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. 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. 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.