<sec>
<title>Objectives</title>
<p>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.</p></sec>
<sec>
<title>Methods</title>
<p>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.</p></sec>
<sec>
<title>Results</title>
<p>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 ( <italic>p</italic> < 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 ( <italic>p</italic> < 0.05). Beclin-1, a biomarker of autophagy, was also induced by transfection with VSV wt or M51R-mMPs at 48 hours post-transfection.</p></sec>
<sec>
<title>Conclusion</title>
<p>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.</p></sec>
Citations
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Exogenous expression of both matrix protein and glycoprotein facilitates infectious viral particle production of Borna disease virus 1 Takehiro Kanda, Madoka Sakai, Akiko Makino, Keizo Tomonaga
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.2022;[Epub] CrossRef
La herencia de Prometeo. Las enfermedades ocupacionales en el Corpus Hippocraticum César Sierra Martín Asclepio.2022; 74(1): p587. CrossRef
Analyses of cell death mechanisms related to amino acid substitution at position 95 in the rabies virus matrix protein Isshu Kojima, Fumiki Izumi, Makoto Ozawa, Yoshikazu Fujimoto, Misuzu Okajima, Naoto Ito, Makoto Sugiyama, Tatsunori Masatani
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.2021;[Epub] CrossRef
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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
<sec>
<title>Objectives</title>
<p>Human rhinoviruses (HRVs) are the major cause of the common cold. Currently there is no registered, clinically effective, antiviral chemotherapeutic agent to treat diseases caused by HRVs. In this study, the antiviral activity of dexamethasone (DEX) against HRV1B was examined.</p></sec>
<sec>
<title>Methods</title>
<p>The anti–HRV1B activity of DEX was assessed by sulforhodamine B assay in HeLa cells, and by RT-PCR in the lungs of HRV1B-infected mice. Histological evaluation of HRV1B-infected lungs was performed and a histological score was given. Anti-HRV1B activity of DEX via the glucocorticoid receptor (GCR)-dependent autophagy activation was assessed by blocking with chloroquine diphosphate salt or bafilomycin A1 treatment.</p></sec>
<sec>
<title>Results</title>
<p>In HRV1B-infected HeLa cells, treatment with DEX in a dose-dependent manner, resulted in a cell viability of > 70% indicating that HRV1B viral replication was reduced by DEX treatment. HRV1B infected mice treated with DEX, had evidence of reduced inflammation and a moderate histological score. DEX treatment showed antiviral activity against HRV1B via GCR-dependent autophagy activation.</p></sec>
<sec>
<title>Conclusion</title>
<p>This study demonstrated that DEX treatment showed anti-HRV1B activity via GCR-dependent autophagy activation in HeLa cells and HRV1B infected mice. Further investigation assessing the development of topical formulations may enable the development of improved DEX effectiveness.</p></sec>
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Intracellular translocation of HMGB1 is important for Zika virus replication in Huh7 cells Kim-Ling Chin, Nurhafiza Zainal, Sing-Sin Sam, Pouya Hassandarvish, Rafidah Lani, Sazaly AbuBakar Scientific Reports.2022;[Epub] CrossRef
Pharmacological Modulators of Autophagy as a Potential Strategy for the Treatment of COVID-19 Gustavo José da Silva Pereira, Anderson Henrique França Figueredo Leão, Adolfo Garcia Erustes, Ingrid Beatriz de Melo Morais, Talita Aparecida de Moraes Vrechi, Lucas dos Santos Zamarioli, Cássia Arruda Souza Pereira, Laís de Oliveira Marchioro, Letícia P International Journal of Molecular Sciences.2021; 22(8): 4067. CrossRef
MSTN Attenuates Cardiac Hypertrophy through Inhibition of Excessive Cardiac Autophagy by Blocking AMPK /mTOR and miR-128/PPARγ/NF-κB Hanping Qi, Jing Ren, Lina Ba, Chao Song, Qianhui Zhang, Yonggang Cao, Pilong Shi, Bowen Fu, Yongsheng Liu, Hongli Sun Molecular Therapy - Nucleic Acids.2020; 19: 507. CrossRef
Autophagy Augmentation to Alleviate Immune Response Dysfunction, and Resolve Respiratory and COVID-19 Exacerbations Garrett Pehote, Neeraj Vij Cells.2020; 9(9): 1952. CrossRef
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