{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRecent evidence has revealed that the long non‐coding RNA SNHG20 functions as a potent oncogenic regulator across a diverse range of human malignancies. In a comprehensive overview, SNHG20 has been implicated in tumor progression and poor patient prognosis, underscoring its potential as both a diagnostic marker and therapeutic target."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn cancers of the respiratory system, SNHG20 is markedly up‐regulated in non‐small cell lung cancer and lung adenocarcinoma. Mechanistic studies indicate that SNHG20 can modulate cell cycle regulators—for example, by cooperating with epigenetic modifiers to repress p21—and act as a competing endogenous RNA to sequester specific microRNAs. Such molecular actions have been reported via analyses in NSCLC cell models, where SNHG20 sponges miRNAs (for instance, affecting the miR‐2467/E2F3 axis), thereby contributing to enhanced proliferation, migration, and invasion."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "2", "end_ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nWithin the gastrointestinal and hepatic realm, SNHG20 has been shown to be significantly overexpressed in colorectal cancer, where its high levels correlate with aggressive tumor features and metastasis. In gastric cancer, SNHG20 promotes tumor growth by regulating key signaling axes. Moreover, in hepatocellular carcinoma—in both HBV‐related contexts and in nonalcoholic fatty liver disease progressing to HCC—SNHG20 deregulation (including reports of altered expression patterns) contributes to tumor cell proliferation and disease progression. Additional studies in cholangiocarcinoma have further implicated SNHG20 in accelerating malignant behavior by acting as a molecular sponge."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nSNHG20 also plays critical roles in gynecologic and head and neck cancers. In ovarian cancer, studies have documented elevated SNHG20 expression in both serous ovarian carcinoma and epithelial ovarian cancer, where it promotes cell proliferation, migration, and invasion via distinct mechanisms including activation of Wnt/β‐catenin signaling and modulation of the miR‐148a/ROCK1 axis. Similarly, the progression of cervical cancer has been linked to SNHG20 dysregulation. In oral and laryngeal squamous cell carcinomas, SNHG20 enhances tumorigenesis by influencing cancer stem cell properties and epithelial–mesenchymal transition via several ceRNA axes (for example, involving miR‐197/LIN28 and miR‐19b-3p/RAB14)."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "22"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its roles in the aforementioned solid tumors, SNHG20 has been implicated in neoplasms of bone and the nervous system. In osteosarcoma, SNHG20 up‐regulation promotes tumorigenesis by modulating the miR‐139/RUNX2 axis and perturbing mitochondrial apoptotic pathways. Similarly, in glioma, its aberrant expression contributes to cellular proliferation and resistance to apoptosis. In retinoblastoma, SNHG20 enhances oncogenic behaviors via regulation of the miR‐335-5p/E2F3 axis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "23", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jiling Zeng, Zhuoyi Liu, Chao Zhang, et al. 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