乳腺癌是女性最常见的恶性肿瘤之一。据报道，细胞分裂周期相关 5 (CDCA5) 是姐妹染色单体凝聚力的主要调节因子，在多种癌症中表达上调。在此，探讨CDCA5在乳腺癌中的功能和调节机制。通过免疫组化染色鉴定乳腺癌标本中CDCA5的表达。利用组织微阵列分析CDCA5表达与乳腺癌患者临床病理特征和预后的相关性。在CDCA5过表达/敲低细胞和小鼠模型中探讨了CDCA5在乳腺癌中的功能。通过Co-IP、ChIP和双荧光素酶报告基因检测来阐明潜在的分子机制。我们发现CDCA5在乳腺癌组织和细胞系中以较高水平表达，并且CDCA5的过度表达与患者的不良预后显着相关患有乳腺癌。此外，CDCA5敲低显着抑制增殖和迁移，同时促进体外细胞凋亡。从机制上讲，我们揭示了CDCA5在促进E2F转录因子1（E2F1）与叉头盒M1（FOXM1）启动子结合方面发挥着重要作用。此外，体外和体内数据表明，FOXM1的缺失减轻了CDCA5过表达对乳腺癌的影响。此外，我们发现Wnt/β-catenin信号通路是CDCA5诱导乳腺癌进展所必需的。我们认为CDCA5通过CDCA5/FOXM1/Wnt轴促进乳腺癌进展，CDCA5可能作为乳腺癌的新治疗靶点癌症治疗。© 2024。作者。

Breast cancer is one of the most common malignant tumors in women. Cell division cycle associated 5 (CDCA5), a master regulator of sister chromatid cohesion, was reported to be upregulated in several types of cancer. Here, the function and regulation mechanism of CDCA5 in breast cancer were explored.CDCA5 expression was identified through immunohistochemistry staining in breast cancer specimens. The correlation between CDCA5 expression with clinicopathological features and prognosis of breast cancer patients was analyzed using a tissue microarray. CDCA5 function in breast cancer was explored in CDCA5-overexpressed/knockdown cells and mice models. Co-IP, ChIP and dual-luciferase reporter assay assays were performed to clarify underlying molecular mechanisms.We found that CDCA5 was expressed at a higher level in breast cancer tissues and cell lines, and overexpression of CDCA5 was significantly associated with poor prognosis of patients with breast cancer. Moreover, CDCA5 knockdown significantly suppressed the proliferation and migration, while promoted apoptosis in vitro. Mechanistically, we revealed that CDCA5 played an important role in promoting the binding of E2F transcription factor 1 (E2F1) to the forkhead box M1 (FOXM1) promoter. Furthermore, the data of in vitro and in vivo revealed that depletion of FOXM1 alleviated the effect of CDCA5 overexpression on breast cancer. Additionally, we revealed that the Wnt/β-catenin signaling pathway was required for CDCA5 induced progression of breast cancer.We suggested that CDCA5 promoted progression of breast cancer via CDCA5/FOXM1/Wnt axis, CDCA5 might serve as a novel therapeutic target for breast cancer treatment.© 2024. The Author(s).