{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐592 has emerged as a critical regulatory microRNA whose dysregulation has been documented in a wide spectrum of human diseases. Multiple studies have demonstrated that abnormal miR‐592 expression is involved in the control of cell proliferation, apoptosis, metabolism, migration, and differentiation. Notably, miR‐592 has been implicated in various cancers—including colorectal, hepatocellular, thyroid (both papillary and medullary), breast, glioma, uveal, ovarian, and medulloblastoma—as well as in non‐malignant conditions such as polycystic ovary syndrome, suggesting that its function is highly context‐dependent. In some settings, aberrant miR‐592 expression correlates with the deregulation of key oncogenes and tumor suppressors, thereby contributing to tumor initiation and progression"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "19"}]}, {"type": "t", "text": "\n \n<br><br>\nIn several studies, miR‐592 appears to function as a tumor suppressor. Downregulated miR‐592 in hepatocellular carcinoma was associated with enhanced aerobic glycolysis and cell proliferation through its direct regulation of targets such as DEK and WSB1. Similarly, in glioma and thyroid cancer, restoration of miR‐592 levels suppressed cell growth and invasiveness via targeting oncogenic factors including ROCK1, IGFBP2, and NOVA1. In ovarian cancer, increased miR‐592 expression inhibited tumor cell proliferation and invasion by downregulating ERBB3, and in polycystic ovary syndrome, diminished circulating miR‐592 correlated inversely with luteinizing hormone receptor levels and cell cycle progression. Furthermore, in breast cancer and medulloblastoma, re‐establishing miR‐592 expression led to marked reductions in malignant phenotypes"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "2", "end_ref": "4"}, {"type": "fg_f", "ref": "7"}, {"type": "fg_f", "ref": "10"}, {"type": "fg_f", "ref": "12"}, {"type": "fg_fs", "start_ref": "17", "end_ref": "19"}]}, {"type": "t", "text": "\n \n<br><br>\nConversely, other investigations have reported oncogenic functions for miR‐592 in certain tumor contexts. In colorectal and gastric cancers, miR‐592 is frequently upregulated, and its elevated levels promote cell proliferation, migration, and invasion through suppression of tumor suppressors such as SPARC. Similarly, in medullary thyroid carcinoma, increased miR‐592 expression accelerates cell proliferation via targeting CDK8, while analyses in breast cancer and uveal melanoma have underscored its association with adverse clinical outcomes in selected patient populations. In addition, although its role in acute myeloid leukemia remains to be fully elucidated, these findings collectively highlight the complex, context‐dependent nature of miR‐592’s function in tumorigenesis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}, {"type": "fg_f", "ref": "5"}, {"type": "fg_f", "ref": "9"}, {"type": "fg_fs", "start_ref": "13", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Mulin Liu, Qiaoming Zhi, Wenbin Wang, et al. 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