ArticleCancer medicine2024
Targeting Tumor Endothelial Cells by EGCG Using Specific Liposome Delivery System Inhibits Vascular Inflammation and Thrombosis.
Article in Cancer medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Targeting aging pathways with natural compounds: a review of curcumin, epigallocatechin gallate, thymoquinone, and resveratrol.Immunity & ageing : I & A · 2025Review
- Nanotechnology-driven EGCG: bridging antioxidant and therapeutic roles in metabolic and cancer pathways.Nanomedicine (London, England) · 2025Review
- Epigallocatechin gallate (EGCG) modulates senescent endothelial cell-monocyte communication in age-related vascular inflammation.Frontiers in cardiovascular medicine · 2024Article
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Authors and funding
9 authors.
Funding
Abstract
backgroundInflammation is one of the hallmarks of cancer and is associated with tumor growth. Tumor endothelial cells (TECs) demonstrate inflamed phenotypes. Endothelial inflammation initiates thrombus formation, which is the second cause of cancer-related deaths. Epigallocatechin-3-O-gallate (EGCG), a natural compound in green tea, has demonstrated an anti-inflammatory effect. However, the tumor progression inhibition effect of EGCG by targeting TEC inflammation remains unclear. This study addresses the anti-tumor effect of EGCG, especially its anti-inflammatory role in TECs.
methodsIn vitro, the effect of EGCG on TECs were studied using real-time quantitative PCR and immunofluoresence to analyza gene and protein expression. In vivo, a cyclic RGD liposome delivery system (MEND) was employed to efficiently deliver EGCG to TECs in tumor-bearing mice.
resultsIn vitro, EGCG significantly reduces inflammatory cytokine expression, including tumor necrosis factor-α, interleukin-6, IL-8, and IL-1β through NF-κB signaling inhibition. Additionally, von Willebrand factor reduction in TECs, which is involved in platelet adhesion and thrombosis formation, was analyzed. Our results revealed that EGCG-MEND significantly inhibited TEC inflammation and thrombus formation in tumors. Additionally, EGCG-MEND improved tumor immunity by reducing programmed death-ligand 1 expression and promoting high endothelial venule formation by recruiting CD8
conclusionOur results indicate the anti-tumor potential of EGCG-MEND in normalizing the inflammatory immune microenvironment and inhibiting thrombosis by targeting TEC.
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