{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe MIR181B1 gene, which gives rise to mature miR‐181b, has emerged as a multifaceted regulator whose activity is highly context‐dependent. In certain inflammatory and transformation settings, MIR181B1 is rapidly induced downstream of IL‐6/STAT3 signaling, thereby contributing to an epigenetic switch that converts nontransformed cells into a tumorigenic state via a positive feedback loop—partly through the inhibition of key tumor suppressors such as CYLD. In colon cancer models, transient induction of miR‐181b‐1 cooperates with other STAT3‐activated microRNAs to sustain NF‐κB activity and the transformed phenotype."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn hematologic malignancies, the expression of MIR181B1–derived miR‐181b is of particular importance. In acute myeloid leukemia (AML), higher circulating levels correlate with favorable overall survival and its ectopic expression can promote apoptosis and chemosensitivity—principally by targeting anti‐apoptotic factors such as PBX3, HMGB1, and Mcl‐1. Similarly, in chronic lymphocytic leukemia (CLL), declining miR‐181b levels are associated with disease progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "3", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn several central nervous system tumor models, including gliomas and glioblastoma multiforme, miR‐181b generally functions as a tumor suppressor. Reduced levels in tumor tissues correlate with increased proliferation, migration, invasion and resistance to therapy; mechanistic studies have shown that miR‐181b may inhibit oncogenic drivers such as IGF‐1R or modulate networks involving FOS and miR‐21, and even suppress epithelial–mesenchymal transitions through KPNA4 targeting. Such observations underline its potential utility as both a prognostic biomarker and a therapeutic candidate in malignant brain tumors."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the context of other solid tumors, MIR181B1 displays dual roles. In cervical and gastric cancers, as well as in thyroid papillary and ovarian cancers, elevated miR‐181b expression can promote cell proliferation, migration, and invasion by targeting tumor suppressors like AC9 or CYLD and by facilitating TGF‐β–mediated epithelial–mesenchymal transition. In neuroblastoma, its overexpression correlates with MYCN amplification and aggressive behavior, while in non–small cell lung cancer it has been implicated in driving EMT and metastasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "21"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond cancer, MIR181B1 plays significant roles in non‐malignant conditions. In the liver, miR‐181b is induced by TGF‐β1 in hepatic stellate cells—promoting cell cycle progression by directly targeting molecules such as p27 and PTEN; these actions contribute to liver cirrhosis, fibrosis, and even non‐alcoholic fatty liver disease through modulation of lipid metabolism (and SIRT1 expression). In cartilage, its upregulation in osteoarthritic chondrocytes correlates with enhanced expression of matrix metalloproteinases and cartilage breakdown. Moreover, in cardiovascular settings, its elevated expression in the fibrosa of calcified aortic valves and its association with increased matrix‐degrading activity suggest a role in vascular remodeling. MIR181B1 is further implicated in modulating inflammatory responses—for instance, by promoting TNF‐α mRNA decay in sepsis and by dampening IFN‐γ production in immune cells. These diverse functions have also been linked to alterations in metabolic and endocrine pathways, as revealed in type 2 diabetes mellitus ceRNA network studies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "22", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFinally, in the neuropsychiatric realm, aberrantly high levels of miR‐181b have been noted in schizophrenia—with reductions following antipsychotic treatment correlating with improvement in negative symptoms and treatment responsiveness—underscoring its potential as a peripheral marker of disease severity."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "36"}]}, {"type": "t", "text": " In addition, MIR181B1 has been shown to potentiate endothelial differentiation from pluripotent stem cells, further highlighting its diverse regulatory role in vascular homeostasis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Dimitrios Iliopoulos, Savina A Jaeger, Heather A Hirsch, et al. 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