Cdc23, also related to 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 [2,4]. It is associated with pathways like the cell cycle, and its abnormal regulation can impact various biological processes and disease states. Genetic models, such as in yeast and mice, have been crucial for studying its functions.

In cancer research, knockdown of Cdc23 in liver cancer cell lines and in xenograft models inhibited cell proliferation, migration, and invasion via regulating the epithelial-mesenchymal transition (EMT) process, suggesting it could be a therapeutic target for liver cancer [1]. In papillary thyroid cancer, functional knockdown of Cdc23 led to cell cycle arrest in S and G(2)M phases, inhibiting cellular proliferation, tumor spheroid formation, and anchorage-independent growth, indicating its role in thyroid cancer initiation and progression [3]. In female infertility, homozygous missense variants in Cdc23 in three infertile individuals caused oocyte maturation defects, and Cdc23Y329C/Y329C mice mimicked the patients' phenotype, revealing the gene's importance in oocyte maturation [2]. In porcine skeletal muscle development, in vitro cell experiments showed that Cdc23 promoted myoblast proliferation and positively regulated skeletal muscle satellite cell differentiation [4].

In conclusion, Cdc23 is essential for processes like cell cycle regulation, oocyte maturation, and muscle development. Gene-knockdown and mouse models have revealed its significance in cancer development, such as in liver and thyroid cancer, and in female infertility, providing insights into potential therapeutic targets and genetic markers for these disease areas.