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  1. Article ; Online: Tumour immunogenicity goes with the (mitochondrial electron) flow.

    Ahmed, Asma / Tait, Stephen W G

    Molecular oncology

    2024  

    Abstract: Mitochondrial metabolism and electron transport chain (ETC) function are essential for tumour proliferation and metastasis. However, the impact of ETC function on cancer immunogenicity is not well understood. In a recent study, Mangalhara et al. found ... ...

    Abstract Mitochondrial metabolism and electron transport chain (ETC) function are essential for tumour proliferation and metastasis. However, the impact of ETC function on cancer immunogenicity is not well understood. In a recent study, Mangalhara et al. found that inhibition of complex II leads to enhanced tumour immunogenicity, T-cell-mediated cytotoxicity and inhibition of tumour growth. Surprisingly, this antitumour effect is mediated by succinate accumulation affecting histone methylation. Histone methylation promotes the transcriptional upregulation of major histocompatibility complex-antigen processing and presentation (MHC-APP) genes in a manner independent of interferon signalling. Modulating mitochondrial electron flow to enhance tumour immunogenicity provides an exciting new therapeutic avenue and may be particularly attractive for tumours with reduced expression of MHC-APP genes or dampened interferon signalling.
    Language English
    Publishing date 2024-03-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2415106-3
    ISSN 1878-0261 ; 1574-7891
    ISSN (online) 1878-0261
    ISSN 1574-7891
    DOI 10.1002/1878-0261.13627
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Killing cells using light (activated) sabers.

    Tait, Stephen W G

    The Journal of cell biology

    2022  Volume 221, Issue 6

    Abstract: Many types of regulated cell death exist, however the non-cell autonomous effects of specific forms of cell death remain poorly understood. Addressing this, Shkarina et al. (2022. J. Cell Biol.https://doi.org/10.1083/jcb.202109038) describe an ... ...

    Abstract Many types of regulated cell death exist, however the non-cell autonomous effects of specific forms of cell death remain poorly understood. Addressing this, Shkarina et al. (2022. J. Cell Biol.https://doi.org/10.1083/jcb.202109038) describe an optogenetic method to activate distinct modes of cell death in select cells.
    Language English
    Publishing date 2022-05-16
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.202205018
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Getting more bang for their buck: BCL2 inhibitors boost dendritic-cell function to enhance anti-cancer immune surveillance.

    Montes-Gómez, Alfredo E / Tait, Stephen W G

    Journal of translational medicine

    2024  Volume 22, Issue 1, Page(s) 317

    Abstract: The anti-apoptotic BCL-2 protein family regulates cancer cell survival, thus it represents an important therapeutic target. Indeed, a drug class, called BH3-mimetics, have been developed to directly target BCL2 proteins and promote cancer cell death. ... ...

    Abstract The anti-apoptotic BCL-2 protein family regulates cancer cell survival, thus it represents an important therapeutic target. Indeed, a drug class, called BH3-mimetics, have been developed to directly target BCL2 proteins and promote cancer cell death. Conventional wisdom suggests that the primary anti-cancer effect of BCL-2 inhibition is through induction of cancer cell death. However, a recent study by Zhao and colleagues describes that BCL-2 inhibition also enhances the function of classical dendritic cells, unleashing their role in immunosurveillance, promoting T cell immunity and tumour regression. Thus, inhibiting anti-apoptotic BCL-2 function may have a multi-pronged anti-tumour action.
    MeSH term(s) Humans ; Apoptosis ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Apoptosis Regulatory Proteins/pharmacology ; Apoptosis Regulatory Proteins/therapeutic use ; Cell Line, Tumor
    Chemical Substances Proto-Oncogene Proteins c-bcl-2 ; Antineoplastic Agents ; Apoptosis Regulatory Proteins ; BCL2 protein, human
    Language English
    Publishing date 2024-03-28
    Publishing country England
    Document type Letter
    ZDB-ID 2118570-0
    ISSN 1479-5876 ; 1479-5876
    ISSN (online) 1479-5876
    ISSN 1479-5876
    DOI 10.1186/s12967-024-04961-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Mitochondria and cell death-associated inflammation.

    Vringer, Esmee / Tait, Stephen W G

    Cell death and differentiation

    2022  Volume 30, Issue 2, Page(s) 304–312

    Abstract: Mitochondria have recently emerged as key drivers of inflammation associated with cell death. Many of the pro-inflammatory pathways activated during cell death occur upon mitochondrial outer membrane permeabilization (MOMP), the pivotal commitment point ... ...

