ArticleNature communications2018
Inhibition of the mevalonate pathway enhances cancer cell oncolysis mediated by M1 virus.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 27 citations in OpenAlex.
- Protein farnesylation: from molecular mechanisms to therapeutic targeting in cancer, aging, and beyond.Frontiers in pharmacology · 2026Review
- Polybacterial intracellular macromolecules shape single-cell inflammatory profiles in upper airway epithelia.NPJ biofilms and microbiomes · 2025Article
- Functional-proteomics-based investigation of the cellular response to farnesyltransferase inhibition in lung cancer.iScience · 2025Article
- Global Research Trends and Hotspots in the Role of Cholesterol in Colorectal Cancer: A Bibliometric Analysis.Human mutation · 2025Article
- Arming oncolytic M1 virus with gasdermin E enhances antitumor efficacy in breast cancer.iScience · 2024Article
- Polybacterial Intracellular Macromolecules Shape Single-Cell Epikine Profiles in Upper Airway Mucosa.bioRxiv : the preprint server for biology · 2024Article
- Tutorial: design, production and testing of oncolytic viruses for cancer immunotherapy.Nature protocols · 2024Review
- Evidence of Differences in Cellular Regulation ofViruses · 2024Article
- Directed natural evolution generates a next-generation oncolytic virus with a high potency and safety profile.Nature communications · 2023Article
- In vitro and in vivo effects of 3-indoleacetonitrile-A potential new broad-spectrum therapeutic agent for SARS-CoV-2 infection.Antiviral research · 2023Article
- Overcoming resistance to oncolytic virus M1 by targeting PI3K-γ in tumor-associated myeloid cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Identification of the receptor of oncolytic virus M1 as a therapeutic predictor for multiple solid tumors.Signal transduction and targeted therapy · 2022Article
- Structure of infective Getah virus at 2.8 Å resolution determined by cryo-electron microscopy.Cell discovery · 2022Article
- Manipulating T-cell metabolism to enhance immunotherapy in solid tumor.Frontiers in immunology · 2022Review
- Metabolic barriers to cancer immunotherapy.Nature reviews. Immunology · 2021Review
- Suppression of CCDC6 sensitizes tumor to oncolytic virus M1.Neoplasia (New York, N.Y.) · 2021Article
- Review
- Intravenous injection of the oncolytic virus M1 awakens antitumor T cells and overcomes resistance to checkpoint blockade.Cell death & disease · 2020Article
- Tumors driven by RAS signaling harbor a natural vulnerability to oncolytic virus M1.Molecular oncology · 2020Article
- Targeted Metabolic Reprogramming to Improve the Efficacy of Oncolytic Virus Therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Review
Corrections and comments
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Authors and funding
20 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncolytic virus is an attractive anticancer agent that selectively lyses cancer through targeting cancer cells rather than normal cells. Although M1 virus is effective against several cancer types, certain cancer cells present low sensitivity to it. Here we identified that most of the components in the cholesterol biosynthesis pathway are downregulated after M1 virus infection. Further functional studies illustrate that mevalonate/protein farnesylation/ras homolog family member Q (RHOQ) axis inhibits M1 virus replication. Further transcriptome analysis shows that RHOQ knockdown obviously suppresses Rab GTPase and ATP-mediated membrane transporter system, which may mediate the antiviral effect of RHOQ. Based on this, inhibition of the above pathway significantly enhances the anticancer potency of M1 virus in vitro, in vivo, and ex vivo. Our research provides an intriguing strategy for the rational combination of M1 virus with farnesyl transferase inhibitors to enhance therapeutic efficacy.
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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 Socratic graph.