Background <p>The objective of this research is to determine the relative abundances and clinical significance of the long non-coding RNA (lncRNA) RASAL2-AS1 in cervical cancer. Additionally, this study aims to elucidate its molecular mechanism in influencing malignant progression through the regulation of the microRNA-590-5p (miR-590-5p)/PDCD5 axis and the Wnt/β-catenin signaling pathway.</p> Methods <p>Gene expression of RASAL2-AS1 was assessed in cervical cancer tissues (<i>n</i> = 103) using quantitative real-time PCR (qRT-PCR). The impacts on cellular events, epithelial-mesenchymal transition (EMT), and key signaling pathways were evaluated using CCK-8, Transwell, and Western Blot techniques. The target relationships among RASAL2-AS1, miR-590-5p, and PDCD5 were verified via luciferase reporter assays.</p> Results <p>RASAL2-AS1 exhibited significantly reduced expression in cervical cancer. Its downregulation was markedly associated with advanced FIGO staging (<i>P</i> = 0.014), lymph node metastasis (<i>P</i> = 0.035), and poor prognosis, establishing it as an independent indicator of unfavorable outcomes for cervical cancer patients (HR = 0.201, 95% CI = 0.087–0.464, <i>P</i> &lt; 0.001). Functionally, the upregulation of RASAL2-AS1 inhibited cervical cancer cell growth and EMT. Mechanistically, RASAL2-AS1 acted as a molecular sponge to sequester miR-590-5p, thereby alleviating its inhibitory effect on PDCD5. Furthermore, RASAL2-AS1 obstructs the Wnt/β-catenin pathway through the miR-590-5p/PDCD5 axis.</p> Conclusions <p>RASAL2-AS1 exerts a tumor-suppressive effect in cervical cancer by functioning as a competing endogenous RNA (ceRNA) that modulates the miR-590-5p/PDCD5 axis and regulates the Wnt/β-catenin pathway.</p>