{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n HNF1A‐AS1 is a long noncoding RNA that appears to be frequently dysregulated in various human cancers and exerts context‐dependent functions in tumor biology. In several tumor types – including esophageal adenocarcinoma, gastric cancer, lung adenocarcinoma, gastric cancer, colorectal cancer, bladder cancer, non‐small cell lung cancer (NSCLC), hepatocellular carcinoma (HCC) and glioma – HNF1A‐AS1 is reported to be upregulated and to promote oncogenic processes such as cell proliferation, cell cycle progression, migration, invasion, metastasis, angiogenesis and chemoresistance by acting as a competing endogenous RNA (ceRNA) or “sponge” for specific microRNAs. For example, HNF1A‐AS1 sponges miR‐661 to modulate chromatin/nucleosome assembly and induce H19 expression in esophageal adenocarcinoma"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ", and it functions as a ceRNA for miR‐661, miR‐17‐5p, miR‐30b–3p, miR‐149–5p, miR‐363–3p or related miRNAs to activate cell cycle regulators such as CDC34, cyclin/CDK complexes, or to modulate key signaling pathways including the Wnt/β‐catenin, Notch and PI3K/AKT cascades in gastric cancer, lung adenocarcinoma and NSCLC."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "2", "end_ref": "5"}]}, {"type": "t", "text": " In other studies, HNF1A‐AS1 was found to interact with epigenetic modifiers such as EZH2 and SHP‐1 thereby influencing histone modifications and transcriptional programs that regulate both cell cycle and epithelial–mesenchymal transition—for instance, by repressing inhibitors such as p21 or NKD1 in HCC"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": "and by enhancing Notch signaling in oral squamous cell carcinoma."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Moreover, in colorectal and bladder cancers as well as in glioma, elevated HNF1A‐AS1 expression is correlated with aggressive clinicopathological features and poorer prognoses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "10"}]}, {"type": "t", "text": " In contrast, in laryngeal squamous cell carcinoma, epigenetic hypermethylation leads to HNF1A‐AS1 downregulation, where it appears to act as a tumor suppressor by inhibiting epithelial–mesenchymal transition."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": " Additionally, studies in colon cancer have revealed roles for HNF1A‐AS1 in promoting angiogenesis via a ceRNA mechanism involving transcriptional regulation"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": "and in another colon cancer report, HNF1A‐AS1 was associated with enhanced proliferation and metastatic potential."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": " Finally, in the context of breast cancer, HNF1A‐AS1 has been implicated in tamoxifen resistance through its modulation of microRNA‐mediated gene expression"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": ", and in glioma, it promotes tumor growth by sponging miR‐32–5p to upregulate targets such as SOX4."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, the available evidence suggests that HNF1A‐AS1 primarily acts as an oncogenic factor by regulating key cell cycle, survival, and metastatic pathways in a tissue‐dependent manner. Its capability to interact with microRNAs and epigenetic regulators, and its correlation with advanced tumor stage and poor patient survival, make HNF1A‐AS1 a promising candidate as both a prognostic biomarker and a therapeutic target in multiple cancer types.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Xue Yang, Jee Hoon Song, Yulan Cheng, et al. 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