{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nLong non‐coding RNA SNHG4 has emerged as a multifaceted regulator in human diseases with diverse expression patterns and functions. In some hematologic and skeletal malignancies, such as myelodysplastic syndromes and osteosarcoma, as well as in certain prostate and liver cancers, SNHG4 dysregulation has been observed, although its precise molecular mechanisms remain to be fully elucidated (see."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn numerous solid tumors, SNHG4 predominantly acts as a competing endogenous RNA (ceRNA) that sponges specific microRNAs, thereby modulating the expression of critical downstream targets and contributing to tumorigenesis. For instance, in non‐small cell lung cancer SNHG4 silencing induces G1 arrest and suppresses epithelial–mesenchymal transition, an effect mediated by the upregulation of miR‑98‑5p and subsequent inhibition of cell proliferation and invasion."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": " In acute myeloid leukemia, lower SNHG4 levels relieve its interaction with miR‑10a, resulting in enhanced PTEN expression and reduced proliferation"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": ", while in glioblastoma, elevated SNHG4 sequesters miR‑138 to upregulate c‑Met and promote cellular proliferation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " Similar ceRNA mechanisms have been documented in endometriosis"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": ", neuroblastoma"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": ", and gastric cancer"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": ", as well as in papillary thyroid cancer where SNHG4 modulates the miR‑25/FBXW7 axis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": " Moreover, in nasopharyngeal carcinoma, SNHG4 facilitates tumor progression via the miR‑510‑5p/CENPF pathway, and in colorectal cancer its oncogenic role extends to modulating ferroptosis and chemoresistance by impacting PTEN stability and regulating the c‑Myb/GPX4 and CDO1 axes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "15"}]}, {"type": "t", "text": " Additionally, studies in non‐small cell lung cancer also suggest SNHG4’s potential as a diagnostic and prognostic marker."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in cancer, SNHG4 influences inflammatory and cell injury processes in various pathological states. In the central nervous system, SNHG4 modulates microglial activation during cerebral ischemia–reperfusion injury and in models of neonatal pneumonia."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": " In diabetic retinopathy, SNHG4 downregulation leads to increased miR‑200b activity and cell apoptosis, whereas its overexpression upregulates oxidation resistance 1 (Oxr1), thus protecting retinal pigment epithelial cells."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "19"}]}, {"type": "t", "text": " In chronic obstructive pulmonary disease, SNHG4, via the miR‑144‑3p/EZH2 axis, exhibits potential diagnostic value"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "20"}]}, {"type": "t", "text": ", and in endometriosis abnormal SNHG4 expression may serve as both a biomarker and therapeutic target."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "21"}]}, {"type": "t", "text": " Notably, a novel splice variant of SNHG4—designated Snhg4‑pod—has been identified as a selective marker of podocyte injury in glomerular diseases"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "22"}]}, {"type": "t", "text": ", and emerging evidence also hints at its involvement in mechanisms underlying prostate cancer chemoresistance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Timothy A Graubert, Michelle A Payton, Jin Shao, et al. 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