{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐25 (MIR25) is frequently dysregulated in a wide spectrum of human cancers, where it exerts context‐dependent effects on tumor cell behavior. In several studies, overexpression of MIR25—often as a constituent of the miR‐106b–25 polycistron—has been shown to promote cell proliferation, migration, invasion, and even distant metastasis by directly downregulating key tumor‐suppressor targets (such as regulators of E2F1, Bim, RECK, CDH1, FBXW7, TOB1, and Smad7) and by perturbing p53 and mitochondrial calcium uptake pathways. In contrast, in certain settings such as colon cancer or within prostate cancer stem cells, restoration of MIR25 activity can inhibit tumor growth and dissemination by repressing proinvasive molecules. These findings underscore the multifaceted, sometimes even paradoxical, role of MIR25 in modulating oncogenic transformation and tumor progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMIR25 is also emerging as a key regulatory molecule in several non‐malignant conditions. In the cardiovascular system, aberrantly high MIR25 expression impairs intracellular calcium handling in cardiomyocytes—a change that contributes to the progression of heart failure. In immune‐mediated and metabolic contexts, altered circulating levels of MIR25 have been reported in type 1 diabetes and diabetic complications such as nephropathy and retinopathy, while decreased expression in specific immune cell subsets (for example, regulatory T cells) and neuronal cells under ischemic challenge indicates roles in modulating inflammatory responses and cell survival. Furthermore, MIR25 upregulation in melanocytes subjected to oxidative stress is associated with cell dysfunction observed in vitiligo."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "36", "end_ref": "43"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, the diverse biological activities of MIR25 not only illuminate its essential roles in the regulation of cell fate and intercellular communication but also highlight its promise as a novel biomarker and therapeutic target. In cancer models, for example, experimental inhibition of MIR25 (using antagomiRs) has restored apoptotic sensitivity and reduced metastatic capacity, while in disorders such as heart failure and diabetic complications, modulating MIR25 levels has led to marked improvements in cellular function and survival by normalizing signaling cascades (including those mediated by PTEN/Akt). These encouraging preclinical findings support further exploration of MIR25‐centered interventions with the ultimate goal of improving patient outcomes across a range of pathologic conditions."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "39"}, {"type": "fg_f", "ref": "21"}, {"type": "fg_f", "ref": "27"}, {"type": "fg_fs", "start_ref": "41", "end_ref": "43"}, {"type": "fg_f", "ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Fabio Petrocca, Rosa Visone, Mariadele Rapazzotti Onelli, et al. 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