ArticleMolecular therapy oncolytics2019
Overexpression of Smac by an Armed Vesicular Stomatitis Virus Overcomes Tumor Resistance.
Article in Molecular therapy oncolytics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Drinkable gene therapy foam for the treatment of constrictive esophageal carcinoma.Gene therapy · 2026Article
- Resistance to oncolytic virotherapy: Multidimensional mechanisms and therapeutic breakthroughs (Review).International journal of molecular medicine · 2025Review
- Oncolytic Maraba Virus MG1 Mediates Direct and Natural Killer Cell-Dependent Lysis of Ewing Sarcoma.Cancers · 2025Article
- RNAi Screening in Tumor Cells Identifies Artificial microRNAs That Improve Oncolytic Virus Replication.Pharmaceuticals (Basel, Switzerland) · 2025Article
- SMAC-armed oncolytic virotherapy enhances the anticancer activity of PD1 blockade by modulating PANoptosis.Biomarker research · 2025Article
- Engineering of Vesicular Stomatitis Virus (VSV) for Modulating Cell Death and Antitumor Immunity.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Employing the Oncolytic Vesicular Stomatitis Virus in Cancer Virotherapy: Resistance and Clinical Considerations.Viruses · 2024Review
- Review
- Enhancing the Efficacy of Breast Cancer Immunotherapy Using a Smac-Armed Oncolytic Virus.Cancers · 2024Article
- Cellular resistance to an oncolytic virus is driven by chronic activation of innate immunity.iScience · 2023Article
- Modulation of the tumor microenvironment by armed vesicular stomatitis virus in a syngeneic pancreatic cancer model.Virology journal · 2022Article
- ILP-2: A New Bane and Therapeutic Target for Human Cancers.Frontiers in oncology · 2022Review
- Review
- ANTP-SmacN7 fusion peptide-induced radiosensitization in A549 cells and its potential mechanisms.Thoracic cancer · 2020Article
- New Therapeutic Options for Advanced Hepatocellular Carcinoma.Cancer control : journal of the Moffitt Cancer CenterArticle
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite reports of successful clinical cases, many tumors appear to resist infection by oncolytic viruses (OVs). To circumvent this problem, an armed vesicular stomatitis virus was constructed by inserting a transgene to express Smac/DIABLO during virus infection (VSV-S). Endogenous Smac in HeLa cells was diminished during wtVSV infection, whereas the Smac level was enhanced during VSV-S infection. Apoptosis was readily induced by VSV-S, but not wtVSV, infection. More importantly, the tumor volume was reduced to a larger extent when xenografts of 4T1 cells in BALB/c mice and OV-resistant T-47D cells in nude mice were intratumorally injected with VSV-S. VSV-S represents a novel mechanism to overcome tumor resistance, resulting in more significant tumor regression due to enhanced apoptosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.