{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nLong non‐coding RNA SNHG1 has emerged as a multifaceted regulator in human cancers. It is frequently overexpressed in tumor tissues—including colorectal, lung, hepatocellular, prostate, nasopharyngeal, glioma, osteosarcoma, renal, neuroblastoma, and breast cancers—with high SNHG1 levels correlating with larger tumors, advanced stages, enhanced metastasis, drug resistance, and poor prognosis. Functionally, SNHG1 promotes cell proliferation, cell cycle progression, migration, invasion, epithelial–mesenchymal transition, and even assists in immune escape. Mechanistically, it acts predominantly as a competing endogenous RNA (ceRNA) by sponging tumor‐suppressive microRNAs (such as miR‐101‑3p, miR‐145‑5p, miR‑199a‑3p, miR‑15b‑5p, miR‑326, and others), thereby de‐repressing oncogenic targets—including SOX9, MTDH, CDK7, PDCD4, WNT2B, MYC, and additional cell cycle regulators—and modulating key pathways such as p53 signaling, Wnt/β‑catenin, and PI3K/AKT. These diverse molecular interactions underscore its promise as a prognostic biomarker and therapeutic target in oncology."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "41"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its oncogenic functions, SNHG1 participates in several non‐malignant pathologies. In neuronal models of Parkinson’s and Alzheimer’s diseases, modulation of SNHG1 influences α‑synuclein aggregation, apoptosis, and related neurotoxic outcomes. Similarly, in musculoskeletal disorders such as intervertebral disc degeneration and osteoarthritis, SNHG1 affects extracellular matrix metabolism and inflammatory cytokine expression, thereby contributing to tissue degeneration. SNHG1 also plays roles in bone biology by attenuating osteogenic differentiation in mesenchymal and periodontal ligament stem cells, a mechanism relevant to osteoporosis, and it contributes to cardiac regeneration by engaging in a positive feedback loop with c‑Myc to activate the PI3K/AKT pathway and promote cardiomyocyte proliferation. These findings highlight the diverse regulatory capacity of SNHG1 in modulating cell survival, differentiation, and reparative processes in non‐cancer disorders."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "42", "end_ref": "48"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "J You, N Fang, J Gu, et al. 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