{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n DBH‐AS1 is a long noncoding RNA that has emerged as an important regulator in cancer, yet its functions vary in a context‐dependent manner. In hepatocellular carcinoma (HCC), DBH‐AS1 is upregulated by the hepatitis B virus X protein and promotes oncogenesis by enhancing cell cycle progression, proliferation, and survival through activation of the MAPK signaling pathway and by modulating key cell cycle regulators (e.g. upregulating CDK6, CCND1, CCNE1 and downregulating p16, p21, and p27) while inhibiting apoptosis (also influenced by p53 suppression)."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In addition to these mechanisms, DBH‐AS1 can act as a competing endogenous RNA; for instance, in HCC it sponges miR‐138 to activate the FAK/Src/ERK cascade, thereby further enhancing tumor cell proliferation and survival. Outside of liver cancer, overexpression of DBH‐AS1 has been observed in osteosarcoma and diffuse large B‐cell lymphoma, where it promotes tumorigenesis by engaging distinct signaling pathways. In osteosarcoma, DBH‐AS1 facilitates cell proliferation, migration, and invasion via activation of the PI3K/Akt pathway"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ", whereas in lymphoma it recruits the RNA‐binding protein BUD13 to stabilize FN1 mRNA, contributing to tumor progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In melanoma, although DBH‐AS1 levels are reduced overall, its modulation affects glycolytic activity and tumor cell aggressiveness via the miR‐223‐3p/IGF‐1R/AKT axis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": " Conversely, in non‐small cell lung cancer, down-regulation of DBH‐AS1 is associated with increased cell proliferation through its function as a sponge for miR‐155 that leads to upregulation of AXIN1 and influences WNT/β‐CATENIN signaling."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Moreover, in pancreatic cancer, reduced expression of DBH‐AS1 has been linked to enhanced malignancy and gemcitabine resistance, indicating its potential as a prognostic biomarker and therapeutic target."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": " Finally, DBH‐AS1 has been incorporated into multi‐lncRNA signatures that confer prognostic value in colorectal cancer, further underscoring its potential utility as a biomarker in diverse tumor types."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these studies indicate that DBH‐AS1 exerts oncogenic or tumor-suppressive effects in a tissue-specific manner by interacting with microRNAs, RNA-binding proteins, and key signaling pathways. The context-dependent role of DBH‐AS1 highlights its potential as both a biomarker for cancer prognosis and a promising target for therapeutic intervention.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jin-lan Huang, Ting-yu Ren, Shun-wang Cao, et al. 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