ArticleCell biochemistry and biophysics2025
CAFs-derived Exosomal miR-889-3p Might Repress M1 Macrophage Polarization to Boost ESCC Development by Regulating STAT1.
Article in Cell biochemistry and biophysics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Remodeling the Stroma: The Role of ncRNAs in Cancer-Associated Fibroblasts and Therapeutic Implications for Digestive Tumors.Drug design, development and therapy · 2026Review
- Advances in understanding exosome-mediated regulation of macrophage function.Frontiers in immunology · 2026Review
- Exosome-delivered bioactive molecules regulate macrophage polarization in atherosclerosis and myocardial infarction: mechanisms and therapeutic potential.Frontiers in cardiovascular medicine · 2026Review
- Hypoxia-induced exosomal circNRIP1 activates cancer-associated fibroblasts to promote esophageal squamous cell carcinoma migration and invasion.BMC gastroenterology · 2025Article
- Exosome-loaded tannic acid-thioctic acid hydrogel enhances wound healing in coagulation disorders.Materials today. Bio · 2025Article
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Authors and funding
6 authors.
Funding
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Abstract
Cancer-associated fibroblasts (CAFs) represent one of the major components of the tumor stroma, which might create an immunosuppressive tumor microenvironment by inducing and functionally polarizing protumoral macrophages. Previous studies indicated that exosomes derived from CAFs might transmit regulating signals and boost esophageal squamous cell carcinoma (ESCC) development. This study is designed to explore the role and mechanism of CAFs-derived exosomal microRNA-889-3p (miR-889-3p) in ESCC progression. Macrophage polarization was detected using flow cytometry. miR-889-3p, Tumor necrosis factor alpha (TNF-α), and inducible nitric oxide synthase (iNOS) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, cycle progression, migration, and invasion were assessed using Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), scratch assay, and Transwell assays. α-SMA, FAP, CD63, CD81, and signal transducer and activator of transcription 1 (STAT1) protein levels were detected using western blot. Exosomes were characterized using an electron microscope and nanoparticle tracking analysis (NTA). Binding between miR-889-3p and STAT1 was predicted by Starbase, and verified by a dual-luciferase reporter and RNA pull-down. The effect of CAFs-derived exosomal miR-889-3p on ESCC tumor growth in vivo was detected using mice xenograft assay. miR-889-3p level was decreased in LPS-induced M0 macrophages. CAF-derived exosomal miR-889-3p knockdown suppressed ESCC proliferation, migration, and invasion. CAFs might transfer miR-889-3p to M0 macrophages via exosomes. STAT1 was a target of miR-889-3p. Besides, in vivo studies confirmed that CAFs-derived exosomal miR-889-3p can accelerate ESCC tumor growth by regulating STAT1. CAFs-derived exosomal miR-889-3p facilitates esophageal squamous cell carcinoma cell proliferation, migration, and invasion by inhibiting M1 macrophage polarization through down-regulation of STAT1, providing a promising therapeutic target for ESCC.
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