{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n MAGI2‐AS3 is a long noncoding RNA whose dysregulation has been implicated in a broad spectrum of human diseases, particularly in various cancers where it exerts context‐dependent functions. In several solid tumors—including breast cancer, non‐small cell lung cancer (NSCLC), glioma, clear cell renal cell carcinoma, bladder cancer, hepatocellular carcinoma, and ovarian cancer—MAGI2‐AS3 is frequently downregulated, and its restoration often suppresses cell proliferation, migration, invasion, and angiogenesis while promoting apoptosis. Its tumor‐suppressive functions are generally mediated by acting as a competing endogenous RNA (ceRNA) that “sponges” oncogenic microRNAs (miRNAs) such as miR‐374a/miR‐374b, miR‐23a‐3p, miR‐15b‐5p, miR‐25, miR‐525‐5p, and others, thereby upregulating key tumor‐suppressor targets including Fas/FasL, PTEN, RECK, SMG1, CCDC19, TNS1, MXD1, and ACY1"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": ", and."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": " In contrast, in certain malignancies such as colorectal cancer, pancreatic cancer, nasopharyngeal carcinoma, and a subset of gastric cancers, MAGI2‐AS3 has been reported to be overexpressed and to promote tumor progression and chemoresistance—for instance, by modulating the miR‐3163/TMEM106B axis or interacting with miR‐490‐5p and miR‐218‐5p to regulate downstream targets that drive proliferation and survival"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "14"}]}, {"type": "t", "text": ", and."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": " Beyond cancer, altered MAGI2‐AS3 expression has been observed in other pathological conditions: in intervertebral disc degeneration, its downregulation leads to increased Fas ligand expression in nucleus pulposus cells"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": "; in Alzheimer’s disease models, MAGI2‐AS3 modulates neurotoxicity and neuroinflammation via a miR‐374b‐5p/BACE1 axis"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "18"}]}, {"type": "t", "text": "; and genetic variation affecting its transcriptional regulation has been linked to nicotine dependence and colon adenocarcinoma progression"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "19"}]}, {"type": "t", "text": "and."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "20"}]}, {"type": "t", "text": " Furthermore, in acute myeloid leukemia, MAGI2‐AS3 appears to influence leukemic stem cell self‐renewal"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "21"}]}, {"type": "t", "text": ", and it has been implicated in the regulation of cisplatin resistance in nasopharyngeal carcinoma as well as in mediating epithelial–mesenchymal transition in gastric cancer"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "22"}]}, {"type": "t", "text": "and."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "23"}]}, {"type": "t", "text": " Intriguingly, emerging evidence also supports a regulatory role for MAGI2‐AS3 in developmental contexts, such as in diaphragm formation in congenital diaphragmatic hernia."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "24"}]}, {"type": "t", "text": " Collectively, these studies underscore that MAGI2‐AS3 exhibits multifaceted, context‐dependent roles—principally through ceRNA mechanisms and modulation of epigenetic states or promoter methylation—that can either impede or promote disease progression. Its differential expression and involvement in key signaling pathways render MAGI2‐AS3 a promising diagnostic biomarker and a potential therapeutic target across a range of human malignancies and other disorders"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "25"}]}, {"type": "t", "text": "and."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "26"}]}, {"type": "t", "text": "\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yong Yang, Hong Yang, Miao Xu, et al. 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