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Updated: Jun 9, 2026

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An Enrichment Method for Small Extracellular Vesicles Derived from Liver Cancer Tissue
Published on: February 3, 2023
Tumor Endothelial Cell-Derived Extracellular Vesicles Promote Hepatocellular Carcinoma Progression Through
Mitsuru Yanagaki1, Koichiro Haruki1, Munetoshi Akaoka1
1Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, The Jikei University School of Medicine, Tokyo, Japan.
Summary
Tumor endothelial cells (TECs) release extracellular vesicles (EVs) that promote hepatocellular carcinoma (HCC) progression by altering microRNA (miRNA) levels. Targeting TEC-derived EVs may offer a new therapeutic strategy for HCC patients.
Area of Science:
- Oncology
- Cell Biology
- Molecular Biology
Background:
- Hepatocellular carcinoma (HCC) progression is complex.
- The role of intercellular communication between HCC cells and tumor endothelial cells (TECs) is not fully understood.
- Extracellular vesicles (EVs) mediate cell-to-cell communication and may influence HCC development.
Purpose of the Study:
- To investigate the involvement of extracellular vesicle (EV) interaction between hepatocellular carcinoma (HCC) cells and tumor endothelial cells (TECs) in HCC progression.
- To identify specific microRNAs (miRNAs) within EVs that mediate this interaction.
- To explore the potential of targeting TEC-derived EVs as a therapeutic strategy for HCC.
Main Methods:
- Matched HCC and adjacent tissues were collected from HCC patients.
- TECs and normal endothelial cells (NECs) were isolated.
- Conditioned medium (CM) and EVs from TECs and NECs were co-cultured with HCC cell lines.
- miRNA sequencing was performed on EVs.
- Prognostic significance of miRNA-targeted proteins in HCC tissues was analyzed in 121 HCC patients.
Main Results:
- TECs-derived EVs significantly enhanced HCC cell migration and invasiveness.
- miR-142-3p was upregulated in TEC-derived EVs, reducing RHOBTB3 and promoting HCC progression.
- miR-20a-5p was downregulated in TEC-derived EVs, increasing ITGB8 and promoting HCC progression.
- Low RHOBTB3 and high ITGB8 expression correlated with poor prognosis in HCC patients.
Conclusions:
- TECs-derived EVs accelerate HCC progression via miRNA-mediated intercellular communication.
- TECs represent a potential therapeutic target for HCC treatment.
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