Colorectal cancer (CRC) is a common malignancy with high mortality. However, the roles of miR-425-5p and its underlying mechanism in CRC remain unknown. Here, RT-qPCR confirmed that miR-425-5p expression was increased by miR-425-5p mimic in SW480 cells and decreased by miR-425-5p inhibitor in LOVO cells. CCK-8, flow cytometry, wound healing and transwell assays revealed that the increased miR-425-5p promoted cell viability, cell cycle entry, migration and invasion in CRC. Besides, miR-425-5p overexpression induced epithelial–mesenchymal transition (EMT) with upregulation of Fibronectin, N-cadherin, Vimentin, and downregulation of E-cadherin. Moreover, miR-425-5p overexpression induced c-myc, Cyclin D1 and MMP7 levels, and promoted β-catenin translocation to the nucleus. Knockdown of miR-425-5p exerted opposite effects. Luciferase reporter assay indicated that miR-425-5p directly targeted CTNND1. Overexpression of miR-425-5p repressed CTNND1 expression at mRNA and protein levels. Silencing of CTNND1 had the inhibitory effect of miR-425-5p inhibitor on cell proliferation, migration, invasion, EMT, and the activation of β-catenin signaling pathway. Furthermore, miR-425-5p promoted tumor growth and metastasis in vivo. In conclusion, miR-425-5p may promote tumorigenesis and metastasis through activating CTNND1-mediated β-catenin pathway, which may provide therapeutic targets for human CRC.

结直肠癌（CRC）是一种常见的恶性肿瘤，死亡率很高。然而，miR-425-5p 在 CRC 中的作用及其潜在机制仍不清楚。在此，RT-qPCR证实SW480细胞中miR-425-5p模拟物增加了miR-425-5p表达，而LOVO细胞中miR-425-5p抑制剂减少了miR-425-5p表达。 CCK-8、流式细胞术、伤口愈合和 Transwell 检测表明，miR-425-5p 的增加促进了 CRC 中的细胞活力、细胞周期进入、迁移和侵袭。此外，miR-425-5p过表达诱导上皮间质转化（EMT），纤连蛋白、N-钙粘蛋白、波形蛋白上调，E-钙粘蛋白下调。此外，miR-425-5p过表达可诱导c-myc、Cyclin D1和MMP7水平，并促进β-catenin易位至细胞核。 miR-425-5p 的敲低产生了相反的效果。荧光素酶报告基因检测表明 miR-425-5p 直接靶向 CTNND1。 miR-425-5p 的过表达在 mRNA 和蛋白质水平抑制 CTNND1 表达。沉默CTNND1可抑制miR-425-5p抑制剂对细胞增殖、迁移、侵袭、EMT以及β-catenin信号通路激活的抑制作用。此外，miR-425-5p在体内促进肿瘤生长和转移。总之，miR-425-5p可能通过激活CTNND1介导的β-catenin通路促进肿瘤发生和转移，这可能为人类结直肠癌提供治疗靶点。