Cdc27, a core component of the Anaphase Promoting complex/cyclosome, plays a crucial role in controlling cell cycle transitions during cellular division [1]. This function is essential for normal cell growth and development, and its associated pathway is fundamental to cell cycle regulation. Genetic models, such as gene knockout in zebrafish, can be valuable for studying Cdc27.

In zebrafish, cdc27 knockout led to craniofacial malformation, spine deformity, and cardiac edema, phenotypes similar to Hemifacial microsomia (HFM) [4]. This indicates a functional link between Cdc27 and HFM, likely through inhibiting cranial neural crest cell (CNCC) proliferation and disrupting pharyngeal chondrocyte differentiation.

In various cancers, functional studies have also been revealing. For example, in colorectal cancer, knockdown of Cdc27 in HCT116 cells inhibited proliferation both in vitro and in vivo, arresting the G1/S phase transition via the accumulation of p21 [6]. In gastric cancer, silencing Cdc27 expression effectively inhibited cell proliferation, invasion, and metastasis in vitro and in vivo [5]. In T-cell lymphoblastic lymphoma, CDC27 promoted proliferation in vivo and in vitro, facilitated G1/S transition, and promoted the expression of Cyclin D1 and CDK4 [3]. In neuroblastoma, CDC27 promoted cell growth, metastasis, and sphere-formation ability in vitro and in vivo [2].

In conclusion, Cdc27 is essential for regulating cell cycle transitions. Studies using gene knockout models in zebrafish have revealed its role in HFM, while in vivo studies in cancer cell models have shown its significance in cancer progression. These findings highlight Cdc27's importance in both normal development and disease conditions, providing potential therapeutic targets for treating related diseases.