{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR-139 – encompassing both its ‑5p and ‑3p isoforms – is emerging as a potent tumor suppressor whose expression is frequently down‐regulated across a wide spectrum of human malignancies, including hepatocellular, colorectal, breast, esophageal, bladder, gallbladder, cervical, prostate, oral, laryngeal, and glioblastoma cancers. In these settings, restoration of miR-139 levels has been shown to inhibit cell proliferation, migration, invasion, metastasis, and the epithelial–mesenchymal transition through direct targeting of multiple oncogenes – such as IGF1R, MMP11, ETS1, BCL2, c-Fos, ZEB1/ZEB2, NR5A2, NOB1, CXCR4, HOXA9, and others – thereby interfering with aberrant Ras, Wnt/β-catenin, TGF-β, and PI3K/AKT signaling cascades. Importantly, re-expression of miR-139 not only reverses aggressive cancer phenotypes but also enhances sensitivity to chemotherapeutics and radiotherapy, underscoring its promise as both a prognostic biomarker and a therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its oncologic roles, miR-139 holds significant diagnostic and functional importance in non-malignant contexts. For instance, elevated exosomal miR-139-5p levels have been implicated in major depressive disorder, where they impair neurogenesis by reducing neural stem cell proliferation and differentiation. In parallel, modulation of miR-139-5p influences skeletal biology: its inhibition in bone marrow-derived mesenchymal stem cells promotes osteogenic differentiation, while altered miR-139 expression in osteoarthritis chondrocytes perturbs inflammatory signaling, notably by affecting IL-6 levels. These findings collectively highlight the potential of miR-139 as a biomarker for early disease detection and prognostication in diverse pathophysiologic settings."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "38", "end_ref": "41"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the mechanistic level, miR-139 exerts its regulatory influence by binding directly to the 3′ untranslated regions of target mRNAs, thereby promoting transcript degradation or translational repression. Its own expression is subject to multilayered regulation—epigenetic modifiers such as EZH2 can silence the miR-139 promoter via H3K27 trimethylation, and long noncoding RNAs like XIST and NEAT1 act as molecular sponges that sequester miR-139, effectively derepressing oncogenic targets. Reciprocal feedback interactions with key transcription factors, including TCF-4, further embed miR-139 within signaling networks governing cell survival, metabolism, and the epithelial–mesenchymal transition. These interconnected regulatory circuits not only shed light on the diverse functional roles of miR-139 but also underscore the therapeutic promise of strategies aimed at restoring its expression to counteract tumor progression and treatment resistance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}, {"type": "fg_f", "ref": "23"}, {"type": "fg_f", "ref": "29"}, {"type": "fg_f", "ref": "32"}, {"type": "fg_f", "ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Carmen Chak-Lui Wong, Chun-Ming Wong, Edmund Kwok-Kwun Tung, et al. 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