Necroptosis as a Novel Facet of Mitotic Catastrophe

Egorshina, Aleksandra Yu; Zamaraev, Alexey V.; Kaminskyy, Vitaliy O.; Радыгина, Т. В.; Zhivotovsky, Boris; Kopeina, Gelina S.

doi:10.3390/ijms23073733

Cited by 8 publications

(8 citation statements)

References 37 publications

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“…Apoptosis is highly regulated and is characterized by membrane blebbing, cell shrinkage, and caspase activation. Necroptosis, a more recently characterized form, is triggered by various factors, including caspase inhibition or impairment ( Egorshina et al, 2022 ; Sahoo et al, 2023 ). Necroptosis relies on RIPK1 and RIPK3 activation, and its morphology differs from apoptosis with organelle swelling and membrane rupture ( Vandenabeele et al, 2010 ; Shan et al, 2018 ; Bertheloot et al, 2021 ).…”

Section: Trif-dependent Tlr3 Signalingmentioning

confidence: 99%

TRIF-dependent signaling and its role in liver diseases

Hu,

Cheng,

Chu

et al. 2024

Front. Cell Dev. Biol.

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TIR domain-containing adaptor inducing IFN-β (TRIF) is a crucial adaptor molecule downstream of toll-like receptors 3 (TLR3) and 4 (TLR4). TRIF directly binds to TLR3 through its TIR domain, while it associates with TLR4 indirectly through the bridge adaptor molecule TRIF-related adaptor molecule (TRAM). TRIF plays a pivotal role in regulating interferon beta 1 (IFN-β) response, nuclear factor kappa B (NF-κB) signaling, apoptosis, and necroptosis signaling mediated by TLR3 and TLR4. It accomplishes these by recruiting and activating various kinases or transcription factors via its distinct domains. In this review, we comprehensively summarize the TRIF-dependent signaling pathways mediated by TLR3 and TLR4, elucidating key target molecules and downstream pathways. Furthermore, we provide an overview of TRIF’s impact on several liver disorders, including drug-induced liver injury, ischemia-reperfusion liver injury, autoimmune hepatitis, viral hepatitis, alcohol-associated liver disease (ALD), metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH). We also explore its effects on liver steatosis, inflammation, fibrosis, and carcinogenesis. A comprehensive understanding of the TRIF-dependent signaling pathways, as well as the intricate relationship between TRIF and liver diseases, can facilitate the identification of potential drug targets and the development of novel and effective therapeutics against hepatic disorders.

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Section: Trif-dependent Tlr3 Signalingmentioning

confidence: 99%

TRIF-dependent signaling and its role in liver diseases

Hu,

Cheng,

Chu

et al. 2024

Front. Cell Dev. Biol.

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“…Mitotic catastrophe is another critical non-apoptotic mechanism of cancer cells, defined by the Nomenclature Committee on Cell Death (NCCD) in 2012, which usually occurs after massive damage to DNA following ROS generation ( Galluzzi et al, 2012 ). Cells undergoing mitotic catastrophe are often in partnership with other mechanisms of cell death, such as autophagy, senescence, or, necroptosis ( Eom et al, 2005 ; Zhao W. et al, 2022b ; Egorshina et al, 2022 ). Recent studies have found that the therapeutic efficiency of anticancer modalities such as radiotherapy and chemotherapy can be reinforced by stimulating mitotic catastrophe, which is also a promising way to overcome multidrug resistance ( Pérès et al, 2015 ; Bai et al, 2017 ).…”

Section: Therapeutic Mechanisms Of Quercetin Targeting Non-apoptotic ...mentioning

confidence: 99%

Targeting of non-apoptotic cancer cell death mechanisms by quercetin: Implications in cancer therapy

Yang

Xu²,

Tang³

et al. 2022

Front. Pharmacol.

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The ultimate goal of cancer treatment is to kill cancer cells, based on the use of various therapeutic agents, such as chemotherapy, radiotherapy, or targeted therapy drugs. Most drugs exert their therapeutic effects on cancer by targeting apoptosis. However, alterations in apoptosis-related molecules and thus assisting cells to evade death, eventually lead to tumor cell resistance to therapeutic drugs. The increased incidence of non-apoptotic cell death modes such as induced autophagy, mitotic catastrophe, senescence, and necrosis is beneficial to overcoming multidrug resistance mediated by apoptosis resistance in tumor cells. Therefore, investigating the function and mechanism of drug-induced non-apoptotic cell death modes has positive implications for the development of new anti-cancer drugs and therapeutic strategies. Phytochemicals show strong potential as an alternative or complementary medicine for alleviating various types of cancer. Quercetin is a flavonoid compound widely found in the daily diet that demonstrates a significant role in inhibiting numerous human cancers. In addition to direct pro-tumor cell apoptosis, both in vivo and in vitro experiments have shown that quercetin exerts anti-tumor properties by triggering diverse non-apoptotic cell death modes. This review summarized the current status of research on the molecular mechanisms and targets through which quercetin-mediated non-apoptotic mode of cancer cell death, including autophagic cell death, senescence, mitotic catastrophe, ferroptosis, necroptosis, etc.

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“…When TNF interacts with TNFR1, the intracellular part of TNFR1 binds with the adaptor protein TRADD. This event leads to the assembly of an intracellular complex, which includes caspases and serine protein kinases RIP1 and RIP3 [20,21]. Depending on the activation of these enzymes, alternative processes of cell death are induced in the cells: apoptosis and necroptosis [22,23].…”

Section: Introductionmentioning

confidence: 99%

The 12-Membered TNFR1 Peptide, as Well as the 16-Membered and 6-Membered TNF Peptides, Regulate TNFR1-Dependent Cytotoxic Activity of TNF

Yurkina,

Romanova,

Tvorogova

et al. 2024

IJMS

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Understanding the exact mechanisms of the activation of proinflammatory immune response receptors is very important for the targeted regulation of their functioning. In this work, we were able to identify the sites of the molecules in the proinflammatory cytokine TNF (tumor necrosis factor) and its TNFR1 (tumor necrosis factor receptor 1), which are necessary for the two-stage cytotoxic signal transduction required for tumor cell killing. A 12-membered TNFR1 peptide was identified and synthesized, interacting with the ligands of this receptor protein’s TNF and Tag7 and blocking their binding to the receptor. Two TNF cytokine peptides interacting with different sites of TNFR1 receptors were identified and synthesized. It has been demonstrated that the long 16-membered TNF peptide interferes with the binding of TNFR1 ligands to this receptor, and the short 6-membered peptide interacts with the receptor site necessary for the transmission of a cytotoxic signal into the cell after the ligands’ interaction with the binding site. This study may help in the development of therapeutic approaches to regulate the activity of the cytokine TNF.

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Necroptosis as a Novel Facet of Mitotic Catastrophe

Cited by 8 publications

References 37 publications

TRIF-dependent signaling and its role in liver diseases

TRIF-dependent signaling and its role in liver diseases

Targeting of non-apoptotic cancer cell death mechanisms by quercetin: Implications in cancer therapy

The 12-Membered TNFR1 Peptide, as Well as the 16-Membered and 6-Membered TNF Peptides, Regulate TNFR1-Dependent Cytotoxic Activity of TNF

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