Publisher Correction: Z-nucleic-acid sensing triggers ZBP1-dependent necroptosis and inflammation

Jiao, Huipeng; Wachsmuth, Laurens; Kumari, Snehlata; Schwarzer, Robin; Lin, Juan; Eren, Remzi Onur; Fisher, Amanda; Lane, Rebecca; Young, George R.; Kassiotis, George; Kaiser, William J.; Pasparakis, Manolis

doi:10.1038/s41586-020-2207-y

Cited by 6 publications

(5 citation statements)

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“…The ZBP1 protein senses viral/endogenous nucleic acid ligands and triggers innate immune responses [77]. In detail, once ZBP1 is activated, RIPK3 and caspase-8 are recruited to activate the NLRP3 inflammasome, which initiates both necroptosis and pyroptosis [78][79][80]. In addition, the bioinformatics analysis reported by Miao et al also indicated that the ZBP1, both of the cuproptosis-related and necroptosis-related gene signature, functions as a risk score for prediction of the low-grade glioma patients prognosis [81].…”

Section: Cross Talk Among Components Of Necroptosis Pyroptosis Ferrop...mentioning

confidence: 99%

Targeting cell death pathways for cancer therapy: recent developments in necroptosis, pyroptosis, ferroptosis, and cuproptosis research

et al. 2022

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Many types of human cells self-destruct to maintain biological homeostasis and defend the body against pathogenic substances. This process, called regulated cell death (RCD), is important for various biological activities, including the clearance of aberrant cells. Thus, RCD pathways represented by apoptosis have increased in importance as a target for the development of cancer medications in recent years. However, because tumor cells show avoidance to apoptosis, which causes treatment resistance and recurrence, numerous studies have been devoted to alternative cancer cell mortality processes, namely necroptosis, pyroptosis, ferroptosis, and cuproptosis; these RCD modalities have been extensively studied and shown to be crucial to cancer therapy effectiveness. Furthermore, evidence suggests that tumor cells undergoing regulated death may alter the immunogenicity of the tumor microenvironment (TME) to some extent, rendering it more suitable for inhibiting cancer progression and metastasis. In addition, other types of cells and components in the TME undergo the abovementioned forms of death and induce immune attacks on tumor cells, resulting in enhanced antitumor responses. Hence, this review discusses the molecular processes and features of necroptosis, pyroptosis, ferroptosis, and cuproptosis and the effects of these novel RCD modalities on tumor cell proliferation and cancer metastasis. Importantly, it introduces the complex effects of novel forms of tumor cell death on the TME and the regulated death of other cells in the TME that affect tumor biology. It also summarizes the potential agents and nanoparticles that induce or inhibit novel RCD pathways and their therapeutic effects on cancer based on evidence from in vivo and in vitro studies and reports clinical trials in which RCD inducers have been evaluated as treatments for cancer patients. Lastly, we also summarized the impact of modulating the RCD processes on cancer drug resistance and the advantages of adding RCD modulators to cancer treatment over conventional treatments.

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Section: Cross Talk Among Components Of Necroptosis Pyroptosis Ferrop...mentioning

confidence: 99%

Targeting cell death pathways for cancer therapy: recent developments in necroptosis, pyroptosis, ferroptosis, and cuproptosis research

et al. 2022

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“…It has been well documented that resistance to regulated cell death is one of the hallmarks of human cancers and it maintains the cell survival and significantly limits the effectiveness of conventional drug therapy . Necrosis has been previously considered as a random and passive process that requires no specific molecular events . However, a regulated type of necrosis (so-called necroptosis) has been recently discovered via identification of chemical inhibitors of necrotic cell death, underlining its regulatory nature .…”

Section: Discussionmentioning

confidence: 99%

“…41 Necrosis has been previously considered as a random and passive process that requires no specific molecular events. 42 However, a regulated type of necrosis (so-called necroptosis) has been recently discovered via identification of chemical inhibitors of necrotic cell death, underlining its regulatory nature. 43 Receptorinteracting protein kinase 1 is a critical regulator of necroptosis, which acts as a downstream mediator of RIPK1, and TRAF5 is considered as a critical subunit in necroptosis execution.…”

Section: ■ Discussionmentioning

confidence: 99%

Tumor-Associated Macrophages Promote Oxaliplatin Resistance via METTL3-Mediated m⁶A of TRAF5 and Necroptosis in Colorectal Cancer

