ArticleThe Journal of surgical research2014
Molecular determinants of susceptibility to oncolytic vesicular stomatitis virus in pancreatic adenocarcinoma.
Article in The Journal of surgical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Fostamatinib (R788), a spleen tyrosine kinase inhibitor, sensitizes pancreatic cancer cells to oncolytic vesicular stomatitis virus.Molecular therapy. Oncology · 2025Article
- Biomimetic Tumour Model Systems for Pancreatic Ductal Adenocarcinoma in Relation to Photodynamic Therapy.International journal of molecular sciences · 2025Review
- Resistance signatures to oncolytic vesiculoviruses in pancreatic ductal adenocarcinoma.Molecular therapy. Oncology · 2025Article
- 2-Deoxyglucose, an Inhibitor of Glycolysis, Enhances the Oncolytic Effect of Coxsackievirus.Cancers · 2022Article
- Oncolytic Viruses in the Therapy of Lymphoproliferative Diseases.Molecular biology · 2022Article
- An Extensive Review on Preclinical and Clinical Trials of Oncolytic Viruses Therapy for Pancreatic Cancer.Frontiers in oncology · 2022Review
- Review
- The Role of Vesicular Stomatitis Virus Matrix Protein in Autophagy in the Breast Cancer.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- Oncolytic activity of the rhabdovirus VSV-GP against prostate cancer.International journal of cancer · 2018Article
- Preclinical Development of Oncolytic Immunovirotherapy for Treatment of HPVMolecular therapy oncolytics · 2018Article
- Recent advances in vesicular stomatitis virus-based oncolytic virotherapy: a 5-year update.The Journal of general virology · 2017Article
- Gene expression profiling of hematologic malignant cell lines resistant to oncolytic virus treatment.Oncotarget · 2017Article
- Review
- Murine Tumor Models for Oncolytic Rhabdo-Virotherapy.ILAR journal · 2016Article
- Phase 1 study of intratumoral Pexa-Vec (JX-594), an oncolytic and immunotherapeutic vaccinia virus, in pediatric cancer patients.Molecular therapy : the journal of the American Society of Gene Therapy · 2015Article
- Mechanistic insights into the oncolytic activity of vesicular stomatitis virus in cancer immunotherapy.Oncolytic virotherapy · 2015Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundM protein mutant vesicular stomatitis virus (M51R-VSV) has oncolytic properties against many cancers. However, some cancer cells are resistant to M51R-VSV. Herein, we evaluate the molecular determinants of vesicular stomatitis virus (VSV) resistance in pancreatic adenocarcinoma cells.
methodsCell viability and the effect of β-interferon (IFN) were analyzed using 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. Gene expression was evaluated via microarray analysis. Cell infectability was measured by flow cytometry. Xenografts were established in athymic nude mice and treated with intratumoral M51R-VSV.
resultsFour of five pancreatic cancer cell lines were sensitive to M51R-VSV, whereas Panc 03.27 cells remained resistant (81 ± 3% viability 72 h after single-cycle infection). Comparing sensitive MiaPaCa2 cells with resistant Panc 03.27 cells, significant differences in gene expression were found relating to IFN signaling (P = 2 × 10(-5)), viral entry (P = 3 × 10(-4)), and endocytosis (P = 7 × 10(-4)). MiaPaCa2 cells permitted high levels of VSV infection, whereas Panc 03.27 cells were capable of resisting VSV cell entry even at high multiplicities of infection. Extrinsic β-IFN overcame apparent defects in IFN-mediated pathways in MiaPaCa2 cells conferring VSV resistance. In contrast, β-IFN decreased cell viability in Panc 3.27 cells, suggesting intact antiviral mechanisms. VSV-treated xenografts exhibited reduced tumor growth relative to controls in both MiaPaCa2 (1423 ± 345% versus 164 ± 136%; P < 0.001) and Panc 3.27 (979 ± 153% versus 50 ± 56%; P = 0.002) tumors. Significant lymphocytic infiltration was seen in M51R-VSV-treated Panc 03.27 xenografts.
conclusionsInhibition of VSV endocytosis and intact IFN-mediated defenses are responsible for M51R-VSV resistance in pancreatic adenocarcinoma cells. M51R-VSV treatment appears to induce antitumor cellular immunity in vivo, which may expand its clinical efficacy.
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