    Abstract Mitochondria have recently emerged as key drivers of inflammation associated with cell death. Many of the pro-inflammatory pathways activated during cell death occur upon mitochondrial outer membrane permeabilization (MOMP), the pivotal commitment point to cell death during mitochondrial apoptosis. Permeabilised mitochondria trigger inflammation, in part, through the release of mitochondrial-derived damage-associated molecular patterns (DAMPs). Caspases, while dispensable for cell death during mitochondrial apoptosis, inhibit activation of pro-inflammatory pathways after MOMP. Some of these mitochondrial-activated inflammatory pathways can be traced back to the bacterial ancestry of mitochondria. For instance, mtDNA and bacterial DNA are highly similar thereby activating similar cell autonomous immune signalling pathways. The bacterial origin of mitochondria suggests that inflammatory pathways found in cytosol-invading bacteria may be relevant to mitochondrial-driven inflammation after MOMP. In this review, we discuss how mitochondria can initiate inflammation during cell death highlighting parallels with bacterial activation of inflammation. Moreover, we discuss the roles of mitochondrial inflammation during cell death and how these processes may potentially be harnessed therapeutically, for instance to improve cancer treatment.
    MeSH term(s) Humans ; Mitochondrial Membranes/metabolism ; Mitochondria/metabolism ; Cell Death ; Apoptosis/physiology ; Inflammation/metabolism
    Language English
    Publishing date 2022-11-29
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/s41418-022-01094-w
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  5. Article ; Online: Mitochondrial DNA in cell death and inflammation.

    Heilig, Rosalie / Lee, Jordan / Tait, Stephen W G

    Biochemical Society transactions

    2023  Volume 51, Issue 1, Page(s) 457–472

    Abstract: Cytosolic DNA is recognized by the innate immune system as a potential threat. During apoptotic cell death, mitochondrial DNA (mtDNA) release activates the DNA sensor cyclic GMP-AMP synthase (cGAS) to promote a pro-inflammatory type I interferon response. ...

    Abstract Cytosolic DNA is recognized by the innate immune system as a potential threat. During apoptotic cell death, mitochondrial DNA (mtDNA) release activates the DNA sensor cyclic GMP-AMP synthase (cGAS) to promote a pro-inflammatory type I interferon response. Inflammation following mtDNA release during apoptotic cell death can be exploited to engage anti-tumor immunity and represents a potential avenue for cancer therapy. Additionally, various studies have described leakage of mtDNA, independent of cell death, with different underlying cues such as pathogenic infections, changes in mtDNA packaging, mtDNA stress or reduced mitochondrial clearance. The interferon response in these scenarios can be beneficial but also potentially disadvantageous, as suggested by a variety of disease phenotypes. In this review, we discuss mechanisms underlying mtDNA release governed by cell death pathways and summarize release mechanisms independent of cell death. We further highlight the similarities and differences in mtDNA release pathways, outlining gaps in our knowledge and questions for further research. Together, a deeper understanding of how and when mtDNA is released may enable the development of drugs to specifically target or inhibit mtDNA release in different disease settings.
    MeSH term(s) Humans ; DNA, Mitochondrial/metabolism ; Mitochondria/metabolism ; Inflammation/metabolism ; Apoptosis ; Interferons/metabolism
    Chemical Substances DNA, Mitochondrial ; Interferons (9008-11-1)
    Language English
    Publishing date 2023-02-23
    Publishing country England
    Document type Review ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 184237-7
    ISSN 1470-8752 ; 0300-5127
    ISSN (online) 1470-8752
    ISSN 0300-5127
    DOI 10.1042/BST20221525
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Targeting immunogenic cell death in cancer.

    Ahmed, Asma / Tait, Stephen W G

    Molecular oncology

    2020  Volume 14, Issue 12, Page(s) 2994–3006

    Abstract: Immunogenic cell death (ICD) is a type of cancer cell death triggered by certain chemotherapeutic drugs, oncolytic viruses, physicochemical therapies, photodynamic therapy, and radiotherapy. It involves the activation of the immune system against cancer ... ...

    Abstract Immunogenic cell death (ICD) is a type of cancer cell death triggered by certain chemotherapeutic drugs, oncolytic viruses, physicochemical therapies, photodynamic therapy, and radiotherapy. It involves the activation of the immune system against cancer in immunocompetent hosts. ICD comprises the release of damage-associated molecular patterns (DAMPs) from dying tumor cells that result in the activation of tumor-specific immune responses, thus eliciting long-term efficacy of anticancer drugs by combining direct cancer cell killing and antitumor immunity. Remarkably, subcutaneous injection of dying tumor cells undergoing ICD has been shown to provoke anticancer vaccine effects in vivo. DAMPs include the cell surface exposure of calreticulin (CRT) and heat-shock proteins (HSP70 and HSP90), extracellular release of adenosine triphosphate (ATP), high-mobility group box-1 (HMGB1), type I IFNs and members of the IL-1 cytokine family. In this review, we discuss the cell death modalities connected to ICD, the DAMPs exposed during ICD, and the mechanism by which they activate the immune system. Finally, we discuss the therapeutic potential and challenges of harnessing ICD in cancer immunotherapy.
    MeSH term(s) Alarmins/metabolism ; Animals ; Endoplasmic Reticulum Stress ; Humans ; Immunity/immunology ; Immunogenic Cell Death ; Neoplasms/immunology ; Neoplasms/pathology ; T-Lymphocytes/immunology
    Chemical Substances Alarmins
    Language English
    Publishing date 2020-12-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2415106-3
    ISSN 1878-0261 ; 1574-7891
    ISSN (online) 1878-0261
    ISSN 1574-7891
    DOI 10.1002/1878-0261.12851
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  7. Article ; Online: Parkin inhibits necroptosis to prevent cancer.

