ArticleProceedings of the National Academy of Sciences of the United States of America2004
Reovirus oncolysis: the Ras/RalGEF/p38 pathway dictates host cell permissiveness to reovirus infection.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
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Who cites it
107 citing papers in PubMed, 188 citations in OpenAlex.
- Beyond oncogenesis: the unexplored benefits of viruses in cancer immunity.Nature reviews. Cancer · 2026Review
- Enhanced sialic acid engagement at physiological temperatures by reovirus σ1 mutants facilitates infection of breast cancer cells with low levels of high-affinity receptors.Journal of virology · 2026Article
- Reovirus resistance in tumors mediated by elevated ISG expression: overcoming therapeutic resistance via JAK/STAT pathway modulation.Virology journal · 2026Article
- Spatiotemporal coordination of reovirus peripheral core replication to perinuclear whole virus assembly.PLoS pathogens · 2025Article
- Unusual Partners: γδ-TCR-Based T Cell Therapy in Combination with Oncolytic Virus Treatment for Diffuse Midline Gliomas.International journal of molecular sciences · 2025Article
- Repurposing of lonafarnib as a treatment for SARS-CoV-2 infection.JCI insight · 2025Article
- The heterogeneous sensitivity of pediatric brain tumors to different oncolytic viruses is predicted by unique gene expression profiles.Molecular therapy. Oncology · 2024Article
- Advances in cell-based delivery of oncolytic viruses as therapy for lung cancer.Molecular therapy. Oncology · 2024Review
- Oncolytic viruses: a potential breakthrough immunotherapy for multiple myeloma patients.Frontiers in immunology · 2024Review
- Innovative strategies in genitourinary cancer: the role of oncolytic viruses.Frontiers in oncology · 2024Review
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- p38 Mitogen-Activated Protein Kinase Signaling Enhances Reovirus Replication by Facilitating Efficient Virus Entry, Capsid Uncoating, and Postuncoating Steps.Journal of virology · 2023Article
- Oncolyic Virotherapy for Prostate Cancer: Lighting a Fire in Winter.International journal of molecular sciences · 2022Review
- Reovirus uses temporospatial compartmentalization to orchestrate core versus outercapsid assembly.PLoS pathogens · 2022Article
- Recombinant Viral Vectors for Therapeutic Programming of Tumour Microenvironment: Advantages and Limitations.Biomedicines · 2022Review
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- Engaging Pattern Recognition Receptors in Solid Tumors to Generate Systemic Antitumor Immunity.Cancer treatment and research · 2022Article
- Genetic Modifications That Expand Oncolytic Virus Potency.Frontiers in molecular biosciences · 2022Review
- Oncolytic virus therapy in cancer: A current review.World journal of virology · 2021Review
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reovirus is a benign human virus that was recently found to have oncolytic properties and is currently in clinical trials as a potential cancer therapy. We have previously demonstrated that activation of Ras signaling, a common event in cancer, renders cells susceptible to reovirus oncolysis. In this study, we investigate which elements downstream of Ras are important in reovirus infection. By using a panel of NIH 3T3 cells transformed with activated Ras mutated in the effector-binding domain, we found that only the RasV12G37 mutant, which was unable to signal to Raf or phosphatidylinositol 3-kinase but retained signaling capability to guanine nucleotide-exchange factors (GEFs) for the small G protein, Ral (known as RalGEFs), was permissive to reovirus. Expression of the activated mutant of the RalGEF, Rlf, also allowed reovirus replication. Specific inhibition of the Ral pathway by using dominant-negative RalA rendered normally permissive H-Ras cells (cells expressing activated Ras) resistant to reovirus. To further identify elements downstream of RalGEF that promote reovirus infection, we used chemical inhibitors of the downstream signaling elements p38 and JNK. We found that reovirus infection was blocked in the presence of the p38 inhibitor but not the JNK inhibitor. Together, these results implicate a Ras/RalGEF/p38 pathway in the regulation of reovirus replication and oncolysis.
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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.