{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐125b is emerging as a multifaceted post‐transcriptional regulator in cancer, where its deregulation either promotes or suppresses tumorigenesis in a context‐dependent manner. In several malignancies—including Taxol‐resistant cancers, diffuse large B‐cell lymphoma, cervical, colorectal, ovarian, breast, prostate, and gallbladder carcinomas—overexpression of miR‐125b has been shown to inhibit pro‐apoptotic molecules such as Bak1 and p14(ARF), modulate the p53 network, and enhance NF‐κB signaling, thereby conferring chemoresistance, promoting cell survival and proliferation, and facilitating metastasis. Conversely, in some solid tumors its downregulation leads to de‐repression of targets such as ETS1, E2F3, BCL3, KIAA1522, and SUV39H1 that otherwise drive aggressive growth, epithelial–mesenchymal transition, and invasion."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the setting of hematopoiesis and stem cell biology, miR‐125b plays a key role in maintaining stem cell properties and influencing differentiation. It is highly expressed in hematopoietic stem cells where it supports survival and skews lineage decisions toward lymphoid‐bias, while its modulation in B‐cell precursors regulates the timely expression of transcription factors that drive differentiation. In addition, alterations in miR‐125b levels have been linked to abnormal lineage commitment in pediatric leukemias and age‐associated declines in B lymphopoiesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nWithin the nervous system, miR‐125b has been implicated in neurodegenerative processes and neural differentiation. Its overexpression in primary neurons induces tau hyperphosphorylation by perturbing kinase/phosphatase balance—a mechanism relevant to Alzheimer’s disease—and miR‐125b is enriched in exosomes released by neuronal progenitors that promote differentiation. These findings underscore the dual role of miR‐125b in both neural pathology and development."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "34"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMiR‐125b also governs key inflammatory and immune responses. In psoriatic skin lesions, reduced miR‐125b in keratinocytes is associated with hyperproliferation and aberrant differentiation, while in macrophages its increased expression leads to destabilization of TNF mRNA, contributing to pathogen immune evasion. Moreover, in chondrocytes and rheumatoid arthritis, miR‐125b modulates inflammatory signaling cascades by targeting mediators like TRAF6, and its circulating levels may serve as predictive biomarkers of therapeutic response in chronic inflammatory conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "35", "end_ref": "40"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond these core functions, miR‐125b is integrated within complex regulatory networks that influence cancer progression and metastasis through cross‐talk with other noncoding RNAs and signaling cascades. It is modulated by oxidative stress via promoter methylation, participates in feedback loops with receptors such as CXCR4 and transcription factors including STAT3, and its deregulated expression contributes to altered angiogenesis, epithelial–mesenchymal transition, and metabolic reprogramming in an array of tumors including melanoma, head and neck, and chronic lymphocytic leukemia. Such diverse functions illustrate miR‐125b’s role as a central “rheostat” fine‐tuning multiple oncogenic, developmental and inflammatory pathways."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "41", "end_ref": "46"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ming Zhou, Zixing Liu, Yuhua Zhao, et al. 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