ArticleOncogene2016
Oncolytic reovirus induces intracellular redistribution of Ras to promote apoptosis and progeny virus release.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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
31 citing papers in PubMed, 48 citations in OpenAlex.
- GM-CSF Armed Oncolytic Adenovirus Enhances T-Cell Infiltration and Suppresses Local and Distal Tumor Growth.Viruses · 2026Article
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- Mechanisms of Oncolytic Virus-Induced Multi-Modal Cell Death and Therapeutic Prospects.International journal of molecular sciences · 2025Review
- Review
- Oncolytic Viruses in Ovarian Cancer: Where Do We Stand? A Narrative Review.Pathogens (Basel, Switzerland) · 2025Review
- SMAC-armed oncolytic virotherapy enhances the anticancer activity of PD1 blockade by modulating PANoptosis.Biomarker research · 2025Article
- Oncolytic Virus Senecavirus A Inhibits Hepatocellular Carcinoma Proliferation and Growth by Inducing Cell Cycle Arrest and Apoptosis.Journal of clinical and translational hepatology · 2024Article
- Comparison of differences in immune cells and immune microenvironment among different kinds of oncolytic virus treatments.Frontiers in immunology · 2024Review
- Oncolytic Parapoxvirus induces Gasdermin E-mediated pyroptosis and activates antitumor immunity.Nature communications · 2023Article
- Cell Killing by Reovirus: Mechanisms and Consequences.Current topics in microbiology and immunology · 2023Review
- Oncolytic viruses-modulated immunogenic cell death, apoptosis and autophagy linking to virotherapy and cancer immune response.Frontiers in cellular and infection microbiology · 2023Review
- Altered Glycan Expression on Breast Cancer Cells Facilitates Infection by T3 Seroptype Oncolytic Reovirus.Nano letters · 2021Article
- Egress of non-enveloped enteric RNA viruses.The Journal of general virology · 2021Review
- Review
- β-Adrenergic Receptor Inhibitor and Oncolytic Herpesvirus Combination Therapy Shows Enhanced Antitumoral and Antiangiogenic Effects on Colorectal Cancer.Frontiers in pharmacology · 2021Article
- Oncolytic Viruses and Cancer, Do You Know the Main Mechanism?Frontiers in oncology · 2021Review
- Current Trends in Cancer Immunotherapy.Biomedicines · 2020Review
- Noncanonical Cell Death Induction by Reassortant Reovirus.Journal of virology · 2020Article
- Assessing the oncolytic potential of rotavirus on mouse myeloma cell line Sp2/0-Ag14.Biomedica : revista del Instituto Nacional de Salud · 2020Article
- Development of oncolytic virotherapy: from genetic modification to combination therapy.Frontiers of medicine · 2020Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Reovirus is a naturally oncolytic virus that preferentially replicates in Ras-transformed cells and is currently undergoing clinical trials as a cancer therapeutic. Ras transformation promotes reovirus oncolysis by enhancing virion disassembly during entry, viral progeny production, and virus release through apoptosis; however, the mechanism behind the latter is not well understood. Here, we show that reovirus alters the intracellular location of oncogenic Ras to induce apoptosis of H-RasV12-transformed fibroblasts. Reovirus infection decreases Ras palmitoylation levels and causes accumulation of Ras in the Golgi through Golgi fragmentation. With the Golgi being the site of Ras palmitoylation, treatment of target cells with the palmitoylation inhibitor, 2-bromopalmitate (2BP), prompts a greater accumulation of H-RasV12 in the Golgi, and a dose-dependent increase in progeny virus release and subsequent spread. Conversely, tethering H-RasV12 to the plasma membrane (thereby preventing its movement to the Golgi) allows for efficient virus production, but results in basal levels of reovirus-induced cell death. Analysis of Ras downstream signaling reveals that cells expressing cycling H-RasV12 have elevated levels of phosphorylated JNK (c-Jun N-terminal kinase), and that Ras retained at the Golgi body by 2BP increases activation of the MEKK1/MKK4/JNK signaling pathway to promote cell death. Collectively, our data suggest that reovirus induces Golgi fragmentation of target cells, and the subsequent accumulation of oncogenic Ras in the Golgi body initiates apoptotic signaling events required for virus release and spread.
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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.