{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‑152 has emerged as an important epigenetic regulator that, in a number of human malignancies, functions predominantly as a tumor‐suppressive factor. In several studies, reduced levels of miR‑152 were observed in cancers such as hepatocellular carcinoma, endometrial, breast, ovarian, glioblastoma, and non‑small cell lung cancer. In these settings, miR‑152 restoration inhibited cell proliferation, migration, invasion and induced apoptosis, in part through its direct targeting of DNA methyltransferase 1 (DNMT1) thereby reducing aberrant global DNA methylation and re‐expressing silenced tumor suppressor genes. Such studies underscore miR‑152’s role in modulating the epigenetic landscape and its potential utility to restore normal gene expression programs in tumor cells."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to regulating DNMT1, miR‑152 has been implicated in controlling a variety of other oncogenic and immunomodulatory targets. For instance, miR‑152 can directly downregulate the expression of HLA‑G – a molecule involved in immune tolerance – as well as other targets such as members of growth factor and adhesion receptor families (e.g., FGF2, TFRC, CD151) and metabolic regulators like PKM2. Its expression is intricately regulated by long non‑coding RNAs – including HOTAIR, H19, and PVT1 – that can act as “sponges” to sequester miR‑152, thereby further modulating oncogenic signals. miR‑152 is also responsive to upstream signaling (for example, following TLR3 activation) that modulate epigenetic programs, and its deregulation has been linked to context‑dependent effects on metastasis, chemoresistance and even cell proliferation in prostate and bladder cancers."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nClinically, aberrant miR‑152 expression – often as a consequence of promoter hypermethylation – has been associated with adverse features such as chemoresistance, enhanced metastatic potential and poor prognosis, suggesting its promise as both a therapeutic target and a non‑invasive biomarker. Circulating levels and the methylation status of miR‑152 regulatory regions have been explored for early cancer detection in several tumor types, while modulation of its expression has been shown to resensitize cancer cells to drugs like cisplatin and to re‐establish normal cellular functions. These findings, spanning diverse contexts from preeclampsia to osteosarcoma and prostate to bladder cancers, collectively support the clinical relevance of miR‑152 in disease management."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "34"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jinfeng Huang, Yue Wang, Yingjun Guo, et al. 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