Mechanistic studies of miR-582-3p targeting of PTPRCAP affecting lung adenocarcinoma via the Wnt/β-catenin pathway

Objective To investigate the regulatory mechanism by which MicroRNA-582-3p ( miR -582-3p) targets protein tyrosine phosphatase receptor type C-associated protein ( PTPRCAP ) and modulates Wnt/β-catenin signaling in lung adenocarcinoma pathogenesis. Methods Bioinformatics analysis of TCGA data assessed miR -582-3p expression and its clinicopathological relevance in LUAD. PTPRCAP mRNA and protein levels were evaluated via RT-qPCR and immunohistochemistry. The miR -582-3p -PTPRCAP interaction was validated using TargetScan8.0 and dual-luciferase reporter assays. Functional assays (CCK-8, scratch, Transwell) determined the effects of miR -582-3p and PTPRCAP on LUAD cell proliferation, migration, and invasion. Western blotting analyzed Wnt/β-catenin pathway components (β-catenin, GSK3β, p-GSK3β). Results miR -582-3p was significantly upregulated in LUAD tissues and cell lines (A549, H1299), correlating with advanced disease features. PTPRCAP , a predicted target of miR -582-3p, showed reduced expression in LUAD. Dual-luciferase assays confirmed miR -582-3p directly binds the PTPRCAP 3′-UTR (P < 0.05). Overexpressing miR -582-3p suppressed PTPRCAP , enhanced malignant phenotypes (P < 0.05), and activated Wnt/β-catenin signaling (increased β-catenin and p-GSK3β; decreased GSK3β). Conversely, PTPRCAP overexpression inhibited tumorigenic behaviors and Wnt pathway activity. Rescue experiments demonstrated that PTPRCAP restoration counteracted miR -582-3p–mediated oncogenic effects (P < 0.05). Conclusion Our findings reveal a novel miR -582-3p/ PTPRCAP /Wnt/β-catenin axis in LUAD progression, where miR -582-3p drives tumor growth by silencing PTPRCAP and activating Wnt signaling. These results highlight miR -582-3p as a potential therapeutic target and PTPRCAP as a tumor suppressor in LUAD, offering new insights for targeted intervention strategies.