ArticleAnnals of translational medicine2020
Extracellular ubiquitin promotes hepatoma metastasis by mediating M2 macrophage polarization via the activation of the CXCR4/ERK signaling pathway.
Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Exogenous Ubiquitin Differentially Modulates the Phenotype and Function of M1 and M2 Macrophages.Cells · 2025Article
- Biological impact and therapeutic implication of tumor-associated macrophages in hepatocellular carcinoma.Cell death & disease · 2024Review
- Almost 50 Years of Monomeric Extracellular Ubiquitin (eUb).Pharmaceuticals (Basel, Switzerland) · 2024Review
- Prognostic and Immune Landscape Analysis of Ubiquitination-related Genes in Hepatocellular Carcinoma: Based on Bulk and Single-cell RNA Sequencing Data.Journal of Cancer · 2024Article
- Macrophages in the Inflammatory Phase following Myocardial Infarction: Role of Exogenous Ubiquitin.Biology · 2023Review
- Extracellular Matrix/Glycopeptide Hybrid Hydrogel as an Immunomodulatory Niche for Endogenous Cardiac Repair after Myocardial Infarction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Post-ischemic cardioprotective potential of exogenous ubiquitin in myocardial remodeling late after ischemia/reperfusion injury.Life sciences · 2023Article
- Maintenance of Epstein-Barr virus latency through interaction of LMP2A with CXCR4.Archives of virology · 2022Article
- Current Strategies for the Treatment of Hepatocellular Carcinoma by Modulating the Tumor Microenvironment via Nano-Delivery Systems: A Review.International journal of nanomedicine · 2022Review
- Mesenchymal stem cells transfected with anti-miRNA-204-3p inhibit acute rejection after heart transplantation by targeting C-X-C motif chemokine receptor 4 (CXCR4)Journal of thoracic disease · 2021Article
- Exosomal DLX6-AS1 from hepatocellular carcinoma cells induces M2 macrophage polarization to promote migration and invasion in hepatocellular carcinoma through microRNA-15a-5p/CXCL17 axis.Journal of experimental & clinical cancer research : CR · 2021Article
- Macrophage Polarization and Its Role in Liver Disease.Frontiers in immunology · 2021Review
- Tanyu Tongzhi Formula Delays Atherosclerotic Plaque Progression by Promoting Alternative Macrophage ActivationFrontiers in pharmacology · 2021Article
- Emerging Importance of Chemokine Receptor CXCR4 and Its Ligand in Liver Disease.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundStored red blood cell (RBC) transfusion has been shown to enhance the risk of cancer recurrence. However, the underlying mechanism remains unknown. At our lab, we have demonstrated that the extracellular ubiquitin (eUb) released by aged RBCs could promote tumor metastasis in a melanoma mouse model. This study aimed to confirm the pro-tumor effect of eUb on hepatocellular carcinoma (HCC) and explore the related immunoregulatory mechanisms.
methodsForty HCC tissue specimens and the corresponding adjacent nontumor and normal liver tissues were collected. Two human hepatoma cell lines (MHCC-97H and HepG2.2.15), one murine hepatoma cell line (Hepa1-6), and one human monocyte cell line (THP-1) were adopted in this study. The coculture of hepatoma cells with macrophages was initiated with Transwell inserts. Cell migration
resultsUb and CXCR4 were significantly upregulated in HCC tissues, and a positive correlation existed between them.
conclusionsExtracellular ubiquitin promoted hepatoma metastasis through M2 macrophage polarization via the activation of the CXCR4/ERK signaling pathway, indicating that a personalized transfusion strategy is needed for the treatment of HCC patients. Neutralizing Ub in stored RBC units could lessen the detrimental clinical outcomes induced by the transfusion of stored RBCs.
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