bims-exocan Biomed News
on Exosomes roles in cancer
Issue of 2026–04–12
six papers selected by
Muhammad Rizwan, COMSATS University
  1. Dual role of exosomes in pancreatic cancer: Underlying mechanisms and research advances (Review).
  2. B7-H3 (CD276) in exosome biogenesis and the tumor microenvironment: a new therapeutic nexus.
  3. Exosomes and cholangiocarcinoma: mechanisms, diagnostic, and therapeutic perspectives.
  4. Engineering exosomes with iRGD for targeted RNAi therapy against pancreatic cancer mediated by long non-coding RNA PLBD1-AS1.
  5. Exosomes: Redefining intercellular communication and the future of translational medicine.
  6. Exosomal miR-92a-3p promotes pancreatic cancer cells' extravasation by inducing vascular permeability through inhibition of DAB2IP.
  1. Oncol Lett. 2026 May;31(5): 192
    Dual role of exosomes in pancreatic cancer: Underlying mechanisms and research advances (Review).
    Zhao Guo, Qingfeng Liu.
      Pancreatic cancer is one of the most common malignant tumors. Due to late diagnosis and a lack of effective treatments, pancreatic cancer has a poor prognosis and a high mortality rate. Further understanding of the mechanisms underlying the development and progression of pancreatic cancer is key to developing rational diagnostic and therapeutic strategies. Exosomes are small vesicles secreted by most cells, carrying a rich cargo of lipids, proteins and nucleic acids. Exosomes serve various roles in intercellular communication, biological processes and signal transduction. Notably, exosomes exhibit a dual role in pancreatic cancer: Exosomes can directly promote tumor cell proliferation, growth and metastasis, modulate the complex immunosuppressive microenvironment and contribute to chemoresistance; by contrast, exosomes can serve as biomarkers for diagnosis and drug delivery vehicles. The present study systematically reviewed the mechanisms through which exosomes exert their dual functions via their specific biomolecular cargo in pancreatic cancer, as well as their potential applications in diagnosis and treatment, thereby laying a research foundation for exosomes to potentially serve a more active role in pancreatic cancer in the future.
    Keywords:  drug delivery; exosomes; intercellular communication; pancreatic cancer; tumor microenvironment
    DOI:  https://doi.org/10.3892/ol.2026.15547
  2. Cell Commun Signal. 2026 Apr 11.
    B7-H3 (CD276) in exosome biogenesis and the tumor microenvironment: a new therapeutic nexus.
    Khaled Omran, Iqra Kousar, Jianrong Lu, Ming Tan.
      Tumor-derived exosomes are powerful mediators of cancer progression, influencing the tumor microenvironment (TME) to promote immune evasion, metastasis, and therapy resistance. B7-H3 (CD276), a member of the B7 immune checkpoint family, is gaining attention as a multifunctional promoter of tumor progression. In addition to its well-known expression on tumor and immune cells, B7-H3 is also enriched in exosomes, where it influences both extracellular vesicle production and signaling. This review examines how B7-H3 impacts exosome biology and contributes to tumor progression. We discuss the mechanisms of exosome biogenesis, including ESCRT-dependent and ESCRT-independent pathways. Emerging evidence indicates that B7-H3 enhances vesicular release, remodels cargo composition, and modulates recipient cell behavior. Mechanistically, B7-H3 activates pathways such as STAT3, PI3K, and lipid metabolism, thereby amplifying oncogenic signaling and promoting a pro-tumor TME. Clinically, B7-H3-enriched exosomes show promise as diagnostic, prognostic, and predictive biomarkers in colorectal, prostate, and non-small cell lung cancers. Additionally, we discuss strategies for therapeutically targeting exosomal B7-H3, including monoclonal and bispecific antibodies, CAR-T cells, and exosome inhibitors, as well as their potential synergy with immunotherapies. Overall, current evidence positions B7-H3 as a crucial link between checkpoint proteins and exosome-mediated cancer progression, offering new avenues for biomarker development and precision oncology.
    Keywords:  B7-H3; Exosomal-B7-H3; Exosome biogenesis; Exosomes; Immunomodulation
    DOI:  https://doi.org/10.1186/s12964-026-02872-6
  3. Front Immunol. 2026 ;17 1779516
    Exosomes and cholangiocarcinoma: mechanisms, diagnostic, and therapeutic perspectives.
    Jing Zhang, Maoshan Chen.
      Cholangiocarcinoma (CCA) is a highly malignant solid tumor originating from the biliary tract epithelium. Due to its aggressive behavior and late clinical presentation, it poses significant diagnostic and therapeutic challenges. Therefore, finding specific biomarkers and early screening of CCA susceptible people are the current top priorities. Exosomes, a subtype of extracellular vesicles, are secreted by many cells and widely distributed in body fluids. In recent years, exosomes are known to play pivotal roles in cell communication, tumorigenesis, metastasis, and immune modulation. This review summarizes recent advances in our understanding of the relationship between exosomes and cholangiocarcinoma, with a focus on their biological functions, diagnostic implications, and therapeutic potentials.
