BECN1-dependent CASP2 incomplete autophagy induction by binding to rabies virus phosphoprotein

Liu, Juan; Wang, Hailong; Gu, Jinyan; Deng, Tingjuan; ZhuangChuan, Yuan; Hu, Boli; Xu, Yunbin; Yan, Yan; Zan, Jie; Liao, Min; DiCaprio, Erin; Lǐ, Jiànróng; Su, Shuo; Zhou, Jiyong

doi:10.1080/15548627.2017.1280220

Cited by 58 publications

(82 citation statements)

References 64 publications

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“…Such inhibition of SVCV replication was potentiated when the autophagy blockers were used in combination with the CRPs, MBCD or 25-HOC. Therefore, together with the decrease in the neutralization of the infection, the results from the combination of each of these three compounds with the autophagy-enhancer rapamycin 55 indicate that the inhibition of SVCV infection observed when cells were treated with the CRPs, MBCD or 25-HOC is due to the blockade of either autophagy or an element common to the autophagy and viral endocytosis pathways, as has also been reported previously for the rabies virus 56 . Since CRP treatment of the cells resulted in an accumulation of autophagosomes, we suggest that the inhibitory effect on autophagy occurs at a late stage such that it affects the fusion of autophagosomes and lysosomes in a fashion similar to CQ 61,67,81 .…”

Section: Discussionsupporting

confidence: 77%

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Zebrafish C-reactive protein isoforms inhibit SVCV replication by blocking autophagy through interactions with cell membrane cholesterol

Belló-Pérez

Pereiro

Coll

et al. 2020

Sci Rep

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Phosphorylcholine works not only as a pathogen-associated molecular pattern (PAMP) 10,18-20 , but also as a danger-associated molecular pattern (DAMP) 18,21-24. This phosphorylcholine-binding site of the soluble CRP is also involved in interactions with, for instance, oxidized low-density lipoprotein (LDL) 21 , nuclear materials (such as chromatin, histones, small nuclear ribonucleoproteins) 25,26 , and other compounds that may not contain phosphorylcholine but are abundant in bacteria 27 , fungi 28,29 and parasites 30,31. In mammals, CRPs are usually triggered during both viral and bacterial infections 32 , although associated serum CRP level increases are more characteristic of bacterial infections, during which they increase by 3-fold logs, while viruses induce lower but significant 10 1 serum CRP levels 2,32,33. Furthermore, the few existing studies that have analysed C-reactive-like protein (CRP) levels in fish show moderate serum level increases in response to both bacterial and viral infections, suggesting an antiviral effect for CRPs 34-36. For example, in common carp (Cyprinus carpio), the serum CRP levels increase up to 2-, 6-and 10-fold in response to Aeromonas salmonicida 37 , Aeromonas hydrophila 34 and cyprinid herpesvirus-3 (CyHV-3) 35 infections, respectively. Further positive correlations between CRP levels and viral infections have been established in fish by transcriptional analysis. For instance, significant upregulation of crp gene expression in several immune-and non-immune-related tissues of diverse fish species has been revealed in response to viruses such as CyHV-3 35 , red seabream iridovirus (RSIV) 38-40 , viral haemorrhagic septicaemia virus (VHSV) 41,42 and spring viraemia of carp virus (SVCV) 42,43. Similarly, higher transcriptional expression of crp genes was observed in common carp treated with polyinosinic:polycytidylic acid (polyI:C, a compound that mimics viral dsRNA) 36 , in DNA-vaccinated rainbow trout (Oncorhynchus mykiss) 44 and zebrafish (Danio rerio) embryos microinjected with an expression plasmid encoding the il6 gene 42 , a cytokine that is upregulated in response to viral infections in humans 45. In this sense, our recent findings show that all previously identified zebrafish CRP1-7 isoforms 46 confer isoform-dependent anti-SVCV protection in vitro and in vivo 47 and exert unexpected anti-SVCV synergistic effects 47 with 25-hydroxycholesterol (25-HOC) 48. Recombinant CRP from tongue sole (Cynoglossus semilaevis) has also been reported to enhance host resistance to RSIV infection when intraperitoneally (i.p.) co-injected with the virus inoculum 40. However, despite the great relevance for evolutionary immunology and therapeutic potential of CRPs, the underlying mechanisms for CRP antiviral effects are not yet known. The present work has been focused on these mechanistic aspects. Results CRP1-7 anti-SVCV activity targets host cells rather than the virus. Our previous studies showed that the treatment with the supernatant from epithelioma papulosum cyprinid (EPC) cells th...

