{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR-539 has emerged as a potent tumor‐suppressive microRNA in a broad spectrum of cancers. In thyroid, osteosarcoma, hepatocellular, breast, nasopharyngeal, prostate, pancreatic, colorectal, renal, Wilms’ tumor, epithelial ovarian cancer, B‐cell acute lymphoblastic leukemia, and even in melanoma models, miR-539 is frequently downregulated, and its reduced expression correlates with increased cell proliferation, migration, invasion, epithelial–mesenchymal transition, and overall tumor progression. Mechanistic studies have shown that miR-539 exerts its suppressive functions by directly targeting key oncogenic regulators – for example, modulating molecules including CARMA1 in thyroid cancer; MMP8 in osteosarcoma; FSCN1 and MAP2K1 in hepatocellular carcinoma; EGFR and SP1 in breast cancer; CDK4 in nasopharyngeal carcinoma; TWIST1, SP1, or IGF-1R in pancreatic cancer; DLX1 in prostate cancer; CDK6 and SOX5 in colorectal and gastric cancers; and HMGA2 in renal cell carcinoma. Furthermore, in several settings, long noncoding RNAs such as LOC100129148, CASC21, TP73-AS1, and others have been found to sponge miR-539, thereby releasing its targets and promoting oncogenic pathways."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "22"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its critical role in cancer, miR-539 participates in several non-malignant cellular processes. In cardiomyocytes, for example, miR-539 targets the mRNA of O-GlcNAcase (OGA), thereby modulating O-GlcNAcylation dynamics that are implicated in heart failure. In ocular tissues, its overexpression has been shown to inhibit experimental choroidal neovascularization through downregulation of CXCR7, while in colon cells, miR-539 attenuates iron influx by targeting the iron-ion transporter SLC11A2. miR-539 also regulates biotin metabolism by suppressing holocarboxylase synthetase (HCS) expression, and in the context of Alzheimer’s disease, enhanced miR-539 levels exert neuroprotective effects by directly targeting APP, caveolin-1, and GSK-3β – thereby reducing amyloid-β accumulation, tau phosphorylation, oxidative stress, and neuronal apoptosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "23", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, these studies underscore that miR-539 is a multifaceted regulatory RNA whose downregulation is frequently associated with the progression of diverse malignancies—through loss of repression of pivotal oncogenes and cell cycle regulators—while its appropriate expression is fundamental for maintaining normal cellular functions in metabolic, vascular, and neurodegenerative contexts. The diverse molecular interactions of miR-539 not only highlight its potential as a diagnostic and prognostic biomarker across diseases but also point to novel therapeutic avenues to restore its function in pathological states.\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Lixue Gu, Weiming Sun "}, {"type": "b", "children": [{"type": "t", "text": "MiR-539 inhibits thyroid cancer cell migration and invasion by directly targeting CARMA1."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biochem Biophys Res Commun (2015)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.bbrc.2015.07.090"}], "href": "https://doi.org/10.1016/j.bbrc.2015.07.090"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "26206083"}], "href": "https://pubmed.ncbi.nlm.nih.gov/26206083"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Y Wang, Z Ou, Y Sun, et al. 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