{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n FAM83A‐AS1 is an oncogenic long noncoding RNA that contributes to tumor progression in multiple cancer types—including lung adenocarcinoma, non‐small cell lung cancer, hepatocellular carcinoma, and esophageal cancer—through dual mechanisms. On one hand, FAM83A‐AS1 functions as a competing endogenous RNA by “sponging” specific microRNAs such as"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "(miR‑150‑5p)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "(miR‑141‑3p), and"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": "(miR‑495‑3p). This sequestration relieves repression on target oncogenes such as matrix metalloproteinase 14 (MMP14) and FAM83A itself, thereby promoting cell proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT)."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n On the other hand, FAM83A‐AS1 enhances the stability of FAM83A mRNA through direct post‐transcriptional mechanisms. In hepatocellular carcinoma, for example, FAM83A‐AS1 binds to the RNA‐binding protein NOP58 to increase FAM83A mRNA stability"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": ", while in non‐small cell lung cancer it forms an RNA duplex and interacts with FBL to similarly stabilize FAM83A pre‐mRNA, resulting in activation of downstream ERK signaling pathways."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In esophageal cancer, upregulation of FAM83A‐AS1 is associated with enhanced migratory potential through its negative regulation of miR‑495‑3p."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": " Across multiple studies, the overexpression of FAM83A‐AS1 has also been incorporated into prognostic lncRNA signatures that correlate with poor overall survival and advanced clinical stage in lung cancers and other malignancies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "13"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these findings indicate that FAM83A‐AS1 serves as a critical regulator of oncogene expression—both by acting as a decoy for tumor‐suppressive microRNAs and by stabilizing FAM83A mRNA—thereby driving aggressive tumor behaviors and offering a promising target for therapeutic intervention.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Guodong Xiao, Peili Wang, Xiaoqiang Zheng, et al. 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