{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐26b is a multifunctional microRNA whose expression is widely deregulated in human disease. In several solid tumors – including glioma, breast, pituitary, oral squamous, tongue, prostate, melanoma, renal, esophageal, triple‐negative breast, and even certain lymphoproliferative disorders – miR‐26b is frequently downregulated. Its restoration suppresses cell proliferation, migration, invasion and tumor growth through direct targeting of key oncogenic or cell‐cycle promoting factors such as SLC7A11, CDC6, MYCBP, LARP1, PFKFB3, COX‑2, KPNA2, FUT4, and DEPDC1, while modulating pathways including NF‑κB, c‑MYC, and PI3K/AKT. Notably, in a subset of colorectal cancers, forced miR‐26b expression has been reported to promote epithelial–mesenchymal transition and stem cell–like features by repressing tumor suppressors including PTEN and WNT5A, indicating that its biological impact may be context dependent."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in oncogenesis, miR‑26b is critical in non‑malignant contexts. In neurodegeneration, elevated miR‑26b in Alzheimer’s disease has been linked to DNA replication aberrancies, tau hyperphosphorylation, and neuronal apoptosis by targeting regulators such as Rb1, while similar regulatory events modulate brain‐derived neurotrophic factor expression. In metabolic tissues, miR‑26b is upregulated during adipocyte differentiation—promoting lipid accumulation and thermogenic characteristics via targets such as ADAM17 and PTEN—and it modulates endothelial cell behavior, thereby influencing angiogenesis relevant to cardiovascular repair. miR‑26b also plays roles in inflammatory and autoimmune conditions; for example, its altered expression in peripheral blood mononuclear cells has been associated with major depressive disorder and HCV‑related lymphoproliferative disorders, and in synovial and chondrocyte models it influences NF‑κB signaling by targeting mediators like KPNA3, ultimately affecting cytokine secretion, extracellular matrix degradation, and fibrosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "41"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, these studies underscore the context‑dependent, pleiotropic functions of miR‑26b. By fine‑tuning diverse biological processes—from cell cycle progression, apoptosis, and epithelial–mesenchymal transition in cancer to neuronal survival, adipogenesis, autophagy, inflammation, and viral replication in non‑malignant tissues—miR‑26b emerges as both a promising biomarker and a potential therapeutic target. Ongoing investigations into its multiple direct targets (for example, Rb1, CDC6, MYCBP, PFKFB3, ULK2, SLC7A11, KPNA2, COX‑2, TRAF5, DEPDC1, ST8SIA4, PIK3CD, among others) will further elucidate how modulation of miR‑26b expression could be exploited in precision medicine.\n \n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ning Wu, Xiangzhong Zhao, Ming Liu, et al. 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