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Original Articles
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
  • 6,672 View
  • 148 Download
  • 9 Crossref
AbstractAbstract 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.

Citations

Citations to this article as recorded by  
  • Evoking pyroptosis with nanomaterials for cancer immunotherapy: Current boom and novel outlook
    Wen-Da Wang, Zhi-Jun Sun
    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
    Amirhossein Mardi, Anastasia V. Shirokova, Rebar N. Mohammed, Ali Keshavarz, Angelina O. Zekiy, Lakshmi Thangavelu, Talar Ahmad Merza Mohamad, Faroogh Marofi, Navid Shomali, Amir Zamani, Morteza Akbari
    Cancer Cell International.2022;[Epub]     CrossRef
  • Oncolytic Viruses: Immunotherapy Drugs for Gastrointestinal Malignant Tumors
    Qingbo Li, Patrick Kwabena Oduro, Rui Guo, Ruiqiao Li, Ling Leng, Xianbin Kong, Qilong Wang, Long Yang
    Frontiers in Cellular and Infection Microbiology.2022;[Epub]     CrossRef
  • Live-attenuated poliovirus-induced extrinsic apoptosis through Caspase 8 within breast cancer cell lines expressing CD155
    Hossein Vazeh, Emad Behboudi, Anahita Hashemzadeh-Omran, Abdolvahab Moradi
    Breast Cancer.2022; 29(5): 899.     CrossRef
  • 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
    Journal of General Virology .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
    Journal of General Virology .2021;[Epub]     CrossRef
  • The role of non-apoptotic cell death in the treatment and drug-resistance of digestive tumors
    Yang Yang, LiangLiang Bai, Weiting Liao, Mingyang Feng, Mengxi Zhang, Qiuji Wu, Kexun Zhou, Feng Wen, Wanting Lei, Nan Zhang, Jiaxing Huang, Qiu Li
    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
Anti-Human Rhinovirus 1B Activity of Dexamethasone viaGCR-Dependent Autophagy Activation
Jae-Sug Lee, Seong-Ryeol Kim, Jae-Hyoung Song, Yong-Pyo Lee, Hyun-Jeong Ko
Osong Public Health Res Perspect. 2018;9(6):334-339.   Published online December 31, 2018
DOI: https://doi.org/10.24171/j.phrp.2018.9.6.07
  • 5,195 View
  • 66 Download
  • 4 Crossref
AbstractAbstract PDF
Objectives

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.

Methods

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.

Results

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.

Conclusion

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.

Citations

Citations to this article as recorded by  
  • 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

PHRP : Osong Public Health and Research Perspectives