{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRecent studies have demonstrated that the long non‐coding RNA SNHG16 is frequently overexpressed in a wide spectrum of malignancies—including colorectal, gastric, cervical, bladder, breast, glioma, hepatocellular, lung, ovarian, diffuse large B‐cell lymphoma, osteosarcoma and neuroblastoma—as well as in various inflammatory and other pathological conditions. Elevated SNHG16 levels have been associated with advanced tumor stage, enhanced cell proliferation, migration, invasion, impaired apoptosis and poor clinical prognosis, which underscores its potential value as a prognostic biomarker and therapeutic target in cancer management."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, SNHG16 exerts its oncogenic influence primarily by acting as a competing endogenous RNA (ceRNA), directly interacting with—and sequestering—a variety of tumor‐suppressive microRNAs (for example, miR‑16‑5p, miR‑98, miR‑216‑5p, miR‑4500, let‑7b‑5p, miR‑30a, miR‑17‑5p and others). This “sponging” activity relieves repression of crucial downstream effectors such as SMAD5, E2F5, PIM1, CDC25B, TIMP3, FGF19, and RRM2, thereby promoting cell cycle progression, epithelial–mesenchymal transition (EMT), invasion and migration. These molecular events have been documented in several cancer models including non–small‐cell lung cancer, glioma, osteosarcoma and diffuse large B‐cell lymphoma, highlighting a central role for the SNHG16‐mediated regulatory network in tumorigenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in cancer cell intrinsic processes, SNHG16 also contributes to other pathogenic mechanisms such as therapeutic resistance, immune modulation and intercellular signaling. For instance, SNHG16 has been implicated in conferring sorafenib resistance in hepatocellular carcinoma, modulating CD73 expression to promote immunosuppressive phenotypes in specific T‐cell subsets, and even influencing vascular smooth muscle cell proliferation in atherosclerosis. Its presence in tumor‐derived exosomes further suggests a role in remodeling the tumor microenvironment and facilitating metastasis. Collectively, these findings reveal SNHG16 as a multifaceted regulator whose ceRNA‐mediated interplay with specific microRNAs and target genes underpins diverse cellular functions and positions it as an attractive candidate for both diagnostic and therapeutic strategies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "30", "end_ref": "46"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Lise Lotte Christensen, Kirsten True, Mark P Hamilton, et al. 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