ArticleCancer cell international2023
ROS impairs tumor vasculature normalization through an endocytosis effect of caveolae on extracellular SPARC.
Article in Cancer cell international, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- GPR81 Regulates MCT1 Membrane Translocation Through a PKA-Dependent Signaling Pathway in Rat Podocytes.International journal of molecular sciences · 2026Article
- A novel Au-Se nanoplatform for co-delivery of cGAMP and acriflavine synergizes with photothermal therapy to enhance anti-tumor immunity via STING activation and HIF-1α inhibition.Journal of nanobiotechnology · 2026Article
- Reverse cardio-oncology: neuroendocrine axis activation and cardiovascular-disease-derived factors synergistically remodel the tumor microenvironment.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Exploring the Role of SPARC in Atherosclerosis: Mechanisms and Potential Implications.Current atherosclerosis reports · 2025Review
- Role of Matricellular Proteins in Endothelial Cell Inflammation and Atherosclerosis.Antioxidants (Basel, Switzerland) · 2025Review
- SPARC: a key mediator of apoptosis in human umbilical vein endothelial cells and its role in hypertension mechanism.In vitro cellular & developmental biology. Animal · 2025Article
- The critical roles of caveolin-1 in lung diseases.Frontiers in pharmacology · 2024Review
- Chinese Herbal Compound Xiaoliu Pingyi Recipe Inhibits the Growth of Lung Adenocarcinoma by Regulating the Tumor Vascular Microenvironment.Integrative cancer therapiesArticle
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundThe accumulation of reactive oxygen species (ROS) in tumor microenvironment (TME) is an important player for tumorigenesis and progression. We aimed to explore the outcomes of ROS on tumor vessels and the potential regulated mechanisms.
methodsExogenous H
resultUnder the context of oxidative stress, the pericyte recruitment of neovascularization in mouse lung cancer and melanoma tissues would be aberrated, which subsequently led to the disruption of the tumor vascular architecture and perfusion dysfunction. In vitro, HUVEC extracellularly SPARC was down-regulated, whereas intracellularly it was up-regulated. By electron microscopy and immunofluorescence staining, we observed that SPARC might undergo transmembrane transport via caveale-1-mediated endocytosis. Finally, the binding of SPARC to phosphorylated-caveale-1 was also detected in B16F10 tissues.
conclusionIn the oxidative stress environment, neovascularization within the tumor occurs structural deterioration and decreased perfusion capacity. One of the main regulatory mechanisms is the migration of extracellular SPARC from the endothelium to intracellular compartments via Caveolin-1 carriers.
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Registered trials
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