Selenop, also known as selenoprotein P, is an extracellular antioxidant, selenium transporter, and hepatokine. It plays a crucial role in selenium metabolism, transporting selenium from the liver to essential tissues like endocrine glands and the brain, and its levels can serve as a biomarker of selenium status [2,4]. It is also involved in various biological processes such as glucose and lipid metabolism, and may interact with important signaling pathways like the WNT signaling pathway [2]. Genetic models, such as knockout mouse models, are valuable for studying its functions.

In a mouse adenoma model with conditional, intestinal epithelium-specific deletion of the tumor suppressor Apc, Selenop KO decreased colon tumor incidence and size. Selenop-KO tumor organoids had defects in organoid formation and decreases in WNT target gene expression, which could be reversed by SELENOP restoration. This indicates that SELENOP modulates the WNT signaling pathway in sporadic colorectal carcinogenesis [1]. Additionally, in extremely preterm infants, the SELENOP rs3877899A allele, associated with reduced selenium bioavailability, may contribute to the risk of retinopathy of prematurity (ROP) and visual impairment [3].

In conclusion, Selenop is essential for selenium transport and metabolism, and plays a role in multiple biological processes. Studies using Selenop KO mouse models have revealed its significance in sporadic colorectal cancer and ROP, highlighting its potential as a key factor in understanding these disease mechanisms.