{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nA substantial body of research has demonstrated that the long noncoding RNA SOX2‐OT functions as a critical oncogenic regulator in a wide spectrum of cancers. In numerous studies, SOX2‐OT is overexpressed in malignant tissues—including pancreatic, lung (both non–small cell and squamous cell carcinomas), breast (including triple‐negative subtypes), esophageal, gastric, hepatocellular, osteosarcoma, nasopharyngeal, laryngeal, cervical, and papillary thyroid cancers—and is frequently co‐expressed with its embedded gene SOX2. In these contexts, SOX2‐OT promotes tumor initiation, cell proliferation, epithelial–mesenchymal transition, metastasis, and chemoresistance. Its molecular mechanisms often involve acting as a competing endogenous RNA to sponge multiple microRNAs (for example, members of the miR‐200 family, miR‐194‐5p, miR‐942‐5p, miR‐146b‐5p, miR‐627‐3p, miR‐192‐5p, among others), recruiting chromatin modifiers such as EZH2, and interacting with regulatory proteins including FUS and ALKBH5 to stabilize transcripts. In addition, diverse splice variants of SOX2‐OT have been identified, emphasizing its role in maintaining cancer stem cell properties while participating in exosome‐mediated intercellular signaling that modulates the tumor microenvironment and drug responses via pathways such as Wnt/β‐catenin, PI3K/AKT, and ERK."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its central role in cancer biology, SOX2‐OT is increasingly recognized as a multifaceted regulator in non‐tumor pathologies. Altered expression of SOX2‐OT has been linked to neurodegenerative disorders such as Parkinson’s disease, while in diabetic nephropathy, its dysregulation is associated with enhanced oxidative stress and apoptosis in renal cells. In cardiovascular contexts, aberrant SOX2‐OT expression contributes to myocardial injury—such as that induced by lipopolysaccharide exposure—and has been implicated in the pathogenesis of myocardial infarction. Furthermore, by modulating Schwann cell proliferation and migration, SOX2‐OT facilitates peripheral nerve regeneration, and its upregulation correlates with fibrotic processes observed in idiopathic pulmonary fibrosis. Collectively, these studies suggest that SOX2‐OT not only drives malignant transformation and tumor progression but also orchestrates diverse cellular responses during tissue injury and repair, underscoring its potential as a biomarker and therapeutic target across a broad range of diseases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Zhonghu Li, Peng Jiang, Jie Li, et al. 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