{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSmall nucleolar RNA host gene 7 (SNHG7) is emerging as a multifunctional long non‐coding RNA with potent oncogenic properties in a wide spectrum of human cancers. Numerous studies have reported its upregulation in colorectal, lung, gastric, prostate, esophageal, glioblastoma, breast, thyroid, hepatocellular, bladder, cervical, nasopharyngeal, and ovarian tumors. In these malignancies, SNHG7 promotes cell proliferation, migration, invasion, epithelial–mesenchymal transition, and metastasis while its elevated expression is consistently correlated with high tumor grade, advanced stage, and poor prognosis. Mechanistically, SNHG7 exerts its tumor‐promoting effects by functioning as a molecular sponge to sequester tumor‐suppressive microRNAs – including miR‑216b, miR‑34a, miR‑5095, miR‑503, miR‑122‑5p, miR‑9‑5p, miR‑323a‑5p, and miR‑342‑5p – thereby releasing key oncogenes and activating downstream pathways such as Wnt/β‑catenin, cell cycle regulators (e.g., Cyclin D1, CDK4/6), and EMT mediators."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its well‐documented oncogenic roles, SNHG7 also contributes to therapy resistance and metabolic reprogramming in cancer cells. For example, in gastric and ovarian cancers, SNHG7 overexpression has been linked to resistance against cisplatin and paclitaxel, respectively, by modulating glycolytic enzymes and autophagic as well as cell cycle regulators through various microRNA‐mediated axes. In prostate cancer, emerging evidence suggests that SNHG7 may also impact tumor metabolism, thereby influencing drug responsiveness. Furthermore, meta‐analyses have corroborated its prognostic significance across multiple tumor types, reinforcing its potential as both a therapeutic target and a prognostic biomarker."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nSNHG7 functions are not limited to oncogenesis. Its dysregulation has been implicated in several non‐malignant and chronic conditions. In diabetic retinopathy, for instance, SNHG7 overexpression modulates high glucose‑induced angiogenesis by targeting microRNAs that regulate SIRT1/VEGF signaling. In vascular smooth muscle cells, SNHG7 exerts protective effects against oxidized LDL‑induced proliferation and migration via a miR‑mediated SIRT7 axis, highlighting its involvement in atherosclerosis. Moreover, SNHG7 is part of regulatory networks in polycystic ovary syndrome via interactions with miR‑21, in bone marrow‑derived mesenchymal stem cell proliferation through interplay with other lncRNAs, and even in neurodegenerative contexts such as Parkinson’s disease by modulating inflammation and oxidative stress. In neonatal sepsis, elevated serum SNHG7 levels have been correlated with increased inflammatory markers and poorer clinical outcomes, suggesting its utility as a diagnostic and prognostic biomarker in critical care."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "27", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, the body of research indicates that SNHG7 acts as a central regulator in both cancer and non‐cancer pathologies by modulating critical cellular processes—through acting as a competitive endogenous RNA, altering the expression and stability of downstream effectors, and interfacing with key signaling pathways. Its versatile roles in promoting tumor growth, mediating chemoresistance, and influencing inflammatory responses underscore its promise as a novel diagnostic biomarker and therapeutic target across a diverse array of human diseases."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "36"}, {"type": "fg_f", "ref": "12"}, {"type": "fg_f", "ref": "17"}, {"type": "fg_f", "ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Kelin She, Jun Huang, Huaping Zhou, et al. 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