Cdc27, a core component of the Anaphase Promoting complex/cyclosome, plays a crucial role in controlling cell cycle transitions during cellular division. It is involved in the regulation of key processes related to the cell cycle, which are essential for normal cell growth and development [1].

CDC27 has been implicated in various diseases. In cancer, its role seems dual-acting as either a tumor suppressor gene or an oncogene in different neoplasms. In neuroblastoma, it promotes cell growth, metastasis, and sphere-formation ability in an ODC1-dependent manner and also affects ferroptosis [2]. In T-cell lymphoblastic lymphoma, it promotes proliferation, facilitates G1/S transition, inhibits apoptosis, and has a positive correlation with PD-L1 expression [3]. In acute leukemia, patients have significantly higher CDC27 expression levels, suggesting its potential as an oncogene and a biomarker [4]. In gastric and colorectal cancer, it promotes cell proliferation, invasion, and metastasis via epithelial-mesenchymal transition [7,10]. In breast cancer, low cdc27 expression is associated with a poor prognosis [8]. In contrast, in systemic lupus erythematosus (SLE), CDC27 expression is low in lupus patients and is related to disease activity [5]. Also, CDC27 has been identified as a candidate gene for hemifacial microsomia, with its knockout in zebrafish causing craniofacial malformation and other HFM-like phenotypes [6]. Additionally, in idiopathic pulmonary fibrosis, lncRNA TUG1 promotes fibrosis by up-regulating CDC27 and activating the PI3K/Akt/mTOR pathway [9].

In conclusion, Cdc27 is essential for cell cycle regulation. Its dysregulation is associated with multiple diseases, especially various cancers, SLE, and hemifacial microsomia. Studies using different models, such as gene knockout in zebrafish, have provided insights into its role in these disease conditions, highlighting its potential as a biomarker and therapeutic target.