ArticleThe Journal of clinical investigation2015
Motif mimetic of epsin perturbs tumor growth and metastasis.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 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
23 citing papers in PubMed, 29 citations in OpenAlex.
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- A long-term human adipocyte organoid model reveals aging-associated responses to intermittent hypoxia.American journal of physiology. Cell physiology · 2026Article
- Endocytic Adaptor Proteins in Vascular Diseases: Critical Role of Intracellular Trafficking in Regulating Pathobiology of Vascular Disorders.Cardiology discovery · 2026Review
- Development of Long-Term Human Adipocyte Organoids Manifesting Aging in Response to Intermittent Hypoxia.bioRxiv : the preprint server for biology · 2025Article
- Differential Roles of Neuro-Inflammatory Regulator, MAPK11 in Cortex and Hippocampus Following Post-Stroke Cognitive Impairments in Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Elucidating the crosstalk between endothelial-to-mesenchymal transition (EndoMT) and endothelial autophagy in the pathogenesis of atherosclerosis.Vascular pharmacology · 2024Review
- Epsin Endocytic Adaptor Proteins in Angiogenic and Lymphangiogenic Signaling.Cold Spring Harbor perspectives in medicine · 2024Review
- Article
- Panel of Engineered Ubiquitin Variants Targeting the Family of Human Ubiquitin Interacting Motifs.ACS chemical biology · 2022Article
- Epsins Negatively Regulate Aortic Endothelial Cell Function by Augmenting Inflammatory Signaling.Cells · 2021Article
- Epsins in vascular development, function and disease.Cellular and molecular life sciences : CMLS · 2021Review
- Epsins 1 and 2 promote NEMO linear ubiquitination via LUBAC to drive breast cancer development.The Journal of clinical investigation · 2021Article
- Epsin-mediated degradation of IP3R1 fuels atherosclerosis.Nature communications · 2020Article
- Endocytic Adaptors in Cardiovascular Disease.Frontiers in cell and developmental biology · 2020Review
- Endocytic Adaptor Proteins in Health and Disease: Lessons from Model Organisms and Human Mutations.Cells · 2019Review
- Myeloid-Specific Deletion of Epsins 1 and 2 Reduces Atherosclerosis by Preventing LRP-1 Downregulation.Circulation research · 2019Article
- Epsin deficiency promotes lymphangiogenesis through regulation of VEGFR3 degradation in diabetes.The Journal of clinical investigation · 2018Article
- Therapeutic efficacy of a synthetic epsin mimetic peptide in glioma tumor model: uncovering multiple mechanisms beyond the VEGF-associated tumor angiogenesis.Journal of neuro-oncology · 2018Article
- Endothelial epsins as regulators and potential therapeutic targets of tumor angiogenesis.Cellular and molecular life sciences : CMLS · 2017Review
- Insights from Genetic Model Systems of Retinal Degeneration: Role of Epsins in Retinal Angiogenesis and VEGFR2 Signaling.Journal of nature and science · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
27 authors at 1 institution in 1 country.
Funding
Abstract
Tumor angiogenesis is critical for cancer progression. In multiple murine models, endothelium-specific epsin deficiency abrogates tumor progression by shifting the balance of VEGFR2 signaling toward uncontrolled tumor angiogenesis, resulting in dysfunctional tumor vasculature. Here, we designed a tumor endothelium-targeting chimeric peptide (UPI) for the purpose of inhibiting endogenous tumor endothelial epsins by competitively binding activated VEGFR2. We determined that the UPI peptide specifically targets tumor endothelial VEGFR2 through an unconventional binding mechanism that is driven by unique residues present only in the epsin ubiquitin-interacting motif (UIM) and the VEGFR2 kinase domain. In murine models of neoangiogenesis, UPI peptide increased VEGF-driven angiogenesis and neovascularization but spared quiescent vascular beds. Further, in tumor-bearing mice, UPI peptide markedly impaired functional tumor angiogenesis, tumor growth, and metastasis, resulting in a notable increase in survival. Coadministration of UPI peptide with cytotoxic chemotherapeutics further sustained tumor inhibition. Equipped with localized tumor endothelium-specific targeting, our UPI peptide provides potential for an effective and alternative cancer therapy.
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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.