    Keywords:  cholangiocarcinoma; diagnosis; exosomes; immune evasion; immunotherapy
    DOI:  https://doi.org/10.3389/fimmu.2026.1779516
  4. PLoS One. 2026 ;21(4): e0345697
    Engineering exosomes with iRGD for targeted RNAi therapy against pancreatic cancer mediated by long non-coding RNA PLBD1-AS1.
    Wenbo Zhu, Xintong Zhao, Weina Hao, Xianzhu Zhou, Congjia Ma, Jiayu Chen, Yating Zhao, Xiangyu Kong, Yiqi Du, Lei Li.
      Tumor-derived exosomes play critical roles in pancreatic ductal adenocarcinoma (PDAC) progression by mediating intercellular communication within the tumor microenvironment. This study identifies the long non-coding RNA PLBD1-AS1 as a functional oncogenic lncRNA enriched in PDAC exosomes. We demonstrate that PLBD1-AS1 promotes tumor cell proliferation, migration, and invasion by interacting with the glycolytic enzyme ALDOA and enhancing glycolytic flux. Furthermore, tumor exosomes deliver PLBD1-AS1 to pancreatic stellate cells (PSC), augmenting their glycolysis and facilitating their activation into cancer-associated fibroblasts, thereby shaping a pro-tumorigenic microenvironment. To target it, we developed an engineered exosome system modified with the tumor-penetrating peptide iRGD for specific delivery of siPLBD1-AS1 to both tumor and stromal cells. The resulting iRGD-exo-siPLBD1-AS1 construct demonstrated enhanced cellular uptake and effectively suppressed PLBD1-AS1 expression, inhibited glycolysis, impaired PSC activation, and significantly attenuated tumor growth. Our findings reveal a novel mechanism of exosome-mediated metabolic crosstalk in PDAC and establish a promising RNAi-based therapeutic strategy targeting this lethal malignancy.
    DOI:  https://doi.org/10.1371/journal.pone.0345697
  5. Bioimpacts. 2026 ;16 33099
    Exosomes: Redefining intercellular communication and the future of translational medicine.
    Khosro Adibkia, Adel Mahmoudi Gharehbaba.
      Exosomes are promising extracellular vesicles for diagnostics, drug delivery, and regenerative medicine. While we have made significant strides in understanding exosomes biogenesis and cargo variability, the translation of exosome-based methods into clinical applications remains limited by challenges in manufacturing, standardization, and regulatory requirements. This editorial attempts to summarize the diverse field of exosome research including advances in isolation technologies and methodologies, omics characterization, and emerging bioengineering strategies that are elevating profile of exosomes as biomaterials for biomedical applications. We propose that exosomes are not just by-products of biological processes, but active information carriers with exceptional therapeutic potential. Therefore, the advancement of exosome methodologies in practice will ultimately alter the ways clinicians will evaluate diagnostic and therapeutic measures. We anticipate that the coming decades will establish a new, integrated framework for exosome science, one that harmonizes innovation, ethics, and cross-disciplinary collaboration to translate the promise of exosomes into tangible clinical reality.
    Keywords:  Drug delivery; Exosomes; Extracellular vesicles; Nanomedicine; Precision medicine; Translational biotechnology
    DOI:  https://doi.org/10.34172/bi.33099
  6. Cell Death Dis. 2026 Apr 08.
    Exosomal miR-92a-3p promotes pancreatic cancer cells' extravasation by inducing vascular permeability through inhibition of DAB2IP.
    Luhan Li, Yanyan Cui, Miao Zhang, Tianyu Shen, Dekun Wang, Xue Mi, Yuying Zhang, Xiaoyue Tan, Alejandro Vaquero, Thomas Braun, Jihui Hao, Alessandro Ianni, Chunyang Jiang, Shijing Yue.
      Metastasis, the colonization of distant organs by cells derived from primary cancer, is the leading cause of mortality in pancreatic adenocarcinoma (PAAD). Growing evidence indicates that cancer-derived exosomes play pivotal roles in facilitating cancer metastasis by promoting pre-metastatic niche formation. However, the contribution of PAAD-derived exosomal microRNAs (MiRNAs) to this process remains poorly characterized. In this study, we identified specific PAAD-derived exosomal miRNAs involved in metastatic progression. Sequencing of small RNAs extracted from circulating exosomes derived from patients with metastatic or non-metastatic PAAD revealed that miR-92a-3p is associated with a metastatic phenotype. We demonstrated that exosomal miR-92a-3p facilitates cancer cells' extravasation and lung metastasis by disrupting vascular barrier integrity. Mechanistically, exosomal miR-92a-3p directly inhibits the tumor suppressor disabled homolog 2 interacting protein (DAB2IP), thereby activating the PI3K-AKT signaling cascade in endothelial cells (ECs). This activation attenuates expression of intracellular junction markers and stimulates endothelial nitric oxide synthase, leading to increased vascular permeability. Our findings suggest that targeting miR-92a-3p could represent a potential strategy to reduce metastasis in PAAD.
    DOI:  https://doi.org/10.1038/s41419-026-08719-9
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