Lan

Liu

et al. 2021

Mol. Pharmaceutics

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As a third-generation platinum drug, oxaliplatin (OX) is widely used as the first-line chemotherapeutic agent in the treatment of colorectal cancer (CRC). CRC cells acquire resistance to chemotherapy and develop resistance, which is a major challenge for the treatment of advanced CRC. Recent studies have suggested that the therapeutic resistance of tumors is affected by the tumor microenvironment (TME). As a critical role among TME, tumor-associated macrophages (TAMs) play an important role. However, their regulatory mechanism underlying the drug resistance in CRC remains largely unknown. In the present study, we found that the density of macrophages infiltrated into the CRC tissues from OX-resistant patients was significantly higher compared with the OX-sensitive patients. Interestingly, both the total N 6 -methyladenosine (m 6 A) RNA content and the expression of its critical methyltransferase METTL3 were increased in the CRC tissues from OX-resistant patients compared with the OX-sensitive patients. Furthermore, we demonstrated that the M2-polarized TAMs enabled the OX resistance via the elevation of METTL3-mediated m 6 A modification in cells. Through whole-genome CRISPR screening and further validation, we found that TRAF5 contributes to the METTL3-triggered OX resistance in CRC cells. This study unveiled that M2-TAMs were important mediators for the acquisition of OX resistance. Furthermore, we provided evidence that targeting of M2-TAMs and METTL3-mediated m 6 A modification might be a promising adjuvant therapeutic strategy for CRC patients, especially for OX-resistant CRC patients.

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“…Bioinformatics analysis further indicated an association between ZBP1 and cuproptosis as well as necroptosis [ 115 ]. ZBP1 activation led to the recruitment of RIPK3 and caspase-8 to activate the NLRP3 inflammasome, which in turn triggers necroptosis and pyroptosis [ 116 , 117 ].…”

Section: Copper-induced Cell Death and Atherosclerosismentioning

confidence: 99%

Copper homeostasis and cuproptosis in atherosclerosis: metabolism, mechanisms and potential therapeutic strategies

Yang,

Li,

Zhou

et al. 2024

Cell Death Discov.

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Copper is an essential micronutrient that plays a pivotal role in numerous physiological processes in virtually all cell types. Nevertheless, the dysregulation of copper homeostasis, whether towards excess or deficiency, can lead to pathological alterations, such as atherosclerosis. With the advent of the concept of copper-induced cell death, termed cuproptosis, researchers have increasingly focused on the potential role of copper dyshomeostasis in atherosclerosis. In this review, we provide a broad overview of cellular and systemic copper metabolism. We then summarize the evidence linking copper dyshomeostasis to atherosclerosis and elucidate the potential mechanisms underlying atherosclerosis development in terms of both copper excess and copper deficiency. Furthermore, we discuss the evidence for and mechanisms of cuproptosis, discuss its interactions with other modes of cell death, and highlight the role of cuproptosis-related mitochondrial dysfunction in atherosclerosis. Finally, we explore the therapeutic strategy of targeting this novel form of cell death, aiming to provide some insights for the management of atherosclerosis.

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Publisher Correction: Z-nucleic-acid sensing triggers ZBP1-dependent necroptosis and inflammation

Cited by 6 publications

References 0 publications

Targeting cell death pathways for cancer therapy: recent developments in necroptosis, pyroptosis, ferroptosis, and cuproptosis research

Targeting cell death pathways for cancer therapy: recent developments in necroptosis, pyroptosis, ferroptosis, and cuproptosis research

Tumor-Associated Macrophages Promote Oxaliplatin Resistance via METTL3-Mediated m⁶A of TRAF5 and Necroptosis in Colorectal Cancer

Copper homeostasis and cuproptosis in atherosclerosis: metabolism, mechanisms and potential therapeutic strategies

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Publisher Correction: Z-nucleic-acid sensing triggers ZBP1-dependent necroptosis and inflammation

Cited by 6 publications

References 0 publications

Targeting cell death pathways for cancer therapy: recent developments in necroptosis, pyroptosis, ferroptosis, and cuproptosis research

Targeting cell death pathways for cancer therapy: recent developments in necroptosis, pyroptosis, ferroptosis, and cuproptosis research

Tumor-Associated Macrophages Promote Oxaliplatin Resistance via METTL3-Mediated m6A of TRAF5 and Necroptosis in Colorectal Cancer

Copper homeostasis and cuproptosis in atherosclerosis: metabolism, mechanisms and potential therapeutic strategies

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Tumor-Associated Macrophages Promote Oxaliplatin Resistance via METTL3-Mediated m⁶A of TRAF5 and Necroptosis in Colorectal Cancer