ABSTRACT
S100 calcium-binding protein A11 (S100A11) has been proved to be an oncogene of most tumors. However, its role in the tumor microenvironment (TME) in pan-cancer stills remains poorly understood. This study used public data from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) database to evaluate the expression of S100A11. The R package "GSVA" was used for Gene set variation analysis (GSVA) of S100A11. The R package "ESTIMATE" was used to further explore the relationship between S100A11 and TME. The Genomics of Drug Sensitivity in Cancer database was used to investigate the effect of S100A11 on the efficiency of anticancer drugs. We found S100A11 expression was upregulated in most tumors and predicted a poor prognosis. Furthermore, S100A11 expression was closely associated with immune regulation-related pathways. Moreover, S100A11 expression in pan-cancer was significantly related to most immunosuppressive cells, such as tumor-associated macrophages (TAM), tumor-associated fibroblasts (TAF), and Treg cells. The expression of S100A11 was significantly related to immunosuppressive genes and immune checkpoints in most tumor types. Additionally, the upregulation of S100A11 expression made patients with cancer resistant to the treatment of most anticancer drugs, such as sorafenib. In brief, our study showed that S100A11 could be used as a potential carcinogen and prognostic marker for most tumor types. The increased expression of S100A11 was closely related to tumor immunosuppressive TME. The upregulation of S100A11 expression made patients with cancer resistant to sorafenib treatment.