    Cao, Kai / Tait, Stephen W G

    Nature cell biology

    2019  Volume 21, Issue 8, Page(s) 915–916

    MeSH term(s) Animals ; Apoptosis/drug effects ; Apoptosis/physiology ; Cell Death/drug effects ; Cell Death/physiology ; Humans ; Necrosis/drug therapy ; Necrosis/metabolism ; Neoplasms/metabolism ; Ubiquitin-Protein Ligases/metabolism
    Chemical Substances Ubiquitin-Protein Ligases (EC 2.3.2.27) ; parkin protein (EC 2.3.2.27)
    Language English
    Publishing date 2019-07-29
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1474722-4
    ISSN 1476-4679 ; 1465-7392
    ISSN (online) 1476-4679
    ISSN 1465-7392
    DOI 10.1038/s41556-019-0350-1
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  8. Article: Mitochondria and Inflammation: Cell Death Heats Up.

    Vringer, Esmee / Tait, Stephen W G

    Frontiers in cell and developmental biology

    2019  Volume 7, Page(s) 100

    Abstract: Mitochondrial outer membrane permeabilization (MOMP) is essential to initiate mitochondrial apoptosis. Due to the disruption of mitochondrial outer membrane integrity, intermembrane space proteins, notably ... ...

    Abstract Mitochondrial outer membrane permeabilization (MOMP) is essential to initiate mitochondrial apoptosis. Due to the disruption of mitochondrial outer membrane integrity, intermembrane space proteins, notably cytochrome
    Language English
    Publishing date 2019-06-27
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2019.00100
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  9. Article ; Online: Mitochondrial quality control: from molecule to organelle.

    Roca-Portoles, Alba / Tait, Stephen W G

    Cellular and molecular life sciences : CMLS

    2021  Volume 78, Issue 8, Page(s) 3853–3866

    Abstract: Mitochondria are organelles central to myriad cellular processes. To maintain mitochondrial health, various processes co-operate at both the molecular and organelle level. At the molecular level, mitochondria can sense imbalances in their homeostasis and ...

    Abstract Mitochondria are organelles central to myriad cellular processes. To maintain mitochondrial health, various processes co-operate at both the molecular and organelle level. At the molecular level, mitochondria can sense imbalances in their homeostasis and adapt to these by signaling to the nucleus. This mito-nuclear communication leads to the expression of nuclear stress response genes. Upon external stimuli, mitochondria can also alter their morphology accordingly, by inducing fission or fusion. In an extreme situation, mitochondria are degraded by mitophagy. Adequate function and regulation of these mitochondrial quality control pathways are crucial for cellular homeostasis. As we discuss, alterations in these processes have been linked to several pathologies including neurodegenerative diseases and cancer.
    MeSH term(s) Animals ; Humans ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondrial Dynamics ; Mitophagy ; Neoplasms/metabolism ; Neoplasms/pathology ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Protein Kinases/metabolism ; Signal Transduction ; Ubiquitin-Protein Ligases/metabolism
    Chemical Substances Ubiquitin-Protein Ligases (EC 2.3.2.27) ; parkin protein (EC 2.3.2.27) ; Protein Kinases (EC 2.7.-) ; PTEN-induced putative kinase (EC 2.7.11.1)
    Language English
    Publishing date 2021-03-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-021-03775-0
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  10. Article ; Online: Sublethal engagement of apoptotic pathways in residual cancer.

    Killarney, Shane T / Tait, Stephen W G / Green, Douglas R / Wood, Kris C

    Trends in cell biology

    2023  Volume 34, Issue 3, Page(s) 225–238

    Abstract: Cytotoxic chemo-, radio-, and targeted therapies frequently elicit apoptotic cancer cell death. Mitochondrial outer membrane permeabilization (MOMP) is a critical, regulated step in this apoptotic pathway. The residual cancer cells that survive treatment ...

    Abstract Cytotoxic chemo-, radio-, and targeted therapies frequently elicit apoptotic cancer cell death. Mitochondrial outer membrane permeabilization (MOMP) is a critical, regulated step in this apoptotic pathway. The residual cancer cells that survive treatment serve as the seeds of eventual relapse and are often functionally characterized by their transient tolerance of multiple therapeutic treatments. New studies suggest that, in these cells, a sublethal degree of MOMP, reflective of incomplete apoptotic commitment, is widely observed. Here, we review recent evidence that this sublethal MOMP drives the aggressive features of residual cancer cells while templating a host of unique vulnerabilities, highlighting how failed apoptosis may counterintuitively enable new therapeutic strategies to target residual disease (RD).
    MeSH term(s) Humans ; Mitochondrial Membranes/metabolism ; Mitochondria/metabolism ; Neoplasm, Residual/metabolism ; Apoptosis/physiology
    Language English
    Publishing date 2023-08-10
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 30122-x
    ISSN 1879-3088 ; 0962-8924
    ISSN (online) 1879-3088
    ISSN 0962-8924
    DOI 10.1016/j.tcb.2023.07.005
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