Cdc23, also known as Mcm10 in some contexts, is a core subunit of the anaphase - promoting complex or cyclosome (APC/C) and is involved in regulating mitosis in eukaryotes [4]. It also plays a role in DNA replication processes, such as promoting Cdc45 chromatin binding and participating in the activation of the pre - replicative complex [5,6]. Its functions are crucial for cell cycle progression and normal cellular development.

In disease - related studies, knockdown of Cdc23 in liver cancer cell lines and xenograft models inhibited cell proliferation, migration, invasion, and tumor growth, likely through regulating the epithelial - mesenchymal transition (EMT) process, suggesting it could be a therapeutic target for liver cancer [1]. In female infertility cases, homozygous missense variants in Cdc23 led to oocyte maturation defects. Cdc23Y329C/Y329C mice mimicked the patient phenotype, with low expression of CDC23 and APC4 and accumulation of securin and cyclin B1 in oocytes, and AZ3146 treatment could rescue the phenotype [2]. In papillary thyroid cancer, functional knockdown of Cdc23 in thyroid cancer cells increased the number of cells in S and G(2)M phases, inhibited cellular proliferation, tumor spheroid formation, and anchorage - independent growth, indicating its role in thyroid cancer initiation and progression [3].

In conclusion, Cdc23 is essential for cell cycle regulation, DNA replication, and normal development. Studies using gene knockdown or mutant mouse models have revealed its significance in diseases like liver cancer, female infertility, and papillary thyroid cancer, providing insights into potential therapeutic strategies for these conditions.