A Pan-Cancer Analysis of the Role of Selenoprotein P mRNA in Tumorigenesis

Background Selenium (Se) exhibits its anti-carcinogenic properties by regulating the redox system. However, the relationship between selenoprotein P (SeP), mRNA (SELENOP mRNA) and tumorigenesis remains unclear. Plasma SeP transports Se to various target tissues and has antioxidant characteristics. The present study aimed to explore the multifaceted pan-cancer properties of SELENOP in terms of its tissue-specific expression, prognostic value, immune function, and signaling pathway enrichment. Patients and methods The expression profile of SELENOP was determined in 33 tumor types and survival, pathway enrichment, and correlation analyses were conducted based on TCGA database. The relationship between SELENOP expression and immune infiltration and macrophage subtype gene markers was investigated using the TIMER and GEPIA. Results SELENOP gene expression was decreased in many cancer tissues, but was upregulated in brain lower grade glioma (LGG). Furthermore, SELENOP expression was associated with a better prognosis in most cancers, but a poorer prognosis in LGG and uterine corpus endometrioid carcinoma (UCEC). Our results showed that SELENOP was correlated with infiltration level of six immune cell types, where SELENOP also showed a strong correlation with macrophages in some cancer types. However, we failed to determine macrophage polarization in 33 tumor types. SELENOP negatively regulated vascular endothelial cell proliferation in LGG and UCEC and epidermal cell differentiation in six tumor types. In contrast, upregulation was related to immune function, including T cell activation, B cell-mediated immunity, adaptive immune response and immune response regulation cell surface receptor signaling pathways in another six tumor types. Conclusion These findings highlighted the tissue-specific expression, prognostic value and immune characteristics of SELENOP in pan-cancer, and provided insights for illustrating the role of SELENOP in tumorigenesis.