CEP89, also known as centrosomal protein 89, is essential for ciliogenesis, mitochondrial metabolism, and neuronal function. It is involved in pathways related to the assembly of primary cilia, regulation of mitochondrial complex IV activity, and synaptic transmission. It has overall biological importance in processes like cell development and cognitive function, and genetic models such as Drosophila are valuable for its study [2,3,4].

In ovarian cancer, CEP89 is overexpressed, with more than a quarter of patients having copy number gains in the gene. High expression is associated with poor prognosis, as patients with high expression have over a year shorter overall survival compared to those with low expression. In vitro studies on OC cell lines also show differences in CEP89 levels. Additionally, CEP89 is required for mitochondrial metabolism; in Drosophila, its knockdown decreases complex IV activity and is lethal. In cilia formation, CEP89 selectively functions in RAB34+ ciliary vesicle recruitment. Knockout studies in Drosophila show that it is essential for IFT-dependent neuronal cilia formation [1,2,3,4].

In conclusion, CEP89 is crucial for ciliogenesis, mitochondrial metabolism, and neuronal function. Model-based research, including Drosophila knockdown models, has revealed its role in these processes. In ovarian cancer, CEP89's overexpression and copy number gains suggest it may serve as a prognostic predictor and a potential therapeutic target.