bims-exocan Biomed News
on Exosomes roles in cancer
Issue of 2026–01–18
five papers selected by
Muhammad Rizwan, COMSATS University



  1. Eur J Med Res. 2026 Jan 14.
      Exosomes, nanoscale extracellular vesicles secreted by various cell types, have emerged as pivotal mediators of intercellular communication in pancreatic diseases. They carry proteins, lipids, and nucleic acids that mirror the molecular state of their parent cells, thereby influencing inflammation, fibrosis, and tumorigenesis. This review summarizes current evidence on the roles of exosomes in acute and chronic pancreatitis as well as pancreatic cancer. In acute pancreatitis, exosomes regulate inflammatory cascades and contribute to remote organ injury, while mesenchymal stem cell-derived exosomes exhibit protective effects, highlighting their therapeutic potential. In chronic pancreatitis, exosomes mediate acinar-stellate cell interactions and fibrosis progression, with exosomal miRNAs and proteins showing promise for differential diagnosis and targeted interventions. In pancreatic cancer, tumor-derived exosomes foster immune evasion, chemoresistance, and metastasis but also serve as valuable candidates for liquid biopsy and as innovative drug delivery vehicles. Despite these advances, challenges remain, including standardization of exosome isolation and characterization methods, optimization of targeting strategies, and verification of clinical safety and efficacy. Collectively, exosomes represent a promising frontier for improving diagnosis, prognosis, and treatment of pancreatic diseases, though further translational research is needed to fully realize their clinical applications.
    Keywords:  Drug delivery; Exosomes; Inflammation-to-cancer transition; Liquid biopsy; Pancreatic diseases
    DOI:  https://doi.org/10.1186/s40001-026-03858-3
  2. BMC Cancer. 2026 Jan 13.
      Triple-negative breast cancer (TNBC) is a clinically aggressive subtype characterized by poor prognosis and limited therapeutic options. Exosomal microRNAs (miRNAs), enclosed within secretory vesicles, have emerged as promising non-invasive biomarkers for cancer detection and disease monitoring. In this study, we identify a panel of five exosomal miRNAs: hsa-miR-6803, hsa-miR-1180, hsa-miR-4728, hsa-miR-1915, and hsa-miR-940, that are consistently overexpressed in TNBC cells, stem-like subpopulations, and patient tumor tissues. Integrated meta-analysis of public datasets combined with in-vitro validation revealed that elevated expression of these miRNAs correlates with poor overall survival. Functional assays further demonstrated that hsa-miR-1180 and hsa-miR-4728 enhance TNBC cell migration and invasion, implicating them in key oncogenic pathways such as Wnt, Notch, and EGFR. The consistent enrichment of these miRNAs in exosomes underscores their potential as exploratory biomarkers for future liquid-biopsy-based applications. To our knowledge, this discovery-phase investigation is the first to associate this exosomal miRNA panel with TNBC and its stem-like subpopulations, providing a preliminary framework for subsequent mechanistic and translational validation.
    Keywords:  CSC; Exosomes; Extracellular vesicles; MiRNA; Prognosis; TNBC
    DOI:  https://doi.org/10.1186/s12885-025-15499-6
  3. Med Oncol. 2026 Jan 13. 43(2): 117
      Gefitinib Resistance (GR) is a frequent occurrence for non-small cell lung cancer (NSCLC). Here, we aim to explore a novel miR-101-3p shuttled by NSCLC cells in the growth and metastasis of NSCLC cells. Real-time PCR was performed to assess the level of miR-101-3p in cells and exosomes derived from the NSCLC cells. Effect of miR-101-3p on cell proliferation, metastasis and gefitinib sensitivity was then detected. Instinctively, METTL14 expression level was detected, which was positively related to that of miR-101-3p. Function of METTL14 on cell proliferation and metastasis was also investigated. High level of exosomal and intracellular miR-101-3p is correlated with better gefitinib response. miR-101-3p inhibited NSCLC cell proliferation and migration. In terms of mechanism, METTL14 endow NSCLC cells with gefitinib sensitivity via intracellular and exosomal miR-101-3p, leading to modulating of GSK-3β/Akt pathway. Collectively, this study indicated that restored METTL14/miR-101-3p confers gefitinib sensitivity in GR NSCLC by targeting GSK-3β/Akt pathway, indicating METTL14/miR-101-3p may act as a potential biomarker and therapeutic target for gefitinib response in NSCLC.
    Keywords:  Exosomal miR-101-3p; Gefitinib; METTL14; NSCLC
    DOI:  https://doi.org/10.1007/s12032-026-03242-5
  4. Int Rev Immunol. 2026 Jan 14. 1-33
      Exosomes (EXOs), membrane vesicles, have garnered significant attention in cancer treatments as a novel means by which cells communicate with each other. EXOs are recognized for their pathophysiological participation in cancer therapy and their role in immune activation. Moreover, extensive research has been conducted on EXOs-mediated cancer treatment, demonstrating significant potential for targeting cancer stem cells (CSCs). Dendritic cells (DCs), which orchestrate the immune response, have been extensively utilized in immunotherapy. Similar to other cells, DCs can release nanovesicles, predominantly EXOs. Significant attention has been directed toward dendritic cell-derived EXOs (DC-EXOs) as immunotherapeutic agents for cancer treatment. Like DCs, DC-EXOs possess chemicals that engage with immune cells, including costimulatory molecules and functional MHC-peptide complexes on their surface. DC-EXOs offer several benefits over cell-based immunotherapies that employ DCs, including the ability to facilitate immune cell-mediated tumor eradication. Tumor peptide-loaded d DC-EXOs have demonstrated efficacy in Phase I clinical studies; a Phase II clinical trial is underway. This study has examined the therapeutic potential of DC-EXOs for CSCs and various types of cancer. The advantages and disadvantages of this therapeutic method were also reviewed to augment the anticancer efficacy and targeting of DC-EXOs for prospective clinical application.
    Keywords:  Cancer; EXOs; cancer stem cells; dendritic cell; dendritic cell-derived EXOs; treatment
    DOI:  https://doi.org/10.1080/08830185.2026.2614776
  5. Int Immunopharmacol. 2026 Jan 15. pii: S1567-5769(26)00023-8. [Epub ahead of print]172 116180
      Gastric cancer, the fifth most prevalent and lethal malignancy worldwide, represents a significant public health challenge that necessitates urgent intervention. Peritoneal metastasis accounts for the majority of recurrences and fatalities following curative surgery for advanced gastric cancer. This study demonstrated that miR-let-7a inhibits gastric cancer peritoneal metastasis through dual mechanisms. Firstly, it promotes the polarization of macrophages to the M1 phenotype by targeting the 3'UTR of IRS2 mRNA, resulting in reduced IRS2 expression and phosphorylation and consequent suppression of the PI3K/AKT signaling pathway. Secondly, macrophages can release miR-let-7a to gastric cancer cells, directly inhibiting their malignant metastatic potential. Our findings suggest that miR-let-7a and IRS2 are promising targets for the development of immunotherapy for gastric cancer. Moreover, establishing systems for the endogenous delivery of miR-let-7a may provide innovative strategies to impede gastric cancer progression.
    Keywords:  Gastric cancer peritoneal metastasis; IRS2; Macrophage polarization; Tumor microenvironment; miR-let-7a
    DOI:  https://doi.org/10.1016/j.intimp.2026.116180