{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSBF2‐AS1 is an oncogenic long non‐coding RNA that is aberrantly expressed in a wide range of cancers, including non‐small cell lung cancer, hepatocellular carcinoma, colorectal cancer, cervical cancer, glioblastoma, and others. In these tumors, increased SBF2‐AS1 levels correlate with advanced clinical stages, larger tumor sizes, lymph node metastasis, and poor patient prognosis. For example, in glioblastoma SBF2‐AS1 carried in exosomes enhances temozolomide resistance, whereas in colorectal and cervical cancers its overexpression is linked to aggressive tumor behavior and reduced survival rates."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, SBF2‐AS1 acts predominantly as a competing endogenous RNA (ceRNA) to sponge various tumor suppressor microRNAs and thereby upregulate oncogenic targets. In acute myeloid leukemia, it sequesters miR‑188‑5p to elevate ZFP91 expression; in hepatocellular carcinoma and cervical cancer, it binds miR‑140‑5p and miR‑361‑5p, respectively, leading to dysregulation of TGF‑β signaling and FOXM1 expression; and in non‐small cell lung cancer, transcriptional activation by E2F1 elevates SBF2‐AS1 levels that in turn sponge miR‑362‑3p to increase GRB2 expression. In pancreatic cancer, exosomes derived from M2 macrophages deliver SBF2‐AS1 to modulate the miR‑122‑5p/XIAP axis, emphasizing its role in intercellular communication and drug resistance. These studies underline SBF2‐AS1’s central role in various oncogenic signaling pathways."}, {"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": "\nClinically, targeting SBF2‐AS1 offers promise both as a therapeutic strategy and a prognostic biomarker. Its knockdown has been shown to inhibit cell proliferation, migration, invasion, and epithelial–mesenchymal transition in several tumor models, including hepatocellular carcinoma, serous ovarian carcinoma, and gastric cancer, partly through downregulating pathways such as TGF‑β, Wnt/LRP5, and ETS1 signaling. Collectively, these findings highlight that modulation of SBF2‐AS1 or its downstream effectors could improve treatment efficacy and overcome drug resistance in various malignancies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Junjie Lv, Mantang Qiu, Wenjia Xia, et al. 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