushita Y, et al. Depressive symptoms and oxidative DNA damage in Japanese municipal employees. Psychiatry Res 2012;200:318-22. [Crossref] [PubMed]
80. Deng L, Liang H, Xu M, et al. STING-Dependent Cytosolic DNA Sensing Promotes Radiation-Induced Type I Interferon-Dependent Antitumor Immunity in Immunogenic Tumors. Immunity 2014;41:843-52. [Crossref] [PubMed]
81. Feng X, Tubbs A, Zhang C, et al. ATR inhibition potentiates ionizing radiation-induced interferon response via cytosolic nucleic acid-sensing pathways. EMBO J 2020;39:e104036. [Crossref] [PubMed]
82. Shen J, Zhao W, Ju Z, et al. PARPi Triggers the STING-Dependent Immune Response and Enhances the Therapeutic Efficacy of Immune Checkpoint Blockade Independent of BRCAness. Cancer Res 2019;79:311-9. [Crossref] [PubMed]
83. Demaria O, Cornen S, Daëron M, et al. Harnessing innate immunity in cancer therapy. Nature 2019;574:45-56. [Crossref] [PubMed]
84. Kim C, Wang XD, Yu Y. PARP1 inhibitors trigger innate immunity via PARP1 trapping-induced DNA damage response. Elife 2020;9:e60637. [Crossref] [PubMed]
85. Chiu LY, Huang DY, Lin WW. PARP-1 regulates inflammasome activity by poly-ADP-ribosylation of NLRP3 and interaction with TXNIP in primary macrophages. Cell Mol Life Sci 2022;79:108. [Crossref] [PubMed]
86. Lin SC, Lo YC, Wu H. Helical assembly in the MyD88-IRAK4-IRAK2 complex in TLR/IL-1R signalling. Nature 2010;465:885-90. [Crossref] [PubMed]
87. Kim MY, Zhang T, Kraus WL. Poly(ADP-ribosyl)ation by PARP-1: 'PAR-laying' NAD+ into a nuclear signal. Genes Dev 2005;19:1951-67. [Crossref] [PubMed]
88. Sobczak M, Zyma M, Robaszkiewicz A. The Role of PARP1 in Monocyte and Macrophage Commitment and Specification: Future Perspectives and Limitations for the Treatment of Monocyte and Macrophage Relevant Diseases with PARP Inhibitors. Cells 2020;9:2040. [Crossref] [PubMed]
89. Panjwani AA, Aguiar S, Gascon B, et al. Biomarker opportunities in the treatment of cancer-related depression. Trends Mol Med 2022;28:1050-69. [Crossref] [PubMed]
90. Dantzer R. Innate immunity at the forefront of psychoneuroimmunology. Brain Behav Immun 2004;18:1-6. [Crossref] [PubMed]
91. Matsumoto J, Dohgu S, Takata F, et al. TNF-α-sensitive brain pericytes activate microglia by releasing IL-6 through cooperation between IκB-NFκB and JAK-STAT3 pathways. Brain Res 2018;1692:34-44. [Crossref] [PubMed]
92. Li C, Wu J, Dong Q, et al. The crosstalk between oxidative stress and DNA damage induces neural stem cell senescence by HO-1/PARP1 non-canonical pathway. Free Radic Biol Med 2024;223:443-57. [Crossref] [PubMed]
93. Han Y, Wang C, Li X, et al. PARP-1 dependent cell death pathway (Parthanatos) mediates early brain injury after subarachnoid hemorrhage. Eur J Pharmacol 2024;978:176765. [Crossref] [PubMed]
94. Bryant HE, Schultz N, Thomas HD, et al. Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase. Nature 2005;434:913-7. [Crossref] [PubMed]
95. Lord CJ, Ashworth A. PARP inhibitors: Synthetic lethality in the clinic. Science 2017;355:1152-8. [Crossref] [PubMed]
96. Moore K, Colombo N, Scambia G, et al. Maintenance Olaparib in Patients with Newly Diagnosed Advanced Ovarian Cancer. N Engl J Med 2018;379:2495-505. [Crossref] [PubMed]
97. Mirza MR, Benigno B, Dørum A, et al. Long-term safety in patients with recurrent ovarian cancer treated with niraparib versus placebo: Results from the phase III ENGOT-OV16/NOVA trial. Gynecol Oncol 2020;159:442-8. [Crossref] [PubMed]
98. Golan T, Hammel P, Reni M, et al. Maintenance Olaparib for Germline BRCA-Mutated Metastatic Pancreatic Cancer. N Engl J Med 2019;381:317-27. [Crossref] [PubMed]
99. Tutt ANJ, Garber JE, Kaufman B, et al. Adjuvant Olaparib for Patients with BRCA1- or BRCA2-Mutated Breast Cancer. N Engl J Med 2021;384:2394-405. [Crossref] [PubMed]
100. Reiss KA, Mick R, Teitelbaum U, et al. Niraparib plus nivolumab or niraparib plus ipilimumab in patients with platinum-sensitive advanced pancreatic cancer: a randomised, phase 1b/2 trial. Lancet Oncol 2022;23:1009-20. [Crossref] [PubMed]
