Objective: Exploration of molecular markers is an ongoing focus in the field of bladder cancer research. Based on data from public databases, GATA3-AS1 was identified as upregulated in bladder urothelial carcinoma (BLCA); however, its exact function and regulatory mechanism in this context remain unclear. Methods: To investigate the clinical implications of GATA3-AS1, we examined its levels in 90 BLCA and adjoining normal tissue samples. Functional assays were conducted to assess the effects of GATA3-AS1 on BLCA cell proliferation, migration, and invasion. Animal assays were employed to determine the effects of GATA3-AS1 on BLCA tumorigenicity in vivo. 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 GATA3-AS1 on BLCA progression. Results: GATA3-AS1 expression was significantly up-regulated in BLCA tissues and correlated with pathological stage, grade, and poor patient outcome. Altered GATA3-AS1 levels promoted BLCA proliferation, migration, and invasion. Mechanistic studies suggested that GATA3-AS1 interacts with DDX5 protein, enhances its stability, and ultimately leads to BLCA progression through Wnt/(3-catenin signaling pathway activation. Conclusion: GATA3-AS1 overexpression increases the aggressiveness of BLCA by activating the Wnt/(3-catenin pathway through binding to DDX5. GATA3-AS1 has potential as a new molecular predictor of poor prognosis in patients with BLCA.