ArticlePLoS pathogens2019
Identification of viral SIM-SUMO2-interaction inhibitors for treating primary effusion lymphoma.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Oncogenic viral infection triggers LAMP2A SUMOylation and chaperone-mediated autophagy to promote tumorigenesis.Nature microbiology · 2026Article
- A KSHV-targeted small molecule efficiently blocks SARS-CoV-2 infection via inhibiting expression of EGFR and Cyclin A2.Emerging microbes & infections · 2025Article
- Garcinol as an Epigenetic Modulator: Mechanisms of Anti-Cancer Activity and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Decoding microbial carcinogenic strategies: ubiquitination and SUMO modification.Frontiers in microbiology · 2025Review
- A small molecule that selectively inhibits the growth of Epstein-Barr virus-latently infected cancer cells.iScience · 2024Article
- Targeting FoxO proteins induces lytic reactivation of KSHV for treating herpesviral primary effusion lymphoma.PLoS pathogens · 2023Article
- A Tale of Usurpation and Subversion: SUMO-Dependent Integrity of Promyelocytic Leukemia Nuclear Bodies at the Crossroad of Infection and Immunity.Frontiers in cell and developmental biology · 2021Review
- Targeting Host Cellular Factors as a Strategy of Therapeutic Intervention for Herpesvirus Infections.Frontiers in cellular and infection microbiology · 2021Review
- Identification of Mubritinib (TAK 165) as an inhibitor of KSHV driven primary effusion lymphoma via disruption of mitochondrial OXPHOS metabolism.Oncotarget · 2020Article
- Regulation of KSHV Latency and Lytic Reactivation.Viruses · 2020Review
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary effusion lymphoma (PEL) is an aggressive B-cell malignancy without effective treatment, and caused by the infection of Kaposi's sarcoma-associated herpesvirus (KSHV), predominantly in its latent form. Previously we showed that the SUMO2-interacting motif within the viral latency-associated nuclear antigen (LANASIM) is essential for establishment and maintenance of KSHV latency. Here, we developed a luciferase based live-cell reporter system to screen inhibitors selectively targeting the interaction between LANASIM and SUMO2. Cambogin, a bioactive natural product isolated from the Garcinia genus (a traditional herbal medicine used for cancer treatment), was obtained from the reporter system screening to efficiently inhibit the association of SUMO2 with LANASIM, in turn reducing the viral episome DNA copy number for establishment and maintenance of KSHV latent infection at a low concentration (nM). Importantly, Cambogin treatments not only specifically inhibited proliferation of KSHV-latently infected cells in vitro, but also induced regression of PEL tumors in a xenograft mouse model. This study has identified Cambogin as a novel therapeutic agent for treating PEL as well as eliminating persistent infection of oncogenic herpesvirus.
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