ArticleAsian Pacific journal of cancer prevention : APJCP2021
The Role of Vesicular Stomatitis Virus Matrix Protein in Autophagy in the Breast Cancer.
Article in Asian Pacific journal of cancer prevention : APJCP, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Oncolytic Effects of S89K Matrix Protein of Vesicular Stomatitis Virus in Cervical Cancer.Advanced biomedical research · 2026Article
- Cancer-Specific Activation of the Vesicular Stomatitis Virus Matrix by Survivin Promoter in Breast Cancer Cells.Molecular biotechnology · 2026Article
- Mechanisms of Oncolytic Virus-Induced Multi-Modal Cell Death and Therapeutic Prospects.International journal of molecular sciences · 2025Review
- Employing the Oncolytic Vesicular Stomatitis Virus in Cancer Virotherapy: Resistance and Clinical Considerations.Viruses · 2024Review
- Oncolytic viruses-modulated immunogenic cell death, apoptosis and autophagy linking to virotherapy and cancer immune response.Frontiers in cellular and infection microbiology · 2023Review
- NEBL and AKT1 maybe new targets to eliminate the colorectal cancer cells resistance to oncolytic effect of vesicular stomatitis virus M-protein.Molecular therapy oncolytics · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBreast cancer is one of the most difficult malignancies to treat. Therapeutics is used to target and kill the cancer cells. Non-human oncolytic viruses have the ability to cause cell death directly to cancers. The objective here was to investigate the role of Vesicular Stomatitis Virus (VSV) Matrix (M) protein in autophagy in the breast cancer cell line.
methodsTwo different VSV wild type and mutant (M51R) M protein constructs were produced. Breast cancer cell line BT-20 was transfected by either wild type or mutant vectors. Transfection efficiency was measured using a fluorescent microscopy. Expression of VSV M protein was investigated at protein level. Cell cytotoxicity was measured using an MTT assay. The autophagy pathway was studied by Beclin-1 immunoassay. Data were statistically analyzed between different transfected groups.
resultsIt has been shown that the VSV M protein induced higher levels of Beclin-1 than the M51R mutant in the BT-20 cell line. Increased levels of Beclin-1 were also associated with VSV M cell-induced cytotoxicity.
conclusionIt has been shown here that VSV wild type or mutant M proteins can cause autophagy-induced cell death by increasing Beclin-1 expression. This includes the possible role of VSV to be used as an oncolytic virus in breast cancer treatment. <br />.
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