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<p>Extracellular vesicles (EVs) are lipid bilayer nanoparticles secreted by almost all cell types, serving as vital mediators of intercellular communication by transporting bioactive cargos, including proteins, lipids, and nucleic acids. This review summarizes the emerging role of EVs as pivotal carriers in cancer epigenetic regulation, focusing on their functions in cancer pathogenesis through the delivery of non-coding RNAs, such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), as well as the modulation of DNA methylation and histone modifications. Drawing on evidence from various malignancies (including osteosarcoma, breast cancer, gastric cancer, hepatocellular carcinoma, cervical cancer, lung cancer, pancreatic cancer, colorectal cancer, bladder cancer, and esophageal squamous cell carcinoma), we systematically elucidate how tumor- or matrix-derived EVs promote tumor progression by delivering specific epigenetic regulators (e.g., <i>NORAD</i>, <i>miR-3190</i>, and <i>circ_0064516</i>). These EV-encapsulated molecules can inhibit tumor suppressors, activate oncogenic pathways (such as PI3K/AKT and Wnt/β-catenin), and promote epithelial-mesenchymal transition, angiogenesis, immune evasion, and metastasis. Furthermore, EVs reshape the epigenetic landscape of the tumor microenvironment by inducing genomic DNA hypomethylation (e.g., <i>LINE-1</i>) and altering histone modifications. Finally, we discuss the potential of EV-associated epigenetic molecules as diagnostic biomarkers and therapeutic targets, underscoring the clinical significance of EVs as key information carriers in oncology.</p>

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Extracellular vesicle-mediated intercellular epigenetic communication in cancer pathogenesis

  • 期刊论文

  • 发表日期：

    2026年5月6日

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  • Bowen Wu,
  • Minghui Zhang,
  • Zhouzhu Liang,
  • Yintao Su,
  • Jinke Gu

摘要

Extracellular vesicles (EVs) are lipid bilayer nanoparticles secreted by almost all cell types, serving as vital mediators of intercellular communication by transporting bioactive cargos, including proteins, lipids, and nucleic acids. This review summarizes the emerging role of EVs as pivotal carriers in cancer epigenetic regulation, focusing on their functions in cancer pathogenesis through the delivery of non-coding RNAs, such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), as well as the modulation of DNA methylation and histone modifications. Drawing on evidence from various malignancies (including osteosarcoma, breast cancer, gastric cancer, hepatocellular carcinoma, cervical cancer, lung cancer, pancreatic cancer, colorectal cancer, bladder cancer, and esophageal squamous cell carcinoma), we systematically elucidate how tumor- or matrix-derived EVs promote tumor progression by delivering specific epigenetic regulators (e.g., NORAD, miR-3190, and circ_0064516). These EV-encapsulated molecules can inhibit tumor suppressors, activate oncogenic pathways (such as PI3K/AKT and Wnt/β-catenin), and promote epithelial-mesenchymal transition, angiogenesis, immune evasion, and metastasis. Furthermore, EVs reshape the epigenetic landscape of the tumor microenvironment by inducing genomic DNA hypomethylation (e.g., LINE-1) and altering histone modifications. Finally, we discuss the potential of EV-associated epigenetic molecules as diagnostic biomarkers and therapeutic targets, underscoring the clinical significance of EVs as key information carriers in oncology.