ArticleOncogene2019
Latent infection with Kaposi's sarcoma-associated herpesvirus enhances retrotransposition of long interspersed element-1.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 24 citations in OpenAlex.
- LINE-1 transposable element is expressed in Kaposi's sarcoma and regulates gene expression in KSHV-infected cells.bioRxiv : the preprint server for biology · 2026Article
- Human herpesvirus 6B U65 binds to histone proteins and suppresses interferon production.Journal of virology · 2025Article
- Cell-intrinsic regulation of HBV RNAs by the nonsense-mediated mRNA decay pathway controls viral replication.iScience · 2025Article
- Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025Review
- Molecular Mechanisms of Kaposi Sarcoma-Associated Herpesvirus (HHV8)-Related Lymphomagenesis.Cancers · 2024Review
- Suppression of Borna Disease Virus Replication during Its Persistent Infection Using the CRISPR/Cas13b System.International journal of molecular sciences · 2024Article
- Kaposi's sarcoma herpesvirus viral FLICE inhibitory protein modulates A20 deubiquitinase activity.Access microbiology · 2024Article
- Roles of Human Endogenous Retroviruses and Endogenous Virus-Like Elements in Cancer Development and Innate Immunity.Biomolecules · 2023Review
- The Role of DNA Viruses in Human Cancer.Cancer informatics · 2023Review
- Unwinding the roles of RNA helicase MOV10.Wiley interdisciplinary reviews. RNA · 2022Review
- The fifth Japanese meeting on biological function and evolution through interactions between hosts and transposable elements.Mobile DNA · 2022Article
- SARS-CoV-2 infection mediates differential expression of human endogenous retroviruses and long interspersed nuclear elements.JCI insight · 2021Article
- Article
- Characterization of an active LINE-1 in the naked mole-rat genome.Scientific reports · 2021Article
- Enterovirus Infection Restricts Long Interspersed Element 1 Retrotransposition.Frontiers in microbiology · 2021Article
- High levels of LINE-1 transposable elements expressed in Kaposi's sarcoma-associated herpesvirus-related primary effusion lymphoma.Oncogene · 2021Article
- Effects of activation of the LINE-1 antisense promoter on the growth of cultured cells.Scientific reports · 2020Article
- A Traditional Chinese Medicine, Maoto, Suppresses Hepatitis B Virus Production.Frontiers in cellular and infection microbiology · 2020Article
- Identification of a Retroelement-Containing Human Transcript Induced in the Nucleus by Vaccination.International journal of molecular sciences · 2019Article
- Profiling of LINE-1-Related Genes in Hepatocellular Carcinoma.International journal of molecular sciences · 2019Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kaposi's sarcoma (KS)-associated herpesvirus (KSHV), a gamma-2 herpesvirus, is the causative agent of KS, primary effusion lymphoma (PEL), and a plasma cell variant of multicentric Castleman's disease. Although KSHV latency is detected in KS-related tumors, oncogenic pathways activated by KSHV latent infection are not fully understood. Here, we found that retrotransposition of long interspersed element-1 (L1), a retrotransposon in the human genome, was enhanced in PEL cells. Among the KSHV latent genes, viral FLICE-inhibitory protein (vFLIP) enhanced L1 retrotransposition in an NF-κB-dependent manner. Intracellular cell adhesion molecule-1 (ICAM-1), an NF-κB target, regulated the vFLIP-mediated enhancement of L1 retrotransposition. Furthermore, ICAM-1 downregulated the expression of Moloney leukemia virus 10 (MOV10), an L1 restriction factor. Knockdown of ICAM-1 or overexpression of MOV10 relieved the vFLIP-mediated enhancement of L1 retrotransposition. Collectively, during KSHV latency, vFLIP upregulates ICAM-1 in an NF-κB-dependent manner, which, in turn, downregulates MOV10 expression and thereby enhances L1 retrotransposition. Because active L1 retrotransposition can lead to genomic instability, which is commonly found in KS and PEL, activation of L1 retrotransposition during KSHV latency may accelerate oncogenic processes through enhancing genomic instability. Our results suggest that L1 retrotransposition may be a novel target for impeding tumor development in KSHV-infected patients.
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