bims-exocan Biomed News
on Exosomes roles in cancer
Issue of 2026–02–01
six papers selected by
Muhammad Rizwan, COMSATS University



  1. Biochim Biophys Acta Rev Cancer. 2026 Jan 27. pii: S0304-419X(26)00017-X. [Epub ahead of print] 189545
      Colorectal cancer (CRC) progression is profoundly shaped by the tumor microenvironment. Among stromal components, cancer-associated fibroblasts (CAFs) release small extracellular vesicles (exosomes) that deliver miRNAs, lncRNAs, circRNAs, proteins, and metabolites to malignant and immune cells. In CRC, CAF-derived exosomes (CAF-Exo) drive epithelial-mesenchymal transition, sustain stemness, stimulate angiogenesis, suppress antitumor immunity, and promote resistance to fluoropyrimidines and oxaliplatin. Representative mechanisms include exosomal miR-92a-3p activation of Wnt/β-catenin signaling, the lncRNA WEE2-AS1-mediated suppression of Hippo restraint with YAP activation, and circRNA cargos that reprogram autophagy or endothelial dynamics. Circulating CAF-Exo signatures are emerging as minimally invasive biomarkers for diagnosis, prognosis, and therapy stratification. However, translation remains limited by CAF heterogeneity, cargo variability, and incomplete in vivo characterization of vesicle dynamics. Therapeutic opportunities include blockade of exosome biogenesis or uptake, pharmacologic reprogramming of CAFs, and engineering vesicles to deliver targeted inhibitors or RNA-based therapeutics. This review synthesizes current mechanistic insights, evaluates biomarker potential, and outlines clinical priorities for targeting CAF-exosomal pathways in CRC.
    Keywords:  Biomarkers; Cancer-associated fibroblasts; Colorectal cancer; Exosomes; Non-coding RNAs; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.bbcan.2026.189545
  2. Int J Oncol. 2026 Apr;pii: 38. [Epub ahead of print]68(4):
      Breast carcinoma remains a major global health burden requiring innovative diagnostic and therapeutic strategies. Exosomal miRNAs have emerged as key factors in breast carcinoma that influence tumor progression, metastasis and treatment resistance. Recent studies have elucidated their mechanisms of action, including their roles in regulating oncogenic and tumor‑suppressive pathways, modulating the tumor microenvironment and promoting chemo‑resistance. Advances in miRNA‑based therapies such as miRNA mimics and inhibitors have shown promise in combination treatments, enhancing their therapeutic efficacy. Furthermore, exosomal miRNAs play a role in breast carcinoma calcification, offering novel insights into tumor progression. Unlike previous reviews that focus on a single function or therapeutic potential of miRNAs, the present review systematically integrated the multilevel role of exosomal miRNAs in breast cancer from the two dimensions of oncogenicity and tumor inhibition and the regulatory mechanism of breast carcinoma calcification and proposes that the exosomal miRNA calcification axis may be a key link connecting tumor metabolism and pathological calcification. Despite the potential of miRNAs, challenges remain in optimizing exosome isolation techniques and standardizing miRNA detection methods for clinical applications. Future research should focus on refining miRNA‑based liquid biopsies, developing delivery systems that target exosomes to enhance therapeutic efficacy and early detection strategies and ultimately improving patient survival and quality of life. The present review comprehensively explored the roles of exosomal miRNAs and highlighted their importance in breast carcinoma research. The present review illustrated the potential of exosomal miRNAs as non‑invasive biomarkers and therapeutic targets in precision medicine.
    Keywords:  biomarker; breast carcinoma; calcification; combination therapy; exosomal miRNAs
    DOI:  https://doi.org/10.3892/ijo.2026.5851
  3. Brain Res. 2026 Jan 27. pii: S0006-8993(26)00043-0. [Epub ahead of print] 150185
      Exosomes play a vital role in intercellular communication, significantly influencing cell behavior and fate. Their influence is particularly evident in diseases like glioblastoma, one of the most challenging cancers to treat. Due to glioblastoma's high resistance to conventional therapies, novel treatment strategies are urgently needed. Exosomes, being nano-sized vesicles capable of crossing the blood-brain barrier, can deliver bioactive molecules, including nucleic acids, proteins, and metabolites, to suppress tumor-promoting activities in cancer cells. Induced pluripotent stem cells (iPSCs), known for their unlimited proliferation potential and lack of ethical concerns compared to embryonic sources, present a valuable source of exosomes for therapeutic purposes. Although embryonic stem cell-derived exosomes have shown anti-tumor effects against glioblastoma, the therapeutic potential of iPSC-derived exosomes remains largely unexplored. In this study, we demonstrate that exosomes derived from iPSCs exert anti-tumorigenic effects on glioblastoma cells. We also focused on microRNAs (miRNAs), key regulators of cellular proliferation and apoptosis, which are considered promising therapeutic targets in glioblastoma. Specifically, we observed that microRNA-7 (miR-7) significantly inhibits glioblastoma cell proliferation, migration, and invasion. Our findings show that treatment with a miR-7-5p mimic reduces glioblastoma cell proliferation, and its combination with iPSC-derived exosomes leads to either additive or synergistic anti-cancer effects. These results highlight iPSC-derived exosomes and miR-7 as promising therapeutic candidates for glioblastoma and potentially other malignancies.
