ArticleCellular oncology (Dordrecht, Netherlands)2025
Cancer-associated fibroblast-derived extracellular vesicles facilitate metastasis in hepatocellular carcinoma by delivering CTGF.
Article in Cellular oncology (Dordrecht, Netherlands), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- CTGF: The remodeler of the tumor immune microenvironment (Review).Oncology reports · 2026Review
- Targeting cancer-associated fibroblasts: therapeutic strategies, translational challenges, and future perspectives.Journal of hematology & oncology · 2026Review
- Hepatocellular carcinoma metastasis-immune microenvironment crosstalk: emerging mechanisms and immunotherapy.Cellular & molecular biology letters · 2026Review
- Cytokines and cancer-associated fibroblasts.Journal of hematology & oncology · 2026Review
- Sublethal heat stress synergizes with the tumor microenvironment to drive recurrence of hepatocellular carcinoma after thermal ablation: mechanisms, molecular predictors, and targeted interventions.Cell biology and toxicology · 2026Review
- Fusobacterium nucleatum increases CTGF expression through TLR2-YAP signaling axis in cancer-associated fibroblasts, thereby promoting colorectal cancer progression.Cancer cell international · 2025Article
- FBXO42 promotes hepatocellular carcinoma progression via mediating p57Kip2 ubiquitination and degradation.European journal of medical research · 2025Article
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12 authors.
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Abstract
purposeThe tumor microenvironment (TME) plays a crucial role in cancer progression. Cancer-associated fibroblasts (CAFs) are key components of the TME and play critical roles in tumor development and metastasis. However, the mechanisms by which CAFs influence hepatocellular carcinoma (HCC) metastasis are not fully understood.
methodsExtracellular vesicles (EVs) from CAFs and normal fibroblasts (NFs) were characterized via western blotting, transmission electron microscopy, and nanoparticle tracking analysis. An iTRAQ-based proteomic sequencing analysis was conducted to quantify proteins in the EVs from these cells. Colony formation assays and Transwell assays were used to assess tumor cell proliferation and migration. Xenograft tumor models were established in nude mice to evaluate tumor progression in vivo. Coimmunoprecipitation and molecular docking were performed to explore the interactions between CTGF and Notch1.
resultsA high CAF abundance is associated with poor prognosis in HCC patients. EVs from CAFs significantly enhanced the proliferative and invasive abilities of HCC cells in vitro and in vivo. Connective tissue growth factor (CTGF) was found to be highly upregulated in CAF-derived EVs, and CTGF knockdown in CAF-derived EVs attenuated their tumor-promoting capacities. Mechanistically, CTGF derived from CAF-EVs activated the Notch1/Snail1 signaling pathway in recipient cells via interaction with the Notch1 receptor, enhancing HCC cell proliferation and invasion. Furthermore, high CTGF expression was significantly correlated with poor clinicopathological features in HCC patients.
conclusionOur findings revealed that CTGF derived from CAF-EVs promoted the proliferation and invasion of HCC cells via activation of the Notch1/Snail1 pathway, highlighting CTGF derived from CAF-EVs as a prognostic biomarker and therapeutic target in HCC.
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