{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe long noncoding RNA ZEB1‐AS1, which is transcribed from the promoter region of the ZEB1 gene, is emerging as a critical oncogenic regulator across a broad spectrum of human malignancies. Studies have demonstrated that its expression is markedly upregulated in cancers such as glioma, osteosarcoma, bladder, colorectal, esophageal, hepatocellular, gastric, pancreatic, prostate, melanoma, lung cancer, and even in hematological malignancies like B‐lineage acute lymphoblastic leukemia. In many of these studies, high ZEB1‐AS1 levels correlate with advanced clinical stage, enhanced metastasis, and poor overall prognosis, suggesting that this lncRNA plays a key role in disease progression and may function as a prognostic biomarker."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistic investigations have revealed that ZEB1‐AS1 exerts its oncogenic functions by regulating gene expression at multiple levels. Functioning as a competitive endogenous RNA (ceRNA), it “sponges” a variety of tumor‐suppressive microRNAs (for example, members of the miR‐200 family, miR‐181a‐5p, miR‐342‐3p, miR‐505, miR‐299‐3p, miR‐23c, among others), thereby de‐repressing key targets such as ZEB1, TRIB2, CUL4B, and E2F1. In addition, ZEB1‐AS1 can interact with RNA‐binding proteins like ELAVL1, AUF1, and STAT3 to enhance mRNA stability, establishing positive feedback loops that further increase ZEB1 expression. Through these interactions, the lncRNA promotes epithelial‐to‐mesenchymal transition (EMT) and activates oncogenic signaling cascades—including the PI3K/AKT/mTOR and TGF‐β/Smad pathways—that drive cell cycle progression, invasion, and metastasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, these studies underscore that deregulation of ZEB1‐AS1 contributes to tumorigenesis—not only by enhancing proliferation, migration, invasion, and chemoresistance but also by modulating key processes such as apoptosis and ferroptosis. Moreover, its aberrant expression in select nonmalignant conditions (e.g., atherosclerosis) and even in certain neurodegenerative contexts further highlights the multifaceted role of ZEB1‐AS1 in disease pathogenesis. As such, ZEB1‐AS1 represents a promising prognostic biomarker and an attractive therapeutic target, warranting further investigation into its potential for clinical intervention.\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Qiao-Li Lv, Lei Hu, Shu-Hui Chen, et al. 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