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Mavroeidi, D.; Georganta, A.; Panagiotou, E.; Syrigos, K.; Souliotis, V.L. ATR Pathway as a Therapeutic Target for Cancer. Encyclopedia. Available online: (accessed on 16 April 2024).
Mavroeidi D, Georganta A, Panagiotou E, Syrigos K, Souliotis VL. ATR Pathway as a Therapeutic Target for Cancer. Encyclopedia. Available at: Accessed April 16, 2024.
Mavroeidi, Dimitra, Anastasia Georganta, Emmanouil Panagiotou, Konstantinos Syrigos, Vassilis L. Souliotis. "ATR Pathway as a Therapeutic Target for Cancer" Encyclopedia, (accessed April 16, 2024).
Mavroeidi, D., Georganta, A., Panagiotou, E., Syrigos, K., & Souliotis, V.L. (2024, March 07). ATR Pathway as a Therapeutic Target for Cancer. In Encyclopedia.
Mavroeidi, Dimitra, et al. "ATR Pathway as a Therapeutic Target for Cancer." Encyclopedia. Web. 07 March, 2024.
ATR Pathway as a Therapeutic Target for Cancer

The DNA damage response (DDR) system is a complicated network of signaling pathways that detects and repairs DNA damage or induces apoptosis. Critical regulators of the DDR network include the DNA damage kinases ataxia telangiectasia mutated Rad3-related kinase (ATR) and ataxia-telangiectasia mutated (ATM). The ATR pathway coordinates processes such as replication stress response, stabilization of replication forks, cell cycle arrest, and DNA repair. ATR inhibition disrupts these functions, causing a reduction of DNA repair, accumulation of DNA damage, replication fork collapse, inappropriate mitotic entry, and mitotic catastrophe. Data have shown that the inhibition of ATR can lead to synthetic lethality in ATM-deficient malignancies. In addition, ATR inhibition plays a significant role in the activation of the immune system by increasing the tumor mutational burden and neoantigen load as well as by triggering the accumulation of cytosolic DNA and subsequently inducing the cGAS-STING pathway and the type I IFN response. 

ATR DDR ATM kinases inhibition synthetic lethality

1. Introduction

Cells face constant exposure to multiple DNA damage sources, both endogenous (e.g., oxidation, alkylation, hydrolysis, mismatch of DNA bases) and exogenous (genotoxic chemicals, UV light, ionizing radiation, etc.) [1][2][3][4][5]. To neutralize these threats and ensure genomic stability, cells have developed several mechanisms, collectively called the DNA damage response (DDR) network [6]. The DDR system includes damage sensors, transducer kinases, and effectors to maintain genomic integrity. Interestingly, recent data have shown that the deregulated DDR network is capable of activating the host immune system [7]. These results potentially provide a novel strategy for enhancing the efficacy of immunotherapy.
On the other hand, deregulated DDR pathways trigger mutagenesis and genomic instability, thus getting implicated in the onset and progression of cancer. Cancer cells divide continuously due to a breakdown of the mechanisms regulating the cell cycle. The increased proliferation rate and the DNA repair defects in cancer cells make these cells more vulnerable to specific DDR inhibition [8]. Hence, DDR inhibitors, a class of drugs that can modify the DDR network, have recently gained great attention in cancer treatment research. The known DDR inhibitors include drugs that inhibit several DNA repair pathways or molecular components, such as the polyADP-ribose polymerase (PARP), the ataxia telangiectasia mutated kinase (ATM), the ataxia telangiectasia and Rad3-related kinase (ATR), the Checkpoint kinases 1 and 2 (CHK1/2), the Cyclin-dependent kinases 4 and 6, (CDK4/6), the cell-cycle checkpoint kinase WEE1, and the DNA-dependent protein kinase (DNA-PK) [8].
Particularly, ATM and ATR kinases have a critical role in the activation of the DDR network. As for ATR, following the formation of the stable replication protein A (RPA)-single-stranded DNA (ssDNA) complex at DNA damage sites, the ATR-interacting protein (ATRIP) binds to RPA, causing the localization of the ATR kinase to these sites [9]. Next, to give more time for the DNA repair mechanism to proceed, the ATR-CHK1 signaling pathway induces cell-cycle arrest at the G2-M phase. As for ATM, this kinase is activated via the MRN (meiotic recombination protein 11—MRE11, Nijmegen breakage syndrome protein 1—NBS1) complex, a DNA double-strand breaks (DSBs) sensor [10]. Then, ATM phosphorylates the H2A histone family member X at S139 (γH2AX) and induces the CHK2 kinase, resulting in G1-S and intra-S-phase checkpoint activation. Based on the above, ATR and ATM kinases may be promising molecular targets in the treatment of cancer. Currently, several ATM/ATR inhibitors have been identified and are participating in preclinical and clinical evaluation.
Chemotherapy resistance is a common challenge in the treatment of cancer, as the activation of a functional DDR can lead to cell cycle arrest and prolonged DNA repair [6]. Blocking the ATR pathway can reverse this state and enhance the cytotoxicity of genotoxic drugs by abrogating the cell cycle checkpoint [11][12].

