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Faculty of natural sciences, university of tabriz
Abstract:   (8 Views)
Lung cancer remains one of the most prevalent malignancies worldwide, presenting substantial challenges in early detection, effective therapy, and favorable prognosis. Exosomes, extracellular vesicles secreted by cells, play a pivotal role in intercellular communication. In recent years, exosomes and their associated non-coding RNAs (ncRNAs) have garnered significant attention as key contributors to cancer progression and as novel biomarkers. This review examines the functions of exosomal miRNAs, lncRNAs, and circRNAs in lung cancer carcinogenesis, encompassing processes such as angiogenesis, epithelial-mesenchymal transition (EMT), drug resistance, immune modulation, and metastasis. Furthermore, it explores the clinical potential of exosomal ncRNAs in enhancing lung cancer management and emerging paradigms in personalized medicine. Findings from recent studies indicate that the expression profiles of these ncRNAs in exosomes derived from blood, plasma, tissues, or other patient fluids can serve as sensitive and specific biomarkers for early diagnosis, prediction of treatment response (e.g., to chemotherapy or immunotherapy), and disease prognosis determination. For instance, miRNAs such as miR-21 and miR-96 are implicated in drug resistance, whereas lncRNAs like HOTAIR and circRNAs like circVMP1 promote proliferation and metastasis. The tumor microenvironment (TME) is also influenced by exosomes, where ncRNAs regulate interactions among tumor, immune, and stromal cells. Nevertheless, challenges including exosome isolation purity, sample heterogeneity, methodological limitations (such as ultracentrifugation), and restricted clinical applicability warrant further investigation. Ultimately, exosomal ncRNAs may emerge as innovative therapeutic targets, such as drug carriers or prognostic indicators, in personalized lung cancer treatment.
 
Article number: 1
     
Type of Study: review | Subject: Subject 03
Received: 2025/10/19 | Accepted: 2026/05/19

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