{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐24‐1 has emerged as a multifunctional regulator that—in addition to its canonical cytoplasmic roles—can act in the nucleus. For instance, miR‐24‐1 can bind enhancer loci to trigger gene activation by stimulating enhancer RNA production, modifying local histone marks, and recruiting transcriptional co‐activators, while other studies show that it contributes to the downregulation of critical DNA repair factors (e.g. via direct targeting of the H2AX 3′‐UTR) and facilitates c‐Myc mRNA turnover through miRISC recruitment. These findings highlight its unanticipated nuclear functions in modulating transcription and genomic stability."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn cancer, the function of miR‐24 (and related mature forms such as miR‐24‐3p) is highly context‐dependent. In certain tumors—including subsets of breast, gastric, hepatocellular, glioma, and bladder cancers—as well as in nasopharyngeal and small‐cell lung cancers, miR‐24 is either overexpressed to promote proliferation, migration, invasion, autophagy and treatment resistance (via targets such as EGFR regulators, ATG4A, and modulators of apoptosis) or is downregulated to relieve repression of tumor suppressor genes (for example, FOXM1 in bladder cancer, TRIM11 in colon cancer, and genes involved in cell cycle control such as DHFR). Moreover, in pancreatic β‐cells and prostate tumors, aberrant levels of miR‐24 contribute to dysfunctional endocrine signaling and altered cell survival, underscoring a dual oncogenic and tumor‐suppressive potential that is dictated by tumor type and microenvironmental cues."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "4", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond oncogenesis, miR‐24 plays pivotal roles in metabolic and immunomodulatory processes. It contributes to the phenotypic modulation of vascular smooth‐muscle cells and regulates steroid biosynthesis by targeting key enzymes in cortisol and aldosterone production. In the liver and kidney, miR‐24 influences lipid accumulation in nonalcoholic fatty liver disease and exacerbates ischemia–reperfusion injury by promoting apoptosis in endothelial and epithelial cells. Moreover, through its impact on phagocytic activity, antigen processing, and macrophage polarization—often by targeting regulators of the MAPK pathway and other immunomodulatory factors—miR‐24 helps shape inflammatory responses; it has even been implicated in the regulation of serotonin transporter levels in irritable bowel syndrome, in depressive treatment responses, in Parkinson’s disease diagnostics, and in antiviral defense against SARS‐CoV‐2. Collectively, these studies underscore the diverse biological functions of miR‐24‐1 in governing both cellular homeostasis and pathogenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ashish Lal, Yunfeng Pan, Francisco Navarro, et al. 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