2. ATR Inhibition and Synthetic Lethality

A large-scale screening of in vitro and in vivo preclinical models of colorectal cancer has indicated that DDR inhibitors, in general, and ATR inhibitors specifically, are strong candidates for immunotherapy alternatives and has also suggested various response-predictive biomarkers for ATR inhibition, such as ATM protein loss [13]. Interestingly, recent data confirmed preclinical findings that the inhibition of ATR can lead to synthetic lethality in ATM-deficient malignancies. In fact, a study in ATM-deficient/p53-null cancer cells showed that ATR inhibition with VE-821 resulted in increased cytotoxicity after treatment with a variety of genotoxic agents, including platinum-based drugs, radiation, antimetabolites (gemcitabine), and topoisomerase inhibitors (camptothecin and etoposide). Importantly, VE-821 demonstrated a synergistic effect in tumor cells but not in normal cells [14]. Another study has also presented synergy between cisplatin and the ATR inhibitor ceralasertib (AZD6738) in ATM-deficient NSCLC (non-small cell lung cancer) cells [15]. Together, these data suggest that inhibition of ATR can lead to synthetic lethality in ATM-deficient/p53-null cancer cells that depend on alternative pathways to repair DSBs [16]. Strikingly, combining ceralasertib with cisplatin resulted in an enhanced cytotoxic effect even in ATM-proficient cell lines [17]. Of note, although previous studies have shown that ATM facilitates fork stabilization and maintains DNA replication [18] in ATM-proficient tumors, the ATR pathway also plays the most important role in replication stress management. For example, tumors expressing oncogenes (e.g., Ras, Myc), which are known to induce high replication stress [19], exhibited a strong response to ATR inhibition even without additional genotoxic treatment [20][21][22][23]. In fact, ATR appears to be crucial for the survival of those tumors, rendering ATR inhibition monotherapy a potential anticancer treatment [24][25].
Another striking example of induced synthetic lethality and antitumor immunity after ATR inhibition has been recently reported regarding Mismatch Repair (MMR) deficient cancer cells [26]. Also, in tumors with high levels of microsatellite instability (MSI-H) that are characterized by decreased levels of WRN helicase, it has been shown that ATR inhibition may potentiate tumor cell death [27]. MSI-H tumors may also present mutations in the ARID1A chromatin remodeling protein that plays a substantial role in DNA repair [28]. ARID1A loss of function is quite common, mostly among gynecological cancers, and renders the ATR pathway indispensable for ARID1A-deficient cells, as demonstrated in vitro and ex vivo in colorectal cancer (CRC) cells [28][29]. Mechanistically, ARID1A-deficient cells are characterized by loss of the G2/M cell cycle checkpoint and impaired homologous recombination. When treated with ATR inhibitors, genomic instability is induced, leading to cell death [28][29][30].
Taken together, the functionality of specific factors could be exploited as a predictive biomarker of ATR-blockade response, and, in parallel, combined perturbation of these proteins could lead to a synthetic lethality effect.

3. ATR Inhibitors Synergy with Other Anti-Tumor Therapies

ATR inhibitor AZD6738 has been proven to synergize with chemotherapy agents like cisplatin in various solid tumor preclinical models, resulting in augmented antitumor activity [17][31]. Likewise, berzosertib (VE-822, VX-970, M6620) has been found to increase cell death both in cell lines and in patient-derived primary lung xenografts after cisplatin treatment while also exhibiting a strong effect in tumor growth arrest in NSCLC models [32][33]. Other chemotherapy drugs may also be combined with ATR inhibition. Indeed, a recent study has shown synergism of the ATR inhibitor AZD6738 with the topoisomerase I inhibitor belotecan in ovarian cancer models [34], while combination with the antimetabolite gemcitabine in pancreatic models has been shown to instigate high replication stress leading to increased cell death and tumor shrinkage [35].
Recently, it has also been reported that AZD6738 can result in augmented cytotoxicity in vitro and tumor regression in vivo when combined with Trastuzumab Deruxtecan (T-DXd), an anti-HER2 antibody-topoisomerase I inhibitor hybrid [36], as well as improve the effectiveness of PI3K inhibitors, probably by DSBs-induced apoptosis as shown in in vitro and in vivo preclinical models of breast cancer [37].
An intriguing idea has led to testing the combination of ATR inhibition with poly (ADP-ribose) polymerase (PARP) inhibitors. PARP is an essential protein for multiple DDR pathways, and several inhibitors, such as olaparib, have been synthesized and are currently used in clinical practice. Olaparib induces DNA damage and activates BRCA1/2-dependent homologous recombination. Thus, it is used to cause synthetic lethality in BRCA1/2-deficient cancers or with synchronous administration of HR-blocking agents [38]. Accumulating data show that the ATR inhibitor AZD6738 synergizes with olaparib to overcome resistance and achieve induced cytotoxicity in ATM-deficient tumors and/or tumors with impaired HR repair [39][40]. However, it has also been proved that AZD6738 combined with olaparib and radiotherapy can benefit therapeutically even HR-proficient tumors through “PARP trapping” and the formation of PARP-DNA complexes that impede DNA replication [41].
A recent study underlined the significance of ATR inhibition scheduling during therapy [42]. The researchers reported that to achieve increased cytotoxic T cells in the tumor-draining lymph node (DLN), radiation therapy or immune checkpoint inhibition must be followed by a short ATR inhibition rather than a prolonged one.
Interestingly, the contribution of ATM and ATR to the killing effect of the DNA-methylating drug temozolomide was investigated in several cell lines [43][44]. The researchers reported that the knockdown of ATM and ATR increased cell killing of glioblastoma and melanoma cells with a more significant effect in the ATR knockdown cells, suggesting that the combination of temozolomide with an ATR inhibitor might be a promising approach to fight temozolomide resistance.


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