YPEL3, also known as small unstable apoptotic protein (SUAP), is a gene encoding a growth-suppressive protein. It is induced by the p53 tumor suppressor and is involved in important biological processes such as cellular senescence, tumor suppression, and regulation of endometrial function during early pregnancy. It is associated with pathways like the Wnt/β-catenin and Hippo signaling pathways [1,2,3]. Genetic models, including Drosophila and zebrafish models, have been used to study its function [4,6].

In Drosophila, frameshift mutations of dYPEL3 led to reduced nociceptive responses and decreased synaptic contact between nociceptors and second-order neurons, suggesting a role in sensory circuit function [4]. In zebrafish, ypel3 mutants showed defects in oligodendrocyte precursor cells, perineurial glial precursor exit from the CNS, perineurium formation, and Schwann cell maturation, indicating its importance in glial cell development [6]. In human cancer cell lines, overexpression of YPEL3 inhibited processes like epithelial-mesenchymal transition (EMT), migration, invasion, and metastasis in nasopharyngeal carcinoma cells by suppressing the Wnt/β-catenin signaling pathway, and induced cellular senescence in breast cancer cells via the Hippo signaling pathway [3,5]. In goats, YPEL3 negatively regulated endometrial function during early pregnancy through the Wnt/β-catenin pathway [2].

In conclusion, YPEL3 is crucial for multiple biological functions. Its role in tumor suppression, glial cell development, and regulation of endometrial function during pregnancy has been revealed through model-based research. The study of YPEL3 in these models provides insights into the mechanisms of cancer, neurological conditions, and pregnancy-related endometrial function regulation.