Background
Dysregulated expression of miR-532-3p has been observed in several types of cancer and plays a key role in tumor progression and metastasis. In this study, we analyzed the role and molecular mechanism of miR-532-3p in lymphoma progression.
Conclusion
This study demonstrates that miR-532-3p functions as a tumor inhibitor in lymphoma progression by targeting β-catenin, suggesting miR-532-3p/β-catenin as a new diagnosis marker or potential therapeutic target in lymphoma.
Methods
The expression of miR-532-3p in lymphoma sample tissues was analyzed using the GEO database and in cell lines by quantitative reverse transcription (qRT)-PCR. The functions of miR-532-3p in lymphoma cell proliferation and apoptosis were analyzed by CCK-8 assay and Annexin V-FITC/propidium iodide staining, respectively. In vivo, the tumor weight and volume were measured. The target gene of miR-532-3p was predicted using miRanda software, and then luciferase, qRT-PCR, and western blot assays were performed to verify that β-catenin was the downstream target gene of miR-532-3p.
Results
miR-532-3p was decreased in lymphoma tissues and cell lines. In vitro and in vivo experiments showed that overexpression of miR-532-3p inhibited lymphoma cell proliferation and promoted apoptosis. Mechanistic studies demonstrated that β-catenin was a functional target gene of miR-532-3p. Furthermore, we found that overexpression of β-catenin reversed the tumor-suppression activities caused by overexpression of miR-532-3p in lymphoma proliferation and apoptosis.