    Keywords:  Combinational therapy; Exosome; Glioblastoma; Induced pluripotent stem cells; miRNA-7
    DOI:  https://doi.org/10.1016/j.brainres.2026.150185
  4. Lab Chip. 2026 Jan 27.
      Extracellular vesicles (EVs), especially the exosome-sized subset are increasingly exploited as minimally invasive cancer biomarkers. These small vesicles are abundant in biofluids and play crucial roles in intercellular communication and disease progression by transporting bioactive molecules. Exosomes offer distinct diagnostic and prognostic advantages over traditional cancer biomarkers, but purifying and extracting exosomes from blood remains challenging. There is a need to simply and cost-effectively isolate exosomes from milliliter quantities of whole blood for transcriptional and other omics-based research. Addressing this gap, we propose a microfluidic cartridge, the EV-Blade, for size and affinity-based purification of exosomes on a centrifugal microfluidic platform. We demonstrate a method to automate exosome purification from whole blood samples on a single microfluidic cartridge. The EV-Blade system combines blood centrifugation, plasma filtration for EV size selection and immunomagnetic capture using functionalized superparamagnetic nanoparticles targeting CD9, CD63, and CD81 exosomal surface proteins. We report on the device performance, purity of exosome recovery and the quality of RNA collected following on-chip EV lysis. We use this automated method to detect relevant long coding and non-coding RNA transcripts in circulating blood exosomes, showcasing the EV-Blade for use in cancer patient risk stratification. The system presented herein represents a significant advancement in exosome purification, offering a robust and automated platform for liquid biopsy-based cancer research and clinical applications. This innovation holds promise for cancer diagnosis, prognosis, and monitoring through non-invasive biomarkers.
    DOI:  https://doi.org/10.1039/d5lc00977d
  5. Front Immunol. 2025 ;16 1734244
      Gastric cancer peritoneal metastasis (GCPM) is the leading cause of death in patients with advanced gastric cancer. The presence of ascites creates favorable conditions for the formation of the pre-metastatic niche (PMN), thereby providing a conducive environment for cancer cell metastasis. However, the mechanisms behind the formation of the pre-metastatic niche (PMN) are still not fully understood. This review examines the dynamic changes in the PMN of gastric cancer using organoid models combined with high spatiotemporal resolution and looks into the role of extracellular vesicles (EVs) in mediating immune suppression. It gives an overview of the latest advances in organoid modeling technologies, clarifies the biological characteristics of EVs, and discusses their functions in immune regulation. Furthermore, this review also highlights current challenges in this field, proposes future research directions, and identifies potential therapeutic targets. Bringing these insights together is intended to deepen understanding of gastric cancer metastasis and support the development of more effective therapeutic strategies.
    Keywords:  extracellular vesicles; gastric cancer; immune suppression; organoid modeling; peritoneal metastasis; pre-metastatic niche
    DOI:  https://doi.org/10.3389/fimmu.2025.1734244
  6. Cell Biol Toxicol. 2026 Jan 29.
      Acute myeloid leukemia (AML)-derived bone mesenchymal stem cell (MSC) exosomes have been confirmed to have a positive effect on AML progression. This study aim to reveal the underlying molecular mechanism by which AML-MSC-derived exosomes promotes AML progression. AML-MSC was isolated from the bone marrow aspirates of AML patients. After incubated with AML-MSC, AML cell functions were analyzed. The expression levels of methyltransferase-like 14 (METTL14), homeobox A3 (HOXA3), WNT family member 7B (WNT7B) and glycolysis-related markers were examined. Exosomes were isolated from AML-MSC and then the obtained exosomes were co-cultured with AML cells. AML-MSC co-culturing could enhance AML cell proliferation and glycolysis, while repress cell apoptosis. METTL14 was upregulated in exosomes from AML-MSC, which could be ingested by AML cells. METTL14 could enhance HOXA3 mRNA stability via promoting its m6A modification. Knockdown of exosomal METTL14 from AML-MSC inhibited AML cell growth and glycolysis, while were reversed by HOXA3. In addition, HOXA3 bound to WNT7B promoter to increase its transcription, and WNT7B overexpression also eliminated si-HOXA3-mediated inhibitory on AML cell growth and glycolysis. Animal study revealed that knockdown of exosomal METTL14 from AML-MSC reduced AML tumorigenesis by decreasing HOXA3 and WNT7B expression. AML-MSC-derived exosomal METTL14 facilitated AML cell growth and glycolysis by activating the HOXA3/WNT7B axis, providing a new mechanism for understanding AML-MSC-derived exosomes to promote AML progression.
    Keywords:  Acute myeloid leukemia; Bone mesenchymal stem cells; Exosome; METTL14
    DOI:  https://doi.org/10.1007/s10565-026-10143-w