ArticleCancer science2021
A STING inhibitor suppresses EBV-induced B cell transformation and lymphomagenesis.
Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Single-cell profiling of HDAC inhibitor-induced EBV lytic heterogeneity defines abortive and refractory states in B lymphoblasts.PLoS pathogens · 2026Article
- Single-Cell Profiling of HDAC Inhibitor-Induced EBV Lytic Heterogeneity Defines Abortive and Refractory States in B Lymphoblasts.bioRxiv : the preprint server for biology · 2025Article
- Article
- Multi-omics integration reveals the oncogenic role of eccDNAs in diffuse large B-cell lymphoma through STING signalling.Clinical and translational medicine · 2024Article
- Multifaceted roles of cGAS-STING pathway in the lung cancer: from mechanisms to translation.PeerJ · 2024Review
- Growth Transformation of B Cells by Epstein-Barr Virus RequiresMicrobiology spectrum · 2023Article
- Epstein-Barr Virus BBLF1 Mediates Secretory Vesicle Transport to Facilitate Mature Virion Release.Journal of virology · 2023Article
- The battle between the innate immune cGAS-STING signaling pathway and human herpesvirus infection.Frontiers in immunology · 2023Review
- The cyclic guanosine monophosphate synthase-stimulator of interferon genes pathway as a potential target for tumor immunotherapy.Frontiers in immunology · 2023Review
- Epstein-Barr virus tegument protein BGLF2 in exosomes released from virus-producing cells facilitates de novo infection.Cell communication and signaling : CCS · 2022Article
- Strategies of Epstein-Barr virus to evade innate antiviral immunity of its human host.Frontiers in microbiology · 2022Review
- A STING inhibitor suppresses EBV-induced B cell transformation and lymphomagenesis.Cancer science · 2021Article
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
Epstein-Barr virus-associated lymphoproliferative disease (EBV-LPD) is frequently fatal. Innate immunity plays a key role in protecting against pathogens and cancers. The stimulator of interferon genes (STING) is regarded as a key adaptor protein allowing DNA sensors recognizing exogenous cytosolic DNA to activate the type I interferon signaling cascade. In terms of EBV tumorigenicity, the role of STING remains elusive. Here we showed that treatment with the STING inhibitor, C-176, suppressed EBV-induced transformation in peripheral blood mononuclear cells. In an EBV-LPD mouse model, C-176 treatment also inhibited tumor formation and prolonged survival. Treatment with B cells alone did not affect EBV transformation, but suppression of EBV-induced transformation was observed in the presence of T cells. Even without direct B cell-T cell contact in a transwell system, the inhibitor reduced the transformation activity, indicating that intercellular communication by humoral factors was critical to prevent EBV-induced transformation. These findings suggest that inhibition of STING signaling pathway with C-176 could be a new therapeutic target of EBV-LPD.
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