101. Robson ME, Im SA, Senkus E, et al. OlympiAD extended follow-up for overall survival and safety: Olaparib versus chemotherapy treatment of physician's choice in patients with a germline BRCA mutation and HER2-negative metastatic breast cancer. Eur J Cancer 2023;184:39-47. [Crossref] [PubMed]
102. Thiery-Vuillemin A, de Bono J, Hussain M, et al. Pain and health-related quality of life with olaparib versus physician's choice of next-generation hormonal drug in patients with metastatic castration-resistant prostate cancer with homologous recombination repair gene alterations (PROfound): an open-label, randomised, phase 3 trial. Lancet Oncol 2022;23:393-405. [Crossref] [PubMed]
103. Martínez-Zamudio RI, Ha HC. PARP1 enhances inflammatory cytokine expression by alteration of promoter chromatin structure in microglia. Brain Behav 2014;4:552-65. [Crossref] [PubMed]
104. Wallis RA, Panizzon KL, Girard JM. Traumatic neuroprotection with inhibitors of nitric oxide and ADP-ribosylation. Brain Res 1996;710:169-77. [Crossref] [PubMed]
105. Hendryk S, Czuba ZP, Jedrzejowska-Szypulka H, et al. Influence of 5-aminoisoquinolin-1-one (5-AIQ) on neutrophil chemiluminescence in rats with transient and prolonged focal cerebral ischemia and after reperfusion. J Physiol Pharmacol 2008;59:811-22. [PubMed]
106. Ordway GA, Szebeni A, Hernandez LJ, et al. Antidepressant-Like Actions of Inhibitors of Poly(ADP-Ribose) Polymerase in Rodent Models. Int J Neuropsychopharmacol 2017;20:994-1004. [Crossref] [PubMed]
107. Sriram CS, Jangra A, Gurjar SS, et al. Poly (ADP-ribose) polymerase-1 inhibitor, 3-aminobenzamide pretreatment ameliorates lipopolysaccharide-induced neurobehavioral and neurochemical anomalies in mice. Pharmacol Biochem Behav 2015;133:83-91. [Crossref] [PubMed]
108. Molina-Hernández M, Tellez-Alcántara NP, Pérez-García J, et al. Antidepressant-like actions of minocycline combined with several glutamate antagonists. Prog Neuropsychopharmacol Biol Psychiatry 2008;32:380-6. [Crossref] [PubMed]
109. O'Connor JC, Lawson MA, André C, et al. Lipopolysaccharide-induced depressive-like behavior is mediated by indoleamine 2,3-dioxygenase activation in mice. Mol Psychiatry 2009;14:511-22. [Crossref] [PubMed]
110. Arakawa S, Shirayama Y, Fujita Y, et al. Minocycline produced antidepressant-like effects on the learned helplessness rats with alterations in levels of monoamine in the amygdala and no changes in BDNF levels in the hippocampus at baseline. Pharmacol Biochem Behav 2012;100:601-6. [Crossref] [PubMed]
111. Saeedi Saravi SS, Amirkhanloo R, Arefidoust A, et al. On the effect of minocycline on the depressive-like behavior of mice repeatedly exposed to malathion: interaction between nitric oxide and cholinergic system. Metab Brain Dis 2016;31:549-61. [Crossref] [PubMed]
112. Soczynska JK, Kennedy SH, Alsuwaidan M, et al. A pilot, open-label, 8-week study evaluating the efficacy, safety and tolerability of adjunctive minocycline for the treatment of bipolar I/II depression. Bipolar Disord 2017;19:198-213. [Crossref] [PubMed]
113. Husain MI, Chaudhry IB, Husain N, et al. Minocycline as an adjunct for treatment-resistant depressive symptoms: A pilot randomised placebo-controlled trial. J Psychopharmacol 2017;31:1166-75. [Crossref] [PubMed]
114. Dean OM, Kanchanatawan B, Ashton M, et al. Adjunctive minocycline treatment for major depressive disorder: A proof of concept trial. Aust N Z J Psychiatry 2017;51:829-40. [Crossref] [PubMed]
115. Miyaoka T, Wake R, Furuya M, et al. Minocycline as adjunctive therapy for patients with unipolar psychotic depression: an open-label study. Prog Neuropsychopharmacol Biol Psychiatry 2012;37:222-6. [Crossref] [PubMed]
116. Ryan KM, McLoughlin DM. PARP1 and OGG1 in Medicated Patients With Depression and the Response to ECT. Int J Neuropsychopharmacol 2023;26:107-15. [Crossref] [PubMed]