{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Long noncoding RNA DDX11‐AS1 has emerged as a multifunctional regulator with critical roles in both normal cell cycle processes and tumorigenesis. In non‐transformed cells, DDX11‐AS1 was originally shown to be required for proper sister chromatid cohesion and DNA replication through direct modulation of the helicase activity of DDX11 (see."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In numerous cancer types—including hepatocellular carcinoma, gastric cancer, colorectal cancer, osteosarcoma, esophageal cancer, bladder cancer, breast cancer, and non–small cell lung cancer—DDX11‐AS1 is frequently upregulated and correlates with poor clinical outcomes (see"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "2", "end_ref": "8"}]}, {"type": "t", "text": ", and."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Mechanistically, DDX11‐AS1 exerts its oncogenic functions primarily by serving as a competing endogenous RNA (ceRNA) that sponges various microRNAs. By sequestering miR‐873–5p, miR‐326, miR‐30d–5p, miR‐499b–5p, miR‐497, miR‐195–5p, miR‐34a–3p, and miR‐514b–3p (refer to"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "4", "end_ref": "7"}, {"type": "fg_fs", "start_ref": "10", "end_ref": "12"}]}, {"type": "t", "text": ", and"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": ", it derepresses several key oncogenes. These include targets such as DDX11, LATS2, SPC18/SEC11A, IRS1, CDK6, SNAI1, ZEB2, MACC1, TRAF5, and TOP2A, which in turn stimulate cell proliferation, promote cell cycle progression, enhance migration and invasion, induce epithelial–mesenchymal transition, and even contribute to chemoresistance (see"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}, {"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": ", and."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Beyond its ceRNA functions, DDX11‐AS1 also interacts with chromatin modifiers and transcriptional regulators such as EZH2, DNMT1, PARP1, and TAF1. These interactions add an additional epigenetic layer to its regulation of gene expression, further contributing to oncogenic signaling pathways such as PI3K/AKT and Wnt/β‐catenin (see"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}, {"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": ", and."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these findings underscore the multifunctional and oncogenic nature of DDX11‐AS1. Its ability to modulate critical cellular processes—ranging from DNA replication and chromatid cohesion to the regulation of multiple oncogenic pathways via microRNA sponging and epigenetic interactions—positions DDX11‐AS1 as a promising prognostic biomarker and a potential therapeutic target across a wide spectrum of human cancers (see"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "19"}]}, {"type": "t", "text": ", and."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": "\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Francesco P Marchese, Elena Grossi, Oskar Marín-Béjar, et al. 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