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Section: Discussionsupporting

confidence: 77%

“…Although the results described above suggest that CRPs might induce autophagy, this is a debated issue for rhabdoviruses 54,[56][57][58][59] . In this context, Fig.…”

Section: Inhibition Of Autophagy With Crps Inhibits Svcv Infectionmentioning

confidence: 96%

Zebrafish C-reactive protein isoforms inhibit SVCV replication by blocking autophagy through interactions with cell membrane cholesterol

Belló-Pérez

Pereiro

Coll

et al. 2020

Sci Rep

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“…Extensive number of genes and proteins were confirmed to interference autophagy and further promote tumorigenesis through regulation of different mechanisms and signal pathways, including PI3K/AKT/mTOR and JNK signaling pathways [55][56][57][58]. Aberrant activation of signaling pathways led to activation of multiple downstream effectors, including those involved in growth, survival, and autophagy [20,54].…”

Section: Discussionmentioning

confidence: 99%

CUL4B regulates autophagy via JNK signaling in diffuse large B-cell lymphoma

Zhou

Zhang

et al. 2019

Cell Cycle

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Aberrant expression of CUL4B was identified in various types of solid cancers. Cumulative evidences support the oncogenic role of CUL4B in cancers, including regulation of cell proliferation and signal transduction. However, its clinical value and potential pathogenic mechanism in diffuse large B-cell lymphoma (DLBCL) have not been described previously. Therefore, we hypothesize that overexpressed CUL4B may contribute to the pathogenesis of DLBCL. The aim of this study is to assess the expression and the biological function of CUL4B in DLBCL progression. In our study, CUL4B overexpression was observed in DLBCL tissues, and its upregulation was closely associated with poor prognosis in patients. Furthermore, the functional roles of CUL4B was detected both in vitro and in vivo. We demonstrated that silencing CUL4B could not only induce cell proliferation inhibition, cell cycle arrest, and motility attenuation of DLBCL cells in vitro, but also decrease tumor growth in DLBCL xenografts mice. In addition, we identified that CUL4B may act as a potent inductor of JNK phosphorylation in regulation of autophagy. Our findings demonstrated a significant role of CUL4B in the development and progression of DLBCL. CUL4B may act as a useful biomarker and a novel therapeutic target in DLBCL. ARTICLE HISTORY

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“…Seed PC3 cells in six-well plates at a density of 5 × 10 5 cells per well, in a CO 2 incubator overnight and treated with QLXZD (0–30 mg/mL) for 24 h. The total protein were collected as previously described ( Liu et al, 2017 ). The equalized amounts of proteins from each sample were subjected to sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) followed by transfer to polyvinylidene fluoride (PVDF) membranes.…”

Section: Methodsmentioning

confidence: 99%

Qianlie Xiaozheng Decoction Induces Autophagy in Human Prostate Cancer Cells via Inhibition of the Akt/mTOR Pathway

Xu¹,

Cai

Zong³

et al. 2018

Front. Pharmacol.

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Qianlie Xiaozheng decoction (QLXZD), a traditional Chinese medicinal formula, has been used clinically to treat advanced prostate cancer (PCa) for more than 10 years. However, experimental evidence supporting its efficacy is lacking. Here, we investigated the anticancer properties and molecular mechanism of QLXZD in vitro in a human PCa cell line (PC3) and in vivo using PC3 xenografts in nude mice. We confirmed the antineoplastic activity of QLXZD by analyzing cell viability and tumor volume growth, which decreased significantly compared to that of the controls. Autophagy following QLXZD treatment was detected morphologically using transmission electron microscopy and was confirmed by measuring the expression of autophagy markers (LC3-II and p62) using fluorescence analysis, flow cytometry, and western blotting. Increasing autophagic flux induced by QLXZD was monitored via pmCherry-GFP-LC3 fluorescence analysis. QLXZD-induced autophagic cell death was alleviated by the autophagy inhibitors, 3-methyl adenine and hydroxychloroquine. We evaluated the total expression and phosphorylation levels of proteins involved in the Akt/mTOR pathway regulating autophagy. Phosphorylation of Akt, mTOR, and p70S6K, but not total protein levels, decreased following treatment. This is the first study to demonstrate the autophagy-related mechanistic pathways utilized during QLXZD-mediated antitumor activity both in vitro and in vivo. These findings support the clinical use of QLXZD for PCa treatment.

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BECN1-dependent CASP2 incomplete autophagy induction by binding to rabies virus phosphoprotein

Cited by 58 publications

References 64 publications

Zebrafish C-reactive protein isoforms inhibit SVCV replication by blocking autophagy through interactions with cell membrane cholesterol

Zebrafish C-reactive protein isoforms inhibit SVCV replication by blocking autophagy through interactions with cell membrane cholesterol

CUL4B regulates autophagy via JNK signaling in diffuse large B-cell lymphoma

Qianlie Xiaozheng Decoction Induces Autophagy in Human Prostate Cancer Cells via Inhibition of the Akt/mTOR Pathway

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