Comprehensive analysis of the oncogenic and immunological role of SPON2 in human tumors.

ABSTRACT

BACKGROUND: Sapiens spondin-2 (SPON2) is a protein found in the extracellular matrix that plays a role in a number of processes, including immune reactions and cell adhesion, and is closely linked to the emergence of a number of tumor types. However, we know very little about Sapiens spondin-2. Therefore, we performed a systematic pan-carcinogenic analysis to explore the relationship between Sapiens spondin-2 and cancers. MATERIALS AND METHODS: By comprehensive use of datasets from TCGA, GEO, GTEx, HPA, CPTAC, GEPIA2, TIMER2, cBioPortal, STRING, we adopted bioinformatics methods to dig up the potential carcinogenesis of SPON2, including dissecting the correlation between SPON2 and gene expression, prognosis, gene mutation, Immunohistochemistry staining, immune cell infiltration, and constructed the interaction network of a total of 54 SPON2-binding proteins as well as explored the enrichment analysis of SPON2-related partners. RESULTS: The expression of Sapiens spondin-2 in most tumor tissues was higher than that of normal tissues. In addition, SPON2 showed the early diagnostic value in 33 kinds of tumors and was positively or negatively associated with the prognosis of different tumors. It also validates that SPON2 is the gene associated with the majority of immune-infiltrating cells in pan-cancer. High SPON2 expression is associated with tumor progression related pathways. CONCLUSION: We found and validated the potential use of SPON2 in cancer detection for the first time through pan-cancer analysis. The expression levels of SPON2 in various tumors were quite different from those in normal tissues. Furthermore, the performance of SPON2 in tumorigenesis and tumor immunity verified our hypothesis. At the same time, it has high specificity and sensitivity in cancer detection. Therefore, SPON2 can be employed as an auxiliary index for the initial diagnosis of tumors and a prognostic marker for various types of tumors.