LncRNA <i>GATA3-AS1</i> Promotes Bladder Uroepithelial Cancer Progression by Stabilizing DDX5

<b>Objective:</b> Exploration of molecular markers is an ongoing focus in the field of bladder cancer research. Based on data from public databases, <i>GATA3-AS1</i> was identified as upregulated in bladder urothelial carcinoma (BLCA); however, its exact function and regulatory mechanism in this context remain unclear. <b>Methods:</b> To investigate the clinical implications of <i>GATA3-AS1</i>, we examined its levels in 90 BLCA and adjoining normal tissue samples. Functional assays were conducted to assess the effects of <i>GATA3-AS1</i> on BLCA cell proliferation, migration, and invasion. Animal assays were employed to determine the effects of <i>GATA3-AS1</i> on BLCA tumorigenicity <i>in vivo</i>. Immunoblotting, RNA pull-down, RNA immunoprecipitation, TOP/FOP luciferase reporter gene, and coimmunoprecipitation assays were used to explore the molecular mechanism underlying the effects of <i>GATA3-AS1</i> on BLCA progression. <b>Results:</b> <i>GATA3-AS1</i> expression was significantly up-regulated in BLCA tissues and correlated with pathological stage, grade, and poor patient outcome. Altered <i>GATA3-AS1</i> levels promoted BLCA proliferation, migration, and invasion. Mechanistic studies suggested that <i>GATA3-AS1</i> interacts with DDX5 protein, enhances its stability, and ultimately leads to BLCA progression through Wnt/β-catenin signaling pathway activation. <b>Conclusion:</b> <i>GATA3-AS1</i> overexpression increases the aggressiveness of BLCA by activating the Wnt/β-catenin pathway through binding to DDX5. <i>GATA3-AS1</i> has potential as a new molecular predictor of poor prognosis in patients with BLCA.