{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‑124 is a highly conserved microRNA that exerts multifaceted tumor‐suppressive effects in a broad range of human cancers. In diverse malignancies—including hepatocellular carcinoma, medulloblastoma, oral, prostate, breast, colorectal, cervical, nasopharyngeal, gallbladder, bladder, lung cancers and others—loss of miR‑124 function (by epigenetic silencing, DNA hypermethylation, or sequestration by oncogenic circular RNAs such as circHIPK3 and circWDR77) is associated with enhanced cell proliferation, invasion, metastasis, and resistance to radiotherapy or chemotherapy. Mechanistic studies have identified its direct targeting of key oncogenic regulators and signaling mediators such as cell‐cycle proteins (e.g. CDK4, CDK6), transcription factors, epigenetic modulators (e.g. DNMT3B, UHRF1), and critical nodes of the PI3K/AKT and EGFR‐driven pathways (including STAT3, PIK3CA, and SPHK1), as well as proteins that modulate metabolic reprogramming (e.g. Rac1, PTB1). Restoration of miR‑124 levels in tumor cells reverses these oncogenic processes and suppresses tumor growth, underscoring its potential value as both a prognostic biomarker and a therapeutic target in cancer management."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its prominent role in cancer, miR‑124 is essential for normal neural and immune homeostasis. In neuronal systems, it regulates alternative splicing and neuronal excitability—contributing to proper synaptic plasticity and differentiation—and its dysregulation has been linked to Alzheimer’s disease, epilepsy, Parkinson’s disease, and drug addiction. Moreover, miR‑124 modulates the inflammatory response by promoting the polarization of macrophages toward an anti‐inflammatory (M2) phenotype and by fine‑tuning toll‑like receptor signaling, thereby reducing pro‑inflammatory cytokine production. 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