ORIGINAL RESEARCH article
Front. Oncol.
Sec. Cancer Molecular Targets and Therapeutics
Volume 15 - 2025 | doi: 10.3389/fonc.2025.1652176
This article is part of the Research TopicTargeting the Wnt/ß-catenin Signaling Pathway in Cancer Vol IIView all articles
Mechanistic studies of miR-582-3p targeting of PTPRCAP affecting lung adenocarcinoma via the Wnt/β-catenin pathway
Provisionally accepted
- 1Affiliated Hospital of Chengde Medical University, Chengde, China
- 2Laboratory of Panvascular Diseases, Hebei Province, Chengde, Hebei Province, Chengde, China
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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.
Keywords: miR-582-3p, PTPRCAP, Lung Adenocarcinoma, Wnt/β-catenin, Signaling Pathways
Received: 23 Jun 2025; Accepted: 04 Sep 2025.
Copyright: © 2025 Yang, Zhao, Han, Guo, Zhao and Liang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Zongying Liang, Affiliated Hospital of Chengde Medical University, Chengde, China
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