ArticlePLoS pathogens2016
An Oncogenic Virus Promotes Cell Survival and Cellular Transformation by Suppressing Glycolysis.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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.
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Who cites it
53 citing papers in PubMed, 74 citations in OpenAlex.
- KSHV vIRF3-PKM2 interaction induces SMAD5 acetylation, promoting Kaposi's sarcoma progression.Experimental & molecular medicine · 2026Article
- D-glucose uptake inhibits bovine alphaherpesvirus 1 post-binding cell process entry via inhibition of PLC-γ1 signaling in a glucose transporter 1-independent manner.Microbiology spectrum · 2026Article
- STING inhibits viral lytic reactivation and cell growth in primary effusion lymphoma.Frontiers in immunology · 2026Article
- The bittersweet link between glucose metabolism, cellular microenvironment and viral infection.Virulence · 2025Review
- Oncogenic Mechanisms of Kaposi's Sarcoma-Associated Herpesvirus on Cell Metabolism and Cell Transformation.Journal of medical virology · 2025Review
- CypA inhibits respiratory syncytial virus (RSV) replication by suppressing glycolysis through the downregulation of PKM2 expression.Journal of virology · 2025Article
- Article
- Molecular mechanisms of viral oncogenesis in haematological malignancies: perspectives from metabolic reprogramming, epigenetic regulation and immune microenvironment remodeling.Experimental hematology & oncology · 2025Review
- Neospora caninum hijacks host PFKFB3-driven glycolysis to facilitate intracellular propagation of parasites.Veterinary research · 2025Article
- Understanding Metabolic Pathway Rewiring by Oncogenic Gamma Herpesvirus.Journal of microbiology and biotechnology · 2024Review
- Glucose-independent human cytomegalovirus replication is supported by metabolites that feed upper glycolytic branches.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A narrative review: exploring viral-induced malignancies through the lens of dysregulated cellular metabolism and glucose transporters.BMC cancer · 2024Review
- Article
- Pepsin enhances glycolysis to promote malignant transformation of vocal fold leukoplakia epithelial cells with dysplasia.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2023Article
- KSHV hijacks FoxO1 to promote cell proliferation and cellular transformation by antagonizing oxidative stress.Journal of medical virology · 2023Article
- When 3D genome technology meets viral infection, including SARS-CoV-2.Journal of medical virology · 2022Review
- A viral interferon regulatory factor degrades RNA-binding protein hnRNP Q1 to enhance aerobic glycolysis via recruiting E3 ubiquitin ligase KLHL3 and decaying GDPD1 mRNA.Cell death and differentiation · 2022Article
- Impaired mitochondria of Tregs decreases OXPHOS-derived ATP in primary immune thrombocytopenia with positive plasma pathogens detected by metagenomic sequencing.Experimental hematology & oncology · 2022Article
- TLR3 Expression is a Potential Prognosis Biomarker and Shapes the Immune-Active Tumor Microenvironment in Esophageal Squamous Cell Carcinoma.Journal of inflammation research · 2022Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Aerobic glycolysis is essential for supporting the fast growth of a variety of cancers. However, its role in the survival of cancer cells under stress conditions is unclear. We have previously reported an efficient model of gammaherpesvirus Kaposi's sarcoma-associated herpesvirus (KSHV)-induced cellular transformation of rat primary mesenchymal stem cells. KSHV-transformed cells efficiently induce tumors in nude mice with pathological features reminiscent of Kaposi's sarcoma tumors. Here, we report that KSHV promotes cell survival and cellular transformation by suppressing aerobic glycolysis and oxidative phosphorylation under nutrient stress. Specifically, KSHV microRNAs and vFLIP suppress glycolysis by activating the NF-κB pathway to downregulate glucose transporters GLUT1 and GLUT3. While overexpression of the transporters rescues the glycolytic activity, it induces apoptosis and reduces colony formation efficiency in softagar under glucose deprivation. Mechanistically, GLUT1 and GLUT3 inhibit constitutive activation of the AKT and NF-κB pro-survival pathways. Strikingly, GLUT1 and GLUT3 are significantly downregulated in KSHV-infected cells in human KS tumors. Furthermore, we have detected reduced levels of aerobic glycolysis in several KSHV-infected primary effusion lymphoma cell lines compared to a Burkitt's lymphoma cell line BJAB, and KSHV infection of BJAB cells reduced aerobic glycolysis. These results reveal a novel mechanism by which an oncogenic virus regulates a key metabolic pathway to adapt to stress in tumor microenvironment, and illustrate the importance of fine-tuning the metabolic pathways for sustaining the proliferation and survival of cancer cells, particularly under stress conditions.
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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.