ArticleCancer research2012
Kaposi sarcoma herpesvirus promotes endothelial-to-mesenchymal transition through Notch-dependent signaling.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 114 citations in OpenAlex.
- In-depth characterisation of the tumour microenvironment reveals HHV-8-dependent immune regulation in HIV-associated and classic Kaposi sarcoma.British journal of cancer · 2026Article
- Tumor-Intrinsic HEXB Drives Endothelial-To-Mesenchymal Transition and Confers Resistance to Anti-Angiogenic Therapy in Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- 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
- Metabolic Syndrome-Driven Changes in Cardiac Lymphatic Endothelium: mRNA Expression and Emerging Questions.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Article
- Review
- Loss of primary cilia promotes EphA2-mediated endothelial-to-mesenchymal transition in the ovarian tumor microenvironment.Molecular oncology · 2025Article
- Article
- Oncogenic virus hijacks SOX18 pioneer function to enhance viral persistence.Research square · 2025Article
- Oncogenic Mechanisms of Kaposi's Sarcoma-Associated Herpesvirus on Cell Metabolism and Cell Transformation.Journal of medical virology · 2025Review
- Shifting Shapes: The Endothelial-to-Mesenchymal Transition as a Driver for Cancer Progression.International journal of molecular sciences · 2025Review
- HIV-1 Tat-induced disruption of epithelial junctions and epithelial-mesenchymal transition of oral and genital epithelial cells lead to increased invasiveness of neoplastic cells and the spread of herpes simplex virus and cytomegalovirus.Frontiers in immunology · 2025Review
- Review
- The cellular Notch1 protein promotes KSHV reactivation in an Rta-dependent manner.Journal of virology · 2024Article
- Notch signaling regulates pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- Endothelial-to-mesenchymal transition in tumour progression and its potential roles in tumour therapy.Annals of medicine · 2023Review
- Today's Kaposi sarcoma is not the same as it was 40 years ago, or is it?Journal of medical virology · 2023Review
- Endothelial-to-Mesenchymal Transition: Potential Target of Doxorubicin-Induced Cardiotoxicity.American journal of cardiovascular drugs : drugs, devices, and other interventions · 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
- Molecular Mechanisms of Kaposi Sarcoma Development.Cancers · 2022Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Endothelial-to-mesenchymal transition (EndMT) is now widely considered a pivotal contributor to cancer progression. In this study, we show that the Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is a sufficient cause of EndMT, potentially helping to explain the aggressiveness of KS that occurs commonly in AIDS patients. Upon KSHV infection, primary dermal microvascular endothelial cells lost expression of endothelial markers and acquired expression of mesenchymal markers, displaying new invasive and migratory properties along with increased survival. KSHV activated Notch-induced transcription factors Slug and ZEB1, and canonical Notch signaling was required for KSHV-induced EndMT. In contrast, KSHV did not utilize the TGFβ signaling pathway, which has also been linked to EndMT. Within KS lesions, KSHV-infected spindle cells displayed features compatible with KSHV-induced EndMT including a complex phenotype of endothelial and mesenchymal properties, Notch activity, and nuclear ZEB1 expression. Our results show that KSHV engages the EndMT program to increase the invasiveness and survival of infected endothelial cells, traits that likely contribute to viral persistence and malignant progression. One important implication of our findings is that therapeutic approaches to disrupt the Notch pathway may offer novel approaches for KS treatment.
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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.