{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSmall nucleolar RNA host gene 17 (SNHG17) is emerging as a multifunctional long noncoding RNA with potent oncogenic properties in a wide array of human malignancies. Numerous studies have shown that SNHG17 is significantly upregulated in cancers such as colorectal cancer, gastric cancer, melanoma, tongue squamous cell carcinoma, astrocytoma, oral squamous cell carcinoma, ovarian, lung, hepatocellular, esophageal, prostate, and osteosarcoma. Its high expression is closely correlated with advanced tumor stage, deep invasion, lymphatic metastasis, poor differentiation, and unfavorable overall survival. Functionally, SNHG17 promotes cell proliferation, accelerates cell cycle progression, enhances invasion and migration, and drives epithelial‐to‐mesenchymal transition – all of which contribute to tumor growth and metastasis. In many of these studies, SNHG17 has also demonstrated potential diagnostic value by virtue of its altered expression pattern in patient tissues and even plasma samples."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, SNHG17 exerts its oncogenic functions via multiple mechanisms. It interacts with chromatin‐modifying complexes—most notably the polycomb repressive complex 2—to epigenetically silence tumor‐suppressor genes such as cyclin‐dependent kinase inhibitors. In addition, SNHG17 stabilizes oncogenic proteins (for example, c-Myc through binding partners like LRPPRC) and functions as a competing endogenous RNA (ceRNA), sponging microRNAs (including miR‑876, miR‑338‑3p, and members of the miR‑23 family) to upregulate key targets such as SP1, SOX4, OTUB1, and factors involved in DNA repair like Rad51. These interactions not only favor cell cycle progression and tumor proliferation but also redirect DNA repair pathways—shifting the balance from high-fidelity homologous recombination to error-prone nonhomologous end joining—and have been implicated in chemoresistance and radiation-induced epithelial–mesenchymal transition. Moreover, emerging evidence indicates that SNHG17 modulates the tumor microenvironment; for example, by influencing macrophage polarization through exosome-mediated transfer, it contributes to immune evasion processes. Complementing its tumor-promoting roles, SNHG17 exhibits context-dependent functions as exemplified by its downregulation in type 2 diabetes mellitus, where altered expression is correlated with metabolic disturbances."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Zhonghua Ma, Shengying Gu, Min Song, et al. 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