ArticleCancer gene therapy2008
JNK-deficiency enhanced oncolytic vaccinia virus replication and blocked activation of double-stranded RNA-dependent protein kinase.
Article in Cancer gene therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Vaccinia virus for lung cancer therapy: preclinical progress and prospects as a systemic immunotherapy platform.Frontiers in immunology · 2026Review
- Oncolytic Viruses as a Novel Therapeutic Approach for Colorectal Cancer: Mechanisms, Current Advances, and Future Directions.Cancers · 2025Review
- Advancing ORFV-Based Therapeutics to the Clinical Stage.Reviews in medical virology · 2025Review
- The Potential of Oncolytic Virotherapy in the Treatment of Head and Neck Cancer: A Comprehensive Review.International journal of molecular sciences · 2024Review
- The Roles of c-Jun N-Terminal Kinase (JNK) in Infectious Diseases.International journal of molecular sciences · 2021Review
- Review
- Article
- Hazard Characterization of Modified Vaccinia Virus Ankara Vector: What Are the Knowledge Gaps?Viruses · 2017Review
- BX-795 inhibits HSV-1 and HSV-2 replication by blocking the JNK/p38 pathways without interfering with PDK1 activity in host cells.Acta pharmacologica Sinica · 2017Article
- Oncolytic Viruses-Interaction of Virus and Tumor Cells in the Battle to Eliminate Cancer.Frontiers in oncology · 2017Review
- The activation of p38MAPK and JNK pathways in bovine herpesvirus 1 infected MDBK cells.Veterinary research · 2016Article
- Oncolytic viruses in head and neck cancer: a new ray of hope in the management protocol.Annals of medical and health sciences research · 2014Review
- Defective antiviral CD8 T-cell response and viral clearance in the absence of c-Jun N-terminal kinases.Immunology · 2014Article
- A vaccinia virus-driven interplay between the MKK4/7-JNK1/2 pathway and cytoskeleton reorganization.Journal of virology · 2012Article
- JNK1 phosphorylation of Cdt1 inhibits recruitment of HBO1 histone acetylase and blocks replication licensing in response to stress.Molecular cell · 2011Article
- Prognostic significance of RNA-dependent protein kinase on non-small cell lung cancer patients.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010Article
- TRAIL gene-armed oncolytic poxvirus and oxaliplatin can work synergistically against colorectal cancer.Gene therapy · 2010Article
- Intelligent design: combination therapy with oncolytic viruses.Molecular therapy : the journal of the American Society of Gene Therapy · 2010Review
- Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Vaccinia virus has recently been used as an expression vector for gene delivery and an oncolytic agent for cancer therapy. Although it has been established that interferon-induced double-stranded RNA (dsRNA)-activated protein kinase (PKR) and RNase L interfere with viral replication, little else is known about the other host factors that might affect viral replication and virus-mediated host cell killing. In this study, we evaluated the roles of c-Jun NH2-terminal kinase (JNK) in oncolytic vaccinia virus replication and vaccinia virus-mediated host cell killing. We found that JNK knockout mouse embryonic fibroblasts (MEFs) were more susceptible to oncolytic vaccinia virus infection than wild-type MEFs. Moreover, viral replication and the production of infectious viral progeny were up to 100-fold greater in JNK-deficient MEFs than in wild-type MEFs. A similar result was observed for wild-type vaccinia virus. The increased killing of infected cells and the production of viral progeny was also observed in wild-type MEFs that had been treated with JNK inhibitors and in human colon cancer cells that had been transfected with dominant-negative JNK constructs. Moreover, testing on several human lung cancer cell lines and HeLa cells showed an inverse correlation between levels of JNK expression and susceptibility to oncolytic vaccinia virus. Our study also revealed that oncolytic virus infection-mediated PKR activation was blocked or diminished in JNK-deficient MEFs. The adenovirus-mediated ectopic expression of human PKR in JNK-deficient MEFs reduced vaccinia virus replication to the levels observed in wild-type MEFs, indicating that JNK is required for vaccinia virus to efficiently activate PKR. Our results demonstrated that the cellular status of JNK function can dramatically affect oncolytic vaccinia virus replication and vaccinia virus-mediated host cell killing. This finding may enable further improvements in oncolytic virotherapy using vaccinia virus.
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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.