{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐205 is a small non‐coding RNA with multifaceted, context‐dependent functions in cancer. In many epithelial malignancies it acts as a tumor suppressor, helping to preserve epithelial differentiation and counteract epithelial‐to‐mesenchymal transition (EMT). Several studies have shown that reduced miR‐205 levels in non–small cell lung cancer, prostate, breast, melanoma, and glioma are associated with enhanced cell proliferation, migration, invasion and metastasis. Mechanistically, miR‐205 targets a variety of oncogenic mediators – including receptor tyrosine kinases (such as ErbB3), vascular endothelial growth factor A (VEGF‐A), protein kinase Cε, E2F transcription factors, and anti‐apoptotic proteins—that normally drive tumor progression. Its expression is frequently regulated by key transcription factors such as p53 and p63, further linking its loss to EMT induction and aggressive cancer phenotypes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "20"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its role in tumor initiation and progression, miR‐205 has been implicated in modulating therapeutic responses. In various studies, loss of miR‐205 was linked to resistance to chemotherapy and radiotherapy in cancers such as prostate, pancreatic, and esophageal carcinomas, whereas restoration of miR‐205 expression resensitized tumor cells to drugs like docetaxel, cisplatin, gemcitabine, and even ionizing radiation. These effects are mediated in part by its capacity to impair pro‐survival signaling pathways (for example, the AKT cascade) and autophagy, and by reversing EMT through upregulation of epithelial markers such as E-cadherin. Moreover, miR‐205 expression is subject to epigenetic regulation (including promoter hypermethylation) and can be modulated by microenvironment‐derived stimuli, thereby influencing both intrinsic cell behavior and the circulating miRNA signature used as a non‐invasive diagnostic or prognostic biomarker."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "30"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its intracellular regulatory circuits, circulating miR‐205 levels have been evaluated as potential biomarkers in several diseases—not only in cancer types such as cervical, bladder, and glioma but also in disorders like Parkinson’s disease and systemic lupus erythematosus. Furthermore, miR‐205 influences additional aspects of tumor biology, including lipid metabolism in hepatocellular carcinoma by targeting metabolic enzymes, and the maintenance of basement membrane integrity in epithelial tissues. Interactions with long non‐coding RNAs (for example, GAS5 and HOTAIR) further exemplify its diverse impact on gene regulatory networks that affect cancer stem cell maintenance and apoptotic responses. Collectively, these findings support the notion that modulation of miR‐205 expression may represent a promising therapeutic avenue as well as serve as a valuable prognostic tool."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "40"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Athina Markou, Emily G Tsaroucha, Loukas Kaklamanis, et al. 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