CCDC106, or coiled-coil domain-containing protein 106, has emerged as a significant player in multiple biological processes. It is involved in regulating the p53-Mdm2/MdmX signaling axis, which is crucial for maintaining the basal level of the tumor suppressor p53 [1]. By directly interacting with the p53 transactivation domain, CCDC106 competes with Mdm2 and MdmX, influencing the cellular levels of p53 and Mdm2/MdmX.

In cancer-related studies, CCDC106 knockdown enhanced apoptosis by stabilizing p53 and suppressed cell viability, colony formation, migration and invasion in cervical cancer HeLa and breast cancer MCF7 cells with wild-type p53, while overexpression had opposite effects in normal breast epithelial HBL100 and cervical cancer SiHa cells with wild-type p53 [5]. In ovarian cancer, overexpression of CCDC106 promoted proliferation, invasion and epithelial-to-mesenchymal transition (EMT) of mutant p53 ovarian cancer cells via the ATF4-mediated inhibition of p21 [2]. In non-small cell lung cancer, CCDC106 expression correlated with advanced TNM stage, positive regional lymph node metastasis and poor overall survival, and it promoted cell proliferation depending on AKT signaling [3]. Also, HPV-CCDC106 integration in cervical cancer altered local chromosome architecture, hijacked an enhancer, and promoted cancer progression by facilitating high CCDC106 expression after HPV E6 splicing, which led to p53 degradation [4,6].

In conclusion, CCDC106 has a significant impact on cancer-related biological processes, mainly through its interaction with p53 and involvement in cell-cycle-regulating and cancer-promoting pathways. Functional studies using gene knockout or knockdown models in various cancer cell lines have revealed its role in promoting cancer cell proliferation, invasion, and in some cases, p53 degradation. These findings suggest CCDC106 could be a potential therapeutic target in cancer treatment.