ArticleBMC cancer2024
Mesenchymal stem cell-derived exosomes carrying miR-486-5p inhibit glycolysis and cell stemness in colorectal cancer by targeting NEK2.
Article in BMC cancer, 2024. 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.
- Pro-Tumorigenic Signaling Between Small Extracellular Vesicles of Cancer Cells and Bone Marrow-Derived Mesenchymal Stem Cells-An In Vitro Study.International journal of molecular sciences · 2026Article
- Tumor microenvironment-driven microRNA dysregulation: Key interactions in colorectal cancer progression.World journal of gastrointestinal oncology · 2026Review
- Exosomal microRNAs in colorectal cancer communication networks: implications for metastasis, therapy resistance, and precision medicine.Frontiers in immunology · 2026Review
- Application of Human Umbilical Cord Mesenchymal Stem Cells and Their Derived Exosomes in Gastrointestinal Diseases.International journal of nanomedicine · 2026Review
- The multifaceted roles of mesenchymal stem cell-derived exosomes in digestive system malignancies: mechanisms and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Hypoxic preconditioned mesenchymal stem cell-derived exosomes alleviate oxidative stress-induced cardiomyocyte apoptosis through miR-486-5p.World journal of stem cells · 2025Article
- Zinc finger protein 695 facilitates the proliferation of colorectal cancer cells through activation of the NEK2 and PI3K/Akt/mTOR signaling pathways.Oncology reports · 2025Article
- Exosomal miRNAs: Key Regulators of the Tumor Microenvironment and Cancer Stem Cells.International journal of molecular sciences · 2025Review
- Crosstalk Between Metabolic Reprogramming and Epigenetic Modifications in Colorectal Cancer: Mechanisms and Clinical Applications.Current issues in molecular biology · 2025Review
- Glucose Metabolic Reprogramming in Colorectal Cancer: From Mechanisms to Targeted Therapy Approaches.Cancer medicine · 2025Review
- Extracellular Vesicle-Based Drug Delivery Systems in Cancer Therapy.International journal of molecular sciences · 2025Review
- Exploration of RNA-binding proteins identified RPS27 as a potential regulator associated with Kaposi's sarcoma development.BMC cancer · 2025Article
- Molecular mechanism of aerobic exercise in miRNAs and the anti-tumoral effects.Frontiers in oncology · 2025Review
- Biological Nanotherapeutics Derived From Human Umbilical Cord Mesenchymal Stem Cells: Mechanisms and Translational Potential in Multisystem Therapies for Regeneration and Oncology.International journal of nanomedicine · 2025Review
- Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is a major global concern. Mesenchymal stem cell-derived exosomes (MSC-EXOs) have demonstrated efficacy as a therapeutic approach for colorectal cancer. However, the precise mechanism by which MSC-EXOs treat colorectal cancer remains unclear. Human umbilical cord (hUC)-MSC-EXOs were isolated and identified. Cell Counting Kit-8 (CCK-8), Transwell, and colony formation assays were used to assess the activity of CRC cells. Glucose consumption, lactic acid production, and extracellular acidification rate (ECAR) were measured to assess glycolytic activity. Cell stemness was assessed using a sphere-formation assay. Furthermore, MSC-exosomal microRNAs (miRNAs) in CRC tissues were analyzed using the EVmiRNA database, and aberrantly expressed miRNAs in CRC cells were obtained from the Gene Expression Omnibus (GEO) database. The binding relationship between miR-486-5p and the never in mitosis gene A-related kinase 2 (NEK2) was predicted using the Starbase database and validated through RNA binding protein immunoprecipitation (RIP) and dual luciferase assays. These results showed that hUC-MSC-EXOs inhibited the proliferation and metastasis of CRC cells. Moreover, glycolysis and stemness abilities of CRC cells also decreased after treatment with hUC-MSC-EXOs. miR-486-5p was found to be enriched in hUC-MSC-EXOs and significantly downregulated in CRC cells. miR-486-5p directly bound to NEK2. Overexpression of NEK2 reversed the inhibitory effect of miR-486-5p on CRC cell glycolysis and stemness. Our study highlights that hUC-MSC-EXO miR-486-5p inhibits glycolysis and cell stemness in CRC by targeting NEK2. This finding offers compelling evidence supporting the potential application of hUC-MSC-EXOs in the treatment of CRC.
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