{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRecent studies have revealed that members of the miR‐10 family, notably miR‐10b, function as key regulators of tumorigenesis. In malignant brain tumors such as glioblastoma, miR‐10b is strongly upregulated where it promotes cell‐cycle progression and impedes apoptosis by repressing multiple tumor suppressor targets. In oral and breast cancers, miR‐10b overexpression enhances cell migration and invasion, thereby facilitating metastasis. Similarly, in fibrolamellar carcinoma, oncogenic fusions induce miR‐10b‐5p upregulation which drives a proliferative axis by inhibiting tumor suppressor genes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its oncogenic roles, miR‐10b is intimately involved in developmental and differentiation processes. It participates in the modulation of neurotrophic factors—for instance, directly repressing brain‐derived neurotrophic factor (BDNF) expression in both neural and muscle systems—thereby influencing synaptogenesis and neural differentiation. In reproductive biology, miR‐10b promotes spermatogonial stem cell self‐renewal through targeting specific transcription factors, and it regulates osteoblast differentiation by interacting with key modulators of bone formation. Moreover, its processing from Hox gene transcripts has been implicated in embryonic antero–posterior patterning, while altered expression in the hippocampus correlates with impaired neurogenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nThe regulatory spectrum of miR‐10b further extends to cardiovascular, metabolic, and inflammatory pathways. In the heart, miR‐10b‐5p confers protection against hypoxia‐induced apoptosis by targeting PTEN, whereas in bone marrow–derived mesenchymal stem cells its upregulation augments migratory capacity through the downregulation of E‐cadherin. In macrophages, miR‐10b suppresses cholesterol efflux by inhibiting key transporters and thus may contribute to atherosclerotic processes. Furthermore, in adipocytes, decreased miR‐10b‐5p levels facilitate adipogenesis via derepression of target genes, and in skin models, delivery of miR‐10b via extracellular vesicles promotes wound healing through enhanced cellular proliferation and migration. Elevated miR‐10b is additionally linked to aneurysm formation and modulates responses in inflammatory bowel disease, emphasizing its complex role in vascular and inflammatory homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nDistinct from the extensively characterized roles of miR‐10b, emerging evidence has begun to shed light on miR‐5010‐5p—a related, yet separate member of the miR‐10 family. Investigations in the context of diabetic kidney disease indicate that miR‐5010‐5p may modulate the function of renal tubular epithelial cells under diabetic conditions, suggesting an important, albeit still preliminary, role in kidney pathology."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Galina Gabriely, Ming Yi, Ravi S Narayan, et al. 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