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- Cell Death Mechanisms in Esophageal Squamous Cell Carcinoma Induced by Vesicular Stomatitis Virus Matrix Protein
- Yousef Douzandegan, Alireza Tahamtan, Zahra Gray, Hadi Razavi Nikoo, Alijan Tabarraei, Abdolvahab Moradi
- Osong Public Health Res Perspect. 2019;10(4):246-252. Published online August 31, 2019
- DOI: https://doi.org/10.24171/j.phrp.2019.10.4.08
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Abstract
PDF Objectives Vesicular stomatitis virus (VSV) is under development as an oncolytic virus due to its preferential replication in cancer cells and oncolytic activity, however the viral components responsible have not yet been determined. In this study the effects of VSV wild-type (wt) and M51R-mutant matrix proteins (M51R-mMP) on apoptosis, pyroptosis, necroptosis, and autophagy pathways, in an esophagus cancer cell line (KYSE-30) were investigated.
Methods The KYSE-30 cells were transfected with pcDNA3.1 plasmids encoding wt or M51R-mMP, and apoptosis, pyroptosis, necroptosis, and autophagy were evaluated 48 and 72 hours after transfection.
Results KYSE-30 cells transfected with VSV wt and M51R-mMPs significantly reduced cell viability to < 50% at 72 hours post-transfection. M51R-MP significantly increased the concentration of caspase-8 and caspase-9 at 48 and 72 hours post-transfection, respectively (
p < 0.05). In contrast, no significant changes were detected following transfection with the VSV wt plasmid. Moreover, VSV wt and M51R-mMP transfected cells did not change the expression of caspase-3. VSV wt and M51R-mMPs did not mMP change caspase-1 expression (a marker of pyroptosis) at 48 and 72 hours post-transfection. However, M51R-mMP and VSV wt transfected cells significantly increased RIP-1 (a marker of necroptosis) expression at 72 hours post-infection (p < 0.05). Beclin-1, a biomarker of autophagy, was also induced by transfection with VSV wt or M51R-mMPs at 48 hours post-transfection.Conclusion The results in this study indicated that VSV exerts oncolytic activity in KYSE-30 tumor cells through different cell death pathways, suggesting that M51R-mMP may potentially be used to enhance oncolysis.
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Citations
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- Evoking pyroptosis with nanomaterials for cancer immunotherapy: Current boom and novel outlook
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Nano TransMed.2022; 1(1): 9130001. CrossRef - Biological causes of immunogenic cancer cell death (ICD) and anti-tumor therapy; Combination of Oncolytic virus-based immunotherapy and CAR T-cell therapy for ICD induction
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Cancer Cell International.2022;[Epub] CrossRef - Oncolytic Viruses: Immunotherapy Drugs for Gastrointestinal Malignant Tumors
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Experimental Cell Research.2021; 405(2): 112678. CrossRef - NEBL and AKT1 maybe new targets to eliminate the colorectal cancer cells resistance to oncolytic effect of vesicular stomatitis virus M-protein
Zoleikha Mamizadeh, Mohamad Reza Kalani, Masoud Parsania, Mohammad Mehdi Soltan Dallal, Abdolvahab Moradi
Molecular Therapy - Oncolytics.2021; 23: 593. CrossRef
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- Natural Infection with Rabies Virus: A Histopathological and Immunohistochemical Study of Human Brains
- Firouzeh Farahtaj, Leila Alizadeh, Alireza Gholami, Alireza Tahamtan, Sadegh Shirian, Maryam Fazeli, Amir Sasan Mozaffari Nejad, Ali Gorji, Hamid Mahmoudzadeh Niknam, Amir Ghaemi
- Osong Public Health Res Perspect. 2019;10(1):6-11. Published online February 28, 2019
- DOI: https://doi.org/10.24171/j.phrp.2019.10.1.03
- 7,238 View
- 244 Download
- 12 Crossref
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Abstract
PDF
Objectives Despite all the efforts and increased knowledge of rabies, the exact mechanisms of infection and mortality from the rabies virus are not well understood. To understand the mechanisms underlying the pathogenicity of rabies virus infection, it is crucial to study the tissue that the rabies virus naturally infects in humans.
Methods Cerebellum brain tissue from 9 human post mortem cases from Iran, who had been infected with rabies virus, were examined histopathologically and immunohistochemically to evaluate the innate immune responses against the rabies virus.
Results Histopathological examination revealed inflammation of the infected cerebellum and immunohistochemical analyses showed an increased immunoreactivity of heat shock protein 70, interleukin-6, interleukin-1, tumor necrosis factor-alpha, caspase-3, caspase-9, toll-like receptor3 and toll-like receptor4 in the infected brain tissue.
Conclusion These results indicated the involvement of innate immunity in rabies infected human brain tissue, which may aggravate the progression of this deadly disease.
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Citations
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Diagnostic Pathology.2022;[Epub] CrossRef - Mitochondrial Dysfunction in Rabies Virus-Infected Human and Canine Brains
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