ArticleCancer cell international2025
Role of S1PR1 in VEGF-exosomes mediated resistance of hepatocellular carcinoma to anti-angiogenesis therapy.
Article in Cancer cell international, 2025. 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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Who cites it
3 citing papers in PubMed.
- Label-free cell phenotypic profiling of sphingosine-1-phosphate receptor 1 and discovery of its agonist from natural products.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Single-cell and spatial dissection of IGF2BP3-driven endothelial reprogramming underlying microvascular invasion in hepatocellular carcinoma.Frontiers in pharmacology · 2026Article
- Exosomal crosstalk: the metastatic language of hepatocellular carcinoma.Frontiers in immunology · 2025Review
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4 authors.
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Abstract
backgroundAnti-angiogenesis therapy (AAT) triggers vascular endothelial growth factor (VEGF)-exosomes secretion from tumor-associated endothelial cells (TAECs) for hepatocellular carcinoma (HCC) tubulogenesis and metastasis. Sphingosine-1-phosphate receptor 1 (S1PR1) has been implicated in HCC progression, but it was targeted by microRNA-9 (miR-9) that might mediate the formation of TAECs. This study aims to investigate the role of miR-9 and VEGF-exosomes in S1PR1-mediated HCC progression and resistance to AAT.
methodsThe expression and distribution of miR-9 in HCC tissues were analyzed using qRT-PCR and fluorescence in situ hybridization (FISH). The impact of S1PR1 knockdown on VEGF-exosome uptake, as well as miR-9 and VEGF-exosome-induced epithelial-mesenchymal transition (EMT), migration, and invasion of HCC cells, was assessed by Transwell assays, fluorescence microscopy, and Western blotting.
resultsmiR-9 expression was significantly upregulated in HCC tissues and selectively localized in CD34⁺ endothelial cells within paracancerous microvessels, suggesting its role in TAEC transformation.miR-9 promoted EMT and enhanced HCC cell migration and invasion, effects that were further potentiated by VEGF-exosomes. S1PR1 knockdown significantly inhibited VEGF-exosome uptake and suppressed miR-9- and VEGF-exosome-induced EMT, migration, and invasion of HCC cells.
conclusionIn conclusion, miR-9 facilitates HCC progression by enhancing tumor malignancy and promoting AAT resistance through TAEC-mediated VEGF-exosome secretion. S1PR1 is a critical mediator of this process, and its inhibition represents a potential therapeutic strategy to overcome AAT resistance in HCC.
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