ArticlePLoS pathogens2013
Lymphotoxin signaling is initiated by the viral polymerase in HCV-linked tumorigenesis.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Pleiotropic and multicellular roles of lymphotoxin beta receptor in solid tumor immunity and therapeutic targeting.Frontiers in immunology · 2026Review
- New insights into potential biomarkers and their roles in biological processes associated with hepatitis C-related liver cirrhosis by hepatic RNA-seq-based transcriptome profiling.Virus research · 2024Article
- Cancer cell genetics shaping of the tumor microenvironment reveals myeloid cell-centric exploitable vulnerabilities in hepatocellular carcinoma.Nature communications · 2024Article
- CD81 suppresses NF-κB signaling and is downregulated in hepatitis C virus expressing cells.Frontiers in cellular and infection microbiology · 2024Article
- T-cell exhaustion signatures characterize the immune landscape and predict HCC prognosisFrontiers in immunology · 2023Article
- Review
- GOLT1B Activation in Hepatitis C Virus-Infected Hepatocytes Links ER Trafficking and Viral Replication.Pathogens (Basel, Switzerland) · 2021Article
- Targeting Lymphotoxin Beta and Paired Box 5: a potential therapeutic strategy for soft tissue sarcoma metastasis.Cancer cell international · 2021Article
- Review
- Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis.Oncotarget · 2017Review
- Chronic hepatitis C virus infection and pathogenesis of hepatocellular carcinoma.Current opinion in virology · 2016Review
- Article
- NOD1 Participates in the Innate Immune Response Triggered by Hepatitis C Virus Polymerase.Journal of virology · 2016Article
- Elevated NIBP/TRAPPC9 mediates tumorigenesis of cancer cells through NFκB signaling.Oncotarget · 2015Article
- Viruses in cancer cell plasticity: the role of hepatitis C virus in hepatocellular carcinoma.Contemporary oncology (Poznan, Poland) · 2015Review
- Oxidative stress and hepatic Nox proteins in chronic hepatitis C and hepatocellular carcinoma.Free radical biology & medicine · 2014Review
- B-cell-intrinsic hepatitis C virus expression leads to B-cell-lymphomagenesis and induction of NF-κB signalling.PloS one · 2014Article
- Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 3 countries.
Funding
Abstract
Exposure to hepatitis C virus (HCV) typically results in chronic infection that leads to progressive liver disease ranging from mild inflammation to severe fibrosis and cirrhosis as well as primary liver cancer. HCV triggers innate immune signaling within the infected hepatocyte, a first step in mounting of the adaptive response against HCV infection. Persistent inflammation is strongly associated with liver tumorigenesis. The goal of our work was to investigate the initiation of the inflammatory processes triggered by HCV viral proteins in their host cell and their possible link with HCV-related liver cancer. We report a dramatic upregulation of the lymphotoxin signaling pathway and more specifically of lymphotoxin-β in tumors of the FL-N/35 HCV-transgenic mice. Lymphotoxin expression is accompanied by activation of NF-κB, neosynthesis of chemokines and intra-tumoral recruitment of mononuclear cells. Spectacularly, IKKβ inactivation in FL-N/35 mice drastically reduces tumor incidence. Activation of lymphotoxin-β pathway can be reproduced in several cellular models, including the full length replicon and HCV-infected primary human hepatocytes. We have identified NS5B, the HCV RNA dependent RNA polymerase, as the viral protein responsible for this phenotype and shown that pharmacological inhibition of its activity alleviates activation of the pro-inflammatory pathway. These results open new perspectives in understanding the inflammatory mechanisms linked to HCV infection and tumorigenesis.
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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.