ArticleBlood2010
KSHV-induced notch components render endothelial and mural cell characteristics and cell survival.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 65 citations in OpenAlex.
- Oncogenic Mechanisms of Kaposi's Sarcoma-Associated Herpesvirus on Cell Metabolism and Cell Transformation.Journal of medical virology · 2025Review
- The pathogen's playbook in cancer: from oncogenesis to progression.Frontiers in oncology · 2025Review
- The cellular Notch1 protein promotes KSHV reactivation in an Rta-dependent manner.Journal of virology · 2024Article
- Review
- Whole brain radiation therapy resulting in radionecrosis: a possible link with radiosensitising chemoimmunotherapy.BMJ case reports · 2023Article
- Today's Kaposi sarcoma is not the same as it was 40 years ago, or is it?Journal of medical virology · 2023Review
- Dysregulation of the miR-30c/DLL4 axis by circHIPK3 is essential for KSHV lytic replication.EMBO reports · 2022Article
- Article
- Multiple strategies to improve the therapeutic efficacy of oncolytic herpes simplex virus in the treatment of glioblastoma.Oncology letters · 2021Review
- Tetraspanin18 regulates angiogenesis through VEGFR2 and Notch pathways.Biology open · 2021Article
- Downregulation of Notch3 links TIMP3 inhibition to suppress aggressive phenotypes of pancreatic ductal adenocarcinoma.American journal of cancer research · 2021Article
- Oncolytic HSV-Infected Glioma Cells Activate NOTCH in Adjacent Tumor Cells Sensitizing Tumors to Gamma Secretase Inhibition.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- Endothelial-specific YY1 governs sprouting angiogenesis through directly interacting with RBPJ.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Unbiased Screening of Activated Receptor Tyrosine Kinases (RTKs) in Tumor Extracts Using a Mouse Phospho-RTK Array Kit.Bio-protocol · 2019Article
- Molecular mechanisms of viral oncogenesis in humans.Nature reviews. Microbiology · 2018Review
- The Role ofThe oncologist · 2018Review
- KSHV-induced ligand mediated activation of PDGF receptor-alpha drives Kaposi's sarcomagenesis.PLoS pathogens · 2018Article
- KSHV and the Role of Notch Receptor Dysregulation in Disease Progression.Pathogens (Basel, Switzerland) · 2017Review
- Diagnosis and Treatment of Kaposi Sarcoma.American journal of clinical dermatology · 2017Review
- MicroRNA Signature of Human Microvascular Endothelium Infected with Rickettsia rickettsii.International journal of molecular sciences · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Kaposi sarcoma-associated herpesvirus (KSHV) infection is essential to the development of Kaposi sarcoma (KS). Notch signaling is also known to play a pivotal role in KS cell survival and lytic phase entrance of KSHV. In the current study, we sought to determine whether KSHV regulates Notch components. KSHV-infected lymphatic endothelial cells showed induction of receptors Notch3 and Notch4, Notch ligands Dll4 and Jagged1, and activated Notch receptors in contrast to uninfected lymphatic endothelial cells. In addition, KSHV induced the expression of endothelial precursor cell marker (CD133) and mural cell markers (calponin, desmin, and smooth muscle alpha actin), suggesting dedifferentiation and trans-differentiation. Overexpression of latency proteins (LANA, vFLIP) and lytic phase proteins (RTA, vGPCR, viral interleukin-6) further supported the direct regulatory capacity of KSHV viral proteins to induce Notch receptors (Notch2, Notch3), ligands (Dll1, Dll4, Jagged1), downstream targets (Hey, Hes), and endothelial precursor CD133. Targeting Notch pathway with gamma-secretase inhibitor and a decoy protein in the form of soluble Dll4 inhibited growth of KSHV-transformed endothelial cell line. Soluble Dll4 was also highly active in vivo against KS tumor xenograft. It inhibited tumor cell growth, induced tumor cell death, and reduced vessel perfusion. Soluble Dll4 is thus a candidate for clinical investigation.
Indexed as
Identifiers
What OpenQuestion holds
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.