{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐148a plays multifaceted roles in normal physiology by fine‐tuning gene expression at the post‐transcriptional level. In immune cells it binds to conserved motifs in the 3′‐untranslated regions of HLA molecules—such as HLA‑C and HLA‑G—to modulate cell‐surface expression and thereby impact recognition in HIV infection and placental tolerance. In addition, miR‑148a is a critical regulator of cellular differentiation, promoting hepatic maturation via repression of DNMT1 and the c‑Met oncogene, as well as fostering adipocyte differentiation through inhibition of the endogenous Wnt1 inhibitor; it also contributes to chondrocyte metabolism and osteoclastogenesis, with emerging roles noted in neuronal differentiation affecting psychiatric function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn cancer, the functional status of miR‑148a is context dependent, with its dysregulation contributing to disease progression, metastasis and chemoresistance in several tumor types. In many malignancies—including prostate, ovarian, breast, gastric, hepatocellular, lung, laryngeal, and bladder cancers as well as osteosarcoma—down‑regulation of miR‑148a is associated with aggressive behavior and poor outcomes. Mechanistically, miR‑148a exerts tumor‑suppressive effects by targeting key mediators of oncogenic pathways such as DNMT1, MSK1, IGF‑IR, IRS1, Met/Snail and ROCK1, thereby promoting apoptosis, inhibiting cell proliferation and curtailing epithelial‑to‑mesenchymal transition. Conversely, in selected contexts such as HBV‑associated hepatocarcinogenesis and glioblastoma, miR‑148a up‑regulation contributes to oncogenic signaling by suppressing tumor suppressors and facilitating factors that drive proliferation and cancer stem‑like phenotypes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nEmerging evidence also points to novel roles of miR‑148a in the regulation of metabolism, therapeutic resistance, and intercellular communication. By directly modulating LDL receptor expression, miR‑148a influences cholesterol homeostasis—a process linked to cardiovascular risk—while its aberrant expression has been implicated in the development of chemoresistance in gastric cancer. In addition, miR‑148a is involved in controlling apoptotic pathways via targeting Bcl‑2 and participates in the modulation of oncogenic feedback loops that impact cell fate decisions. Recent studies further reveal that miR‑148a can be packaged into exosomes; for example, SARS‑CoV‑2 spike protein expression alters exosomal miR‑148a levels, which upon uptake by microglia disturb inflammatory signaling and may contribute to neuroinflammatory sequelae."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "36", "end_ref": "38"}, {"type": "fg_f", "ref": "31"}, {"type": "fg_f", "ref": "33"}, {"type": "fg_f", "ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Margarita Muiños-Gimeno, Yolanda Espinosa-Parrilla, Monica Guidi, et al. 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