ArticleInternational journal of molecular sciences2023
Overexpression of miR-4669 Enhances Tumor Aggressiveness and Generates an Immunosuppressive Tumor Microenvironment in Hepatocellular Carcinoma: Its Clinical Value as a Predictive Biomarker.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Functional heterogeneity of exosomes in hepatocellular carcinoma (Review).Experimental and therapeutic medicine · 2026Review
- Transcriptomic Profiling of MicroRNA and Non-Coding RNA from Whole Blood of African Americans with MASLD.International journal of molecular sciences · 2026Article
- The possible role of sirtuins and MiRNAs in gastrointestinal cancers: special focus on Sirt1.Cancer cell international · 2026Review
- From immune desert to hot tumor: the tripartite synergy of tumor microenvironment-exosomes-immunogenic cell death in pioneering solutions.Frontiers in immunology · 2026Review
- Resistance of first-line targeted drugs in hepatocellular carcinoma: the epigenetic regulation mechanisms.Cell death & disease · 2025Review
- Combining single-cell and bulk RNA sequencing data to create a reliable prognostic model for predicting clear-cell renal cell carcinoma progression.Translational andrology and urology · 2025Article
- Endometrial Mesenchymal Stem Cell-Derived Exosomal miR-4669 Promotes EMT in Adenomyosis by Inducing M2 Macrophage Polarization via the DUSP6/ERK Pathway.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Crosstalk between exosomes and tumor-associated macrophages in hepatocellular carcinoma: implication for cancer progression and therapy.Frontiers in immunology · 2025Review
- Machine learning identifies neutrophil extracellular traps-related biomarkers for acute ischemic stroke diagnosis.Frontiers in neurology · 2025Article
- MicroRNAs in Hepatocellular Carcinoma Pathogenesis: Insights into Mechanisms and Therapeutic Opportunities.International journal of molecular sciences · 2024Review
- Mechanisms of Tolerance Induction in Liver Transplantation: Lessons Learned from Fetomaternal Tolerance, Autoimmunity and Tumor Immunity.International journal of molecular sciences · 2024Review
- Extracellular vesicles and cancer stemness in hepatocellular carcinoma - is there a link?Frontiers in immunology · 2024Review
- Potential of CDC25 phosphatases in cancer research and treatment: key to precision medicine.Frontiers in pharmacology · 2024Review
- Exosome Cargos as Biomarkers for Diagnosis and Prognosis of Hepatocellular Carcinoma.Pharmaceutics · 2023Review
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10 authors.
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Abstract
Accumulating evidence suggests the involvement of tumor-derived exosomes in the development and recurrence of hepatocellular carcinoma (HCC). We previously identified miR-4669 as a highly expressed microRNA in circulating exosomes obtained from patients with post-transplant HCC recurrence. This study aimed to explore how overexpression of miR-4669 affects HCC development and recurrence. The impact of miR-4669 overexpression in Hep3B cells on tumor cell behavior and the tumor microenvironment was evaluated in vitro. In addition, the clinical value of exosomal miR-4669 for the prediction of treatment response to HCC downstaging therapies and following post-transplant HCC recurrence was explored. Overexpression of miR-4669 enhanced migration ability and led to acquired sorafenib resistance with an elevation of sirtuin 1 and long noncoding RNA associated with microvascular invasion. Active release of tumor-derived exosomes and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) contributed to generating an immunosuppressive tumor microenvironment through the induction of M2 macrophage polarization. The retrospective analysis demonstrated the clinical value of exosomal miR-4669 for predicting treatment response to HCC downstaging therapies and for risk assessment of post-transplant HCC recurrence. In summary, the present data demonstrate the impact of exosomal miR-4669 on HCC recurrence through the enhancement of tumor aggressiveness and generation of an immunosuppressive tumor microenvironment.
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