Mitophagy promotes replication of oncolytic Newcastle disease virus by blocking intrinsic apoptosis in lung cancer cells

Ma, Gang; Mao, Xia; Wang, Diancheng; Chen, Aiping; Wang, Yongshan; Wang, Hongwei; Yu, Decai; Wei, Jiwu

doi:10.18632/oncotarget.2219

Cited by 54 publications

(50 citation statements)

References 39 publications

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“…The inhibition of apoptosis by mitophagy favors viral replication and promotes the pathogenesis of viral infection [56]. Similar findings have been reported with HBV, HCV, VEEV, CSFV, PRRSV, Newcastle disease virus (NDV), and transmissible gastroenteritis virus (TGEV) [35,37,38,40,41,57,58]. These examples share 2 concurrent phenomena: (1) upon infection, viruses induce mitophagy via different mechanisms, and (2) subsequent mitophagy mitigates apoptosis to promote viral infection.…”

Section: Virus-triggered Mitophagy Inhibits Apoptosis For Viral Replisupporting

confidence: 57%

Viral strategies for triggering and manipulating mitophagy

2018

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Viral infection causes many physiological alterations in the host cell, and many of these alterations can affect the host mitochondrial network, including mitophagy induction. A substantial amount of literature has been generated that advances our understanding of the relationship between mitophagy and several viruses. Some viruses trigger mitophagy directly, and indirectly and control the mitophagic process via different strategies. This enables viruses to promote persistent infection and attenuate the innate immune responses. In this review, we discuss the events of virus-regulated mitophagy and the functional relevance of mitophagy in the pathogenesis of viral infection and disease. Abbreviation: ATG: autophagy related; BCL2L13: BCL2 like 13; BNIP3L/NIX: BCL2 interacting protein 3 like; CL: cardiolipin; CSFV: classical swine fever virus; CVB: coxsackievirus B; DENV: dengue virus; DNM1L: dynamin 1 like; FIS1: fission, mitochondrial 1; FUNDC1: FUN14 domain containing 1; HPIV3: human parainfluenza virus 3; HSV-1: herpes simplex virus type 1; IMM: inner mitochondrial membrane; IAV: influenza A virus; IFN: interferon; IKBKE/IKKε: inhibitor of nuclear factor kappa B kinase subunit epsilon; LUBAC: linear ubiquitin assembly complex; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MeV: measles virus; MAVS: mitochondrial antiviral signaling protein; MFF: mitochondria fission factor; NLRP3: NLR family pyrin domain containing 3; NDV: Newcastle disease virus; NR4A1: nuclear receptor subfamily 4 group A member 1; OMM: outer mitochondrial membrane; OPA1: OPA1, mitochondrial dynamin like GTPase; PRKN: parkin RBR E3 ubiquitin protein ligase; PINK1: PTEN induced putative kinase 1; PHB2: prohibitin 2; PRRSV: porcine reproductive and respiratory syndrome virus; PRRs: pattern-recognition receptors; RLRs: RIG-I-like receptors; ROS: reactive oxygen species; RIPK2: receptor interacting serine/threonine kinase 2; SESN2: sestrin 2; SNAP29: synaptosome associated protein 29; STX17: syntaxin 17; TGEV: transmissible gastroenteritis virus; TUFM: Tu translation elongation factor, mitochondrial; TRAF2: TNF receptor associated factor 2; TRIM6: tripartite motif containing 6; Ub: ubiquitin; ULK1: unc-51 like autophagy activating kinase 1; VZV: varicella-zoster virus.

