Selenos, also known as selenoprotein S, is a small, intrinsically disordered membrane protein. It contributes to multiple cellular functions such as inflammatory processes, cellular stress response, protein quality control, and signaling pathways. Selenos is mainly recognized for its role in the ER-associated degradation (ERAD) pathway, extracting misfolded proteins from the ER for proteasomal degradation. It also controls transcription factors and cytokine levels [2].

In yellow catfish, the HSF1-SELENOS pathway was found to mediate dietary inorganic Se-induced lipogenesis via up-regulation of PPARγ expression. Blocking SELENOS by RNA interference demonstrated its critical role in sodium selenite-induced lipid accumulation [1]. In colon cancer cells, knocking down SELENOS sensitized reactive oxygen species (ROS)-mediated anti-tumor effects of regorafenib, enhancing the combined anti-tumor activities of regorafenib and oxaliplatin [4]. In triple negative breast cancer, the combined overexpression of SELENOS and valosin-containing protein (VCP/p97) correlated with advanced stages and poor prognosis [5]. In brain lower-grade glioma, siRNA-mediated knockdown of SELENOS reduced cell proliferation, viability, invasion, and migration, and induced apoptosis, suggesting it as a potential prognostic marker and therapeutic target [3].

In conclusion, Selenos plays diverse roles in various biological processes and diseases. Functional studies, especially through loss-of-function experiments like RNA interference in cell models, have revealed its importance in lipid metabolism, cancer development, and potentially stroke pathogenesis. These findings contribute to understanding the underlying mechanisms of related diseases and may offer new perspectives for disease prevention and treatment.