{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐187 has emerged as a highly context‐dependent regulator in human diseases. In several solid tumors, including hepatocellular carcinoma and clear cell renal cell carcinoma, reduced miR‐187 expression is linked to enhanced cell proliferation, migration, invasion, and epithelial–mesenchymal transition by de‐repressing targets such as RTKN2, S100A4, IGF‑1R, B7‑H3, SOX4, NT5E, PTK6, ALDH1A3, and others. Such loss of miR‑187 function has been observed in hepatocellular carcinoma, colorectal cancer, osteosarcoma, and even in salivary adenoid cystic carcinoma, where restoration of its levels or delivery via mesenchymal stem cell‐derived exosomes attenuates tumor growth and metastatic potential."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nConversely, in a number of malignancies miR‑187 appears to function in an oncogenic manner. Elevated levels have been reported in ovarian cancer and peripheral T‑cell lymphoma, where miR‑187 promotes cellular proliferation and migration by targeting tumor‐suppressor genes such as Dab2 and thereby facilitating Ras/ERK/AKT/MYC activation. Similarly, studies in oral squamous cell carcinoma and gastric cancer indicate that its upregulation sustains tumor growth and metastasis through inhibition of BARX2 and CRMP1. In some non‐small cell lung cancers and endometrial tumors, miR‑187 supports epithelial–mesenchymal transition and chemoresistance by repressing key regulators like PTRF, while in B‑cell acute lymphoblastic leukemia high miR‑187‑5p levels drive proliferation via DKK2 suppression and consequent activation of Wnt/β‑catenin signaling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "21"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond oncogenesis, miR‑187 plays diverse roles in non‐malignant as well as other pathological settings. In innate immunity, for example, miR‑187 is upregulated in IL‑10–stimulated monocytes where it dampens inflammatory cytokine production by directly targeting TNF‑α mRNA. Alterations in miR‑187 expression have also been associated with changes in cell cycle progression and apoptosis in models of breast cancer spheroids, glioma, pituitary adenoma, and cervical cancer, while its dysregulation is implicated in reproductive disorders such as recurrent miscarriage via effects on trophoblast function. In addition, dose‐dependent upregulation of miR‑187 has been reported in chronic opioid use disorder, correlating with altered levels of inflammatory mediators, and emerging evidence suggests that miR‑187 contributes to bone biology by modulating osteogenic differentiation and osteoporotic fracture repair. Its potential utility as a diagnostic and prognostic biomarker further underscores the multifaceted importance of miR‑187 across a wide range of biological processes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "22", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Guanqun Huang, Min Liang, Haiyan Liu, et al. 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