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Section: Virus-triggered Mitophagy Inhibits Apoptosis For Viral Replisupporting

confidence: 57%

Viral strategies for triggering and manipulating mitophagy

2018

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“…Some other viruses, such us Hepatitis B and C virus (HBV and HCV) New Castle Disease virus (NDV) and measles viruses, induce instead mitochondrial fission and mitophagy which also favour viral replication [73][74][75][76]. Also the Influenza A (subtype H1N1) full-length PB1-F2 protein targets MT and causes loss of mitochondrial membrane potential and mitochondrial fragmentation [77].…”

Section: Mitochondria Fusion Governs Innate Immunitymentioning

confidence: 99%

Mitochondrial Dynamics in Basal and Stressful Conditions

Zemirli

Morel

Molino

2018

IJMS

136

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The historical role of mitochondria resides in converting the energy released during the oxidation of macromolecules (carbohydrates, lipids and proteins) into adenosine tri-phosphate, a major form of chemically stored energy which sustains cell growth and homeostasis. Beyond this role in bioenergetics regulation, mitochondria play a role in several other cellular processes including lipid metabolism, cellular calcium homeostasis, autophagy and immune responses. Furthermore, mitochondria are highly dynamic organelles: as all other cellular endomembranes, they are continuously moving along cytoskeleton, and, most importantly, they constantly interact one with each other by membrane tethering, fusion and fission. This review aims to highlight the tight correlation between the morphodynamics of mitochondria and their biological function(s), in physiological as well as stress conditions, in particular nutrient deprivation, pathogen attack and some human diseases. Finally, we emphasize some crosstalk between the fusion/fission machinery and the autophagy pathway to ending on some speculative hypothesis to inspire future research in the field.

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“…In the early stages of infection, viruses need tumor cells to be alive so they can take over and control the cellular molecular cell death machinery, but at later periods of infection, oncolytic viruses lyse and kill tumor cells to release newly assembled viruses (2). Some studies have reported that apoptosis limits the replication of influenza virus and other viruses (37)(38)(39)(40), but others have found that promoting apoptosis activates the replication of human herpes virus and hepatitis B virus (41,42). We found that neither pan-caspase inhibitors (Z-VAD-FMK and Q-VD-Oph) nor a JNK inhibitor (SP600125) abrogated the combined cytotoxicity (Fig.…”

Section: Discussionmentioning

confidence: 99%

Selective replication of oncolytic virus M1 results in a bystander killing effect that is potentiated by Smac mimetics

Cai

Lin

Zhang

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Oncolytic virotherapy is a treatment modality that uses native or genetically modified viruses that selectively replicate in and kill tumor cells. Viruses represent a type of pathogen-associated molecular pattern and thereby induce the up-regulation of dozens of cytokines via activating the host innate immune system. Second mitochondria-derived activator of caspases (Smac) mimetic compounds (SMCs), which antagonize the function of inhibitor of apoptosis proteins (IAPs) and induce apoptosis, sensitize tumor cells to multiple cytokines. Therefore, we sought to determine whether SMCs sensitize tumor cells to cytokines induced by the oncolytic M1 virus, thus enhancing a bystander killing effect. Here, we report that SMCs potentiate the oncolytic effect of M1 in vitro, in vivo, and ex vivo. This strengthened oncolytic efficacy resulted from the enhanced bystander killing effect caused by the M1 virus via cytokine induction. Through a microarray analysis and subsequent validation using recombinant cytokines, we identified IL-8, IL-1A, and TRAIL as the key cytokines in the bystander killing effect. Furthermore, SMCs increased the replication of M1, and the accumulation of virus protein induced irreversible endoplasmic reticulum stress-and c-Jun N-terminal kinase-mediated apoptosis. Nevertheless, the combined treatment with M1 and SMCs had little effect on normal and human primary cells. Because SMCs selectively and significantly enhance the bystander killing effect and the replication of oncolytic virus M1 specifically in cancer cells, this combined treatment may represent a promising therapeutic strategy.oncolytic virus | SMAC mimetics | bystander killing effect

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Mitophagy promotes replication of oncolytic Newcastle disease virus by blocking intrinsic apoptosis in lung cancer cells

Cited by 54 publications

References 39 publications

Viral strategies for triggering and manipulating mitophagy

Viral strategies for triggering and manipulating mitophagy

Mitochondrial Dynamics in Basal and Stressful Conditions

Selective replication of oncolytic virus M1 results in a bystander killing effect that is potentiated by Smac mimetics

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