ArticleLeukemia2012
Syndecan-1 promotes the angiogenic phenotype of multiple myeloma endothelial cells.
Article in Leukemia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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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.
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Who cites it
37 citing papers in PubMed, 68 citations in OpenAlex.
- Glycocalyx disruption, endothelial dysfunction and vascular remodeling as underlying mechanisms and treatment targets of chronic venous disease.International angiology : a journal of the International Union of Angiology · 2024Review
- Gas Plasma Exposure Alters Microcirculation and Inflammation during Wound Healing in a Diabetic Mouse Model.Antioxidants (Basel, Switzerland) · 2024Article
- Targeted therapy for multiple myeloma: an overview on CD138-based strategies.Frontiers in oncology · 2024Review
- Circulating biosignatures in multiple myeloma and their role in multidrug resistance.Molecular cancer · 2023Review
- Antibody-Drug Conjugates for Multiple Myeloma: Just the Beginning, or the Beginning of the End?Pharmaceuticals (Basel, Switzerland) · 2023Review
- Heparan sulfate proteoglycans in cancer: Pathogenesis and therapeutic potential.Advances in cancer research · 2023Article
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- Review
- Immunophenotyping and Transcriptional Profiling of Human Plasmablasts in Dengue.Journal of virology · 2021Article
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- Soluble syndecan-1 and glycosaminoglycans in preeclamptic and normotensive pregnancies.Scientific reports · 2021Article
- Heparan Sulfate Glycosaminoglycans: (Un)Expected Allies in Cancer Clinical Management.Biomolecules · 2021Review
- Update on the Role of the Endothelial Glycocalyx in Angiogenesis and Vascular Inflammation.Frontiers in cell and developmental biology · 2021Review
- Syndecans and Their Synstatins: Targeting an Organizer of Receptor Tyrosine Kinase Signaling at the Cell-Matrix Interface.Frontiers in oncology · 2021Review
- Lineage-dependent gene expression programs influence the immune landscape of colorectal cancer.Nature genetics · 2020Article
- Heparanase-Regulated Syndecan-1 Shedding Facilitates Herpes Simplex Virus 1 Egress.Journal of virology · 2020Article
- Article
- Article
- EPS8-mediated regulation of multiple myeloma cell growth and survival.American journal of cancer research · 2019Article
- Cancer Cell Glycocalyx and Its Significance in Cancer Progression.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiogenesis is considered a hallmark of multiple myeloma (MM) progression. In the present study, we evaluated the morphological and functional features of endothelial cells (ECs) derived from bone marrow (BM) of patients affected by MM (MMECs). We found that MMECs compared with normal BM ECs (BMECs) showed increased expression of syndecan-1. Silencing of syndecan-1 expression by RNA interference technique decreased in vitro EC survival, proliferation and organization in capillary-like structures. In vivo, in severe combined immunodeficient mice, syndecan-1 silencing inhibited MMEC organization into patent vessels. When overexpressed in human umbilical vein ECs and BMECs, syndecan-1 induced in vitro and in vivo angiogenic effects. Flow-cytometric analysis of MMECs silenced for syndecan-1 expression indicated a decreased membrane expression of vascular endothelial growth factor (VEGF) receptor-2 (VEGFR-2). Immunoprecipitation and confocal analysis showed colocalization of VEGFR-2 with syndecan-1. Absence of nuclear translocation of VEGFR-2 in syndecan-1-knockdown cells together with the shift from perinuclear localization to recycling compartments suggest a role of syndecan-1 in modulation of VEGFR-2 localization. This correlated with an in vitro decreased VEGF-induced invasion and motility. These results suggest that syndecan-1 may contribute to the highly angiogenic phenotype of MMECs by promoting EC proliferation, survival and modulating VEGF-VEGFR-2 signalling.
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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.