ArticleCancer research2020
Oncogenic Herpesvirus Engages Endothelial Transcription Factors SOX18 and PROX1 to Increase Viral Genome Copies and Virus Production.
Article in Cancer research, 2020. 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, 25 citations in OpenAlex.
- Vascular Endothelial Growth Factor Receptor 2 (VEGFR2/KDR) Promotes KSHV Lytic Replication and Drives Pro-Inflammatory Cytokine Release and Cancer Signaling.Journal of medical virology · 2026Article
- Spatial Transcriptomics of Patients With Kaposi Sarcoma Identifies Mechanisms of Immune Evasion.Journal of medical virology · 2025Article
- Oncogenic virus hijacks SOX18 pioneer function to enhance viral persistence.Research square · 2025Article
- Heat shock factor 2 regulates oncogenic gamma-herpesvirus gene expression by remodeling the chromatin at the ORF50 and BZLF1 promoter.PLoS pathogens · 2025Article
- Infantile hemangioma: the common and enigmatic vascular tumor.The Journal of clinical investigation · 2024Review
- circFNDC3B Accelerates Vasculature Formation and Metastasis in Oral Squamous Cell Carcinoma.Cancer research · 2023Article
- Today's Kaposi sarcoma is not the same as it was 40 years ago, or is it?Journal of medical virology · 2023Review
- The Kaposi's sarcoma progenitor enigma: KSHV-induced MEndT-EndMT axis.Trends in molecular medicine · 2023Review
- KSHV infection of endothelial precursor cells with lymphatic characteristics as a novel model for translational Kaposi's sarcoma studies.PLoS pathogens · 2023Article
- Meningeal lymphatic vessels mediate neurotropic viral drainage from the central nervous system.Nature neuroscience · 2022Article
- Molecular Mechanisms of Kaposi Sarcoma Development.Cancers · 2022Article
- Kaposi's sarcoma-associated herpesvirus at 27.Tumour virus research · 2021Review
- Kaposi's sarcoma-associated herpesvirus promotes mesenchymal-to-endothelial transition by resolving the bivalent chromatin of PROX1 gene.PLoS pathogens · 2021Article
- Oncogenic herpesvirus KSHV triggers hallmarks of alternative lengthening of telomeres.Nature communications · 2021Article
- Characterizing Expression and Regulation of Gamma-Herpesviral Circular RNAs.Frontiers in microbiology · 2021Article
- Quantitative Proteomics Analysis of Lytic KSHV Infection in Human Endothelial Cells Reveals Targets of Viral Immune Modulation.Cell reports · 2020Article
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Authors and funding
15 authors at 6 institutions in 5 countries.
Funding
Abstract
Kaposi sarcoma is a tumor caused by Kaposi sarcoma herpesvirus (KSHV) infection and is thought to originate from lymphatic endothelial cells (LEC). While KSHV establishes latency in virtually all susceptible cell types, LECs support spontaneous expression of oncogenic lytic genes, high viral genome copies, and release of infectious virus. It remains unknown the contribution of spontaneous virus production to the expansion of KSHV-infected tumor cells and the cellular factors that render the lymphatic environment unique to KSHV life cycle. We show here that expansion of the infected cell population, observed in LECs, but not in blood endothelial cells, is dependent on the spontaneous virus production from infected LECs. The drivers of lymphatic endothelium development, SOX18 and PROX1, regulated different steps of the KSHV life cycle. SOX18 enhanced the number of intracellular viral genome copies and bound to the viral origins of replication. Genetic depletion or chemical inhibition of SOX18 caused a decrease of KSHV genome copy numbers. PROX1 interacted with ORF50, the viral initiator of lytic replication, and bound to the KSHV genome in the promoter region of ORF50, increasing its transactivation activity and KSHV spontaneous lytic gene expression and infectious virus release. In Kaposi sarcoma tumors, SOX18 and PROX1 expression correlated with latent and lytic KSHV protein expression. These results demonstrate the importance of two key transcriptional drivers of LEC fate in the regulation of the tumorigenic KSHV life cycle. Moreover, they introduce molecular targeting of SOX18 as a potential novel therapeutic avenue in Kaposi sarcoma. SIGNIFICANCE: SOX18 and PROX1, central regulators of lymphatic development, are key factors for KSHV genome maintenance and lytic cycle in lymphatic endothelial cells, supporting Kaposi sarcoma tumorigenesis and representing attractive therapeutic targets.
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