ArticleJournal of medical virology2023
KSHV hijacks FoxO1 to promote cell proliferation and cellular transformation by antagonizing oxidative stress.
Article in Journal of medical virology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Cellular signaling crosstalk between osteoporosis and diabetes: Common mechanisms and therapeutic targets (Review).Biomedical reports · 2026Review
- Alkaline sphingomyelinase (ENPP7) attenuates DSS-induced colitis by modulating FOXO1-mediated antioxidative stress responses.BMC gastroenterology · 2026Article
- Effect of Dietary Salt Excess on DNA Methylation and Transcriptional Regulation of Human Angiotensinogen Gene Expression.American journal of hypertension · 2026Article
- A viral Cyclin D homolog protein hijacks the metabolic stress sensor SESN2 to promote primary effusion lymphoma growth.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Oncogenic Mechanisms of Kaposi's Sarcoma-Associated Herpesvirus on Cell Metabolism and Cell Transformation.Journal of medical virology · 2025Review
- Heterogeneous Activation of Signaling Pathways and Therapeutic Vulnerabilities in KSHV-Associated Primary Effusion Lymphoma Cell Lines.Journal of medical virology · 2025Article
- Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025Review
- Protective Action of 3,5-Diiodo-L-Thyronine on Cigarette Smoke-Induced Mitochondrial Dysfunction in Human Alveolar Epithelial Cells.Biomedicines · 2025Article
- Blood-Based Whole-Genome Methylation Analysis of Yili Horses Pre- and Post-Racing.Animals : an open access journal from MDPI · 2025Article
- A comprehensive characterization of metabolic signatures-hypoxia, glycolysis, and lactylation-in non-healing diabetic foot ulcers.Frontiers in molecular biosciences · 2025Article
- RUNX3 inhibits KSHV lytic replication by binding to the viral genome and repressing transcription.Journal of virology · 2024Article
- Article
- Enhancing Anticancer Efficacy of Formononetin Microspheres via Microfluidic Fabrication.AAPS PharmSciTech · 2023Article
- Epigenetic and transcriptional regulation of the human angiotensinogen gene by high salt.bioRxiv : the preprint server for biology · 2023Article
- METTL16 controls Kaposi's sarcoma-associated herpesvirus replication by regulating S-adenosylmethionine cycle.Cell death & disease · 2023Article
- Targeting FoxO proteins induces lytic reactivation of KSHV for treating herpesviral primary effusion lymphoma.PLoS pathogens · 2023Article
- Pioneer factors in viral infection.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) are a group of a highly short-lived molecules that control diverse behaviors of cells. Normal cells maintain ROS balance to ensure their functions. Because of oncogenic stress, cancer cells often have excessive ROS, also known as oxidative stress, which are often counteracted by enhanced antioxidant systems to maintain redox homeostasis. Kaposi's sarcoma-associated herpesvirus (KSHV) is an oncogenic virus associated with Kaposi's sarcoma (KS), which manifests hyper inflammation and oxidative stress as the hallmarks. We have previously shown that excessive ROS can disrupt KSHV latency by inducing viral lytic replication, leading to cell death. Paradoxically, most KS tumor cells are latently infected by KSHV in a highly inflammatory and oxidative stress tumor microenvironment, which is in part due to the activation of alternative complement and TLR4 pathways, indicating the existence of an enhanced antioxidant defense system in KS tumor cells. In this study, we show that KSHV upregulates antioxidant genes, including SOD2 and CAT by hijacking the forkhead box protein O1 (FoxO1), to maintain intracellular ROS level. Moreover, the fine-tuned balance of ROS level in KSHV-transformed cells is essential for cell survival. Consequently, KSHV-transformed cells are extremely sensitive to exogenous ROS insult such as treatment with a low level of hydrogen peroxide (H
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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 Socratic graph.