Ccdc25, Coiled-coil domain containing 25, is a transmembrane protein that has emerged as a crucial molecule in multiple biological processes. It acts as a NET-DNA receptor on cancer cells, activating the ILK-β-parvin pathway to enhance cell motility. It also plays a role in the regulation of neural stem cell (NSC) proliferation, differentiation, and neuronal maturation during brain development, possibly through the Egr1-related pathway. Additionally, it may be involved in metabolic pathways [1,2,3].

In cancer metastasis, NET-DNA, by binding to Ccdc25 on cancer cells, acts as a chemotactic factor to attract cancer cells, promoting distant metastases. CCDC25-knockout cells abrogate NET-mediated metastasis, highlighting its importance in this process [1]. In brain development, suppression of Ccdc25 by shRNAs increases NSC proliferation and inhibits premature terminal mitosis and neuronal differentiation, while overexpression has the opposite effects. RNA sequencing shows that Ccdc25 regulates NSC development through Egr1, as Egr1 knockdown mimics the Ccdc25-knockdown phenotype and Egr1 overexpression can rescue it [2].

In conclusion, Ccdc25 is essential in processes like cancer metastasis and brain development. The use of gene-knockout models, such as CCDC25-knockout cells in cancer metastasis research, has been crucial in revealing its role in promoting metastasis. In brain development, manipulation of Ccdc25 expression in NSCs has provided insights into its role in regulating NSC proliferation, differentiation, and neuronal maturation. These findings offer potential therapeutic targets for preventing cancer metastasis and understanding neurodevelopmental disorders [1,2].