ArticleInternational journal of biological sciences2021
Cancer-associated fibroblasts-derived exosomal miR-3656 promotes the development and progression of esophageal squamous cell carcinoma via the ACAP2/PI3K-AKT signaling pathway.
Article in International journal of biological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Role of Cancer Associated Fibroblast (CAF) derived miRNAs on head and neck malignancies microenvironment: a systematic review.BMC cancer · 2025Pooled it
- Engineered Exosomes for Delivery of Mir-423-5p to Improve Radiation Sensitivity by Inhibiting MAP7D1 in Esophageal Cancer.Annals of surgical oncology · 2026Article
- Targeting the CAF-GDF15 axis attenuates AKT-mediated mitochondrial rewiring and chemoradiation resistance in esophageal adenocarcinoma.Journal of experimental & clinical cancer research : CR · 2026Article
- RNF126 Promotes Ovarian Cancer Progression by Reprogramming Lipid Metabolism Through Degradation of ACAP2.Biochemical genetics · 2026Article
- Advances in epigenetic therapy for esophageal cancer.Clinical epigenetics · 2026Review
- Identification of Small Extracellular Vesicle (sEV)-Related Genes and the Establishment of Diagnostic Models for Esophageal Cancer.Current medicinal chemistry · 2026Article
- Remodeling the Stroma: The Role of ncRNAs in Cancer-Associated Fibroblasts and Therapeutic Implications for Digestive Tumors.Drug design, development and therapy · 2026Review
- Cancer-associated fibroblasts: central players in cancer hallmarks and therapeutic resistance.Cell communication and signaling : CCS · 2025Review
- RGS16-driven cancer-associated fibroblasts promote esophageal squamous cell carcinoma progression via the MDK-SDC1 axis-mediated intercellular crosstalk.Biology direct · 2025Article
- Review
- CAFs-derived Exosomal miR-889-3p Might Repress M1 Macrophage Polarization to Boost ESCC Development by Regulating STAT1.Cell biochemistry and biophysics · 2025Article
- Dual Targeting of Inflammatory and Immune Checkpoint Pathways to Overcome Radiotherapy Resistance in Esophageal Squamous Cell Carcinoma.Journal of inflammation research · 2025Review
- Exosome-Derived Cargos in Immune Microenvironment in Esophageal Carcinoma: A Mini-Review.Recent patents on anti-cancer drug discovery · 2025Review
- Exosomes in esophageal cancer: function and therapeutic prospects.Medical oncology (Northwood, London, England) · 2024Review
- Recent Advances of Small Extracellular Vesicles for the Regulation and Function of Cancer-Associated Fibroblasts.International journal of molecular sciences · 2024Review
- Research Progress of Fibroblasts in Human Diseases.Biomolecules · 2024Review
- Article
- The roles of exosomes in esophageal cancer.Discover oncology · 2024Review
- Non‑coding RNA: A promising diagnostic biomarker and therapeutic target for esophageal squamous cell carcinoma (Review).Oncology letters · 2024Review
- Role of Exosomes in Cancer and Aptamer-Modified Exosomes as a Promising Platform for Cancer Targeted Therapy.Biological procedures online · 2024Review
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal squamous cell carcinoma (ESCC) is one of the most common gastrointestinal tumors, accounting for almost half a million deaths per year. Cancer-associated fibroblasts (CAFs) are the major constituent of the tumor microenvironment (TME) and dramatically impact ESCC progression. Recent evidence suggests that exosomes derived from CAFs are able to transmit regulating signals and promote ESCC development. In this study, we compared different the component ratios of miRNAs in exosomes secreted by CAFs in tumors and with those from normal fibroblasts (NFs) in precancerous tissues. The mRNA level of hsa-miR-3656 was significantly upregulated in the former exosomes. Subsequently, by comparing tumor cell development in vitro and in vivo, we found that the proliferation, migration and invasion capabilities of ESCC cells were significantly improved when miR-3656 was present. Further target gene analysis confirmed ACAP2 was a target gene regulated by miR-3656 and exhibited a negative regulatory effect on tumor proliferation. Additionally, the downregulation of ACAP2 triggered by exosomal-derived miR-3656 further promotes the activation of the PI3K/AKT and β-catenin signaling pathways and ultimately improves the growth of ESCC cells both in vitro and in xenograft models. These results may represent a potential therapeutic target for ESCC and provide a new basis for clinical treatment plans.
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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.