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 的作用及其在 CRC 中的潜在机制仍然未知。在这里，RT-qPCR 证实 miR-425-5p 模拟物在 SW480 细胞中增加了 miR-425-5p 表达，并在 LOVO 细胞中被 miR-425-5p 抑制剂降低了。CCK-8、流式细胞术、伤口愈合和 transwell 测定表明，增加的 miR-425-5p 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) 上调 Fibronectin、N-cadherin、Vimentin 和下调 E-cadherin。此外，miR-425-5p 过表达诱导 c-myc、Cyclin D1 和 MMP7 水平，并促进 β-catenin 易位至细胞核。敲除 miR-425-5p 会产生相反的效果。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 的表达。CTNND1的沉默具有miR-425-5p抑制剂对细胞增殖、迁移、侵袭、EMT和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CRC提供治疗靶点。和β-catenin信号通路的激活。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CRC提供治疗靶点。和β-catenin信号通路的激活。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CRC提供治疗靶点。