Cpne1, a calcium-dependent, phospholipid-binding protein, is ubiquitously expressed in various tissues and organs. It is involved in multiple biological processes and associated with several signaling pathways. For example, it can interact with proteins like 14-3-3γ, Jab1, HAX1, TRAF2, and RACK1, and is related to pathways such as MAPK, PERK-eIF2α, MET, PI3K/AKT/HIF-1α, and AKT/P53 [1-10]. Cpne1 plays an important role in cell proliferation, differentiation, apoptosis, and mitochondrial function, and is also implicated in the development of many diseases, especially various cancers [1-10]. Genetic models, such as knockout mouse models, are valuable for studying its functions.

In gastric, pancreatic, non-small cell lung, breast, and hepatocellular cancers, silencing Cpne1 inhibits cell proliferation, promotes apoptosis, and suppresses tumor growth in vitro and in vivo [1,3,5,6,7]. In sarcopenia, overexpression of Cpne1 in young muscles disrupts mitochondrial function, affects membrane lipid composition, and reduces skeletal muscle fibrosis regeneration and exercise capacity, which can be reversed by a PERK inhibitor [2]. In the context of sperm motility, Cpne1 deficiency preserves sperm motility under Ca2+ channel blockade, suggesting it may be a target of Ca2+ channel inhibitors [4].

In conclusion, Cpne1 is crucial in regulating cell-related biological processes. The use of Cpne1 KO mouse models has significantly contributed to understanding its role in cancer development, sarcopenia, and sperm motility regulation. These findings provide potential therapeutic targets for related diseases.