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Background  Erythropoietin receptor (EPOR), a member of the cytokine class I receptor family, mediates erythropoietin (EPO)-induced erythroblast proliferation and differentiation, but its significance goes beyond that. The expression and prognosis of  EPOR  in cancer remain unclear.    Methods  This study intended to perform a pan-cancer analysis of  EPOR  by bioinformatics methods. Several databases such as GTEx, TCGA, CCLE, and others were used to explore the overall situation of  EPOR  expression, and the correlation of  EPOR  expression with prognosis, microRNAs (miRNAs), immune infiltration, tumor microenvironment, immune checkpoint genes, chemokines, tumor mutation burden (TMB), microsatellite instability (MSI), methyltransferases, and DNA mismatch repair (MMR) genes in 33 tumors was analyzed. In addition, we compared the promoter methylation levels of  EPOR  in cancer tissues with those in normal tissues and performed protein–protein interaction network, gene–disease network, and genetic alteration analyses of  EPOR , and finally enrichment analysis of EPOR-interacting proteins, co-expressed genes, and differentially expressed genes.    Results  The TCGA database showed that  EPOR  expression was upregulated in BLCA, CHOL, HNSC, KIRC, LIHC, STAD, and THCA and downregulated in LUAD and LUSC. After combining the GTEx database,  EPOR  expression was found to be downregulated in 18 cancer tissues and upregulated in 6 cancer tissues. The CCLE database showed that  EPOR  expression was highest in LAML cell lines and lowest in HNSC cell lines. Survival analysis showed that high  EPOR  expression was positively correlated with OS in LUAD and PAAD and negatively correlated with OS in COAD, KIRC, and MESO. Moreover,  EPOR  had a good prognostic ability for COAD, LUAD, MESO, and PAAD and also influenced progression-free survival, disease-specific survival, disease-free survival, and progression-free interval in specific tumors. Further,  EPOR  was found to play a non-negligible role in tumor immunity, and a correlation of  EPOR  with miRNAs, TMB, MSI, and MMR genes and methyltransferases was confirmed to some extent. In addition, the enrichment analysis revealed that  EPOR  is involved in multiple cancer-related pathways.    Conclusion  The general situation of  EPOR  expression in cancer provided a valuable clinical reference.  EPOR  may be target gene of hsa-miR-575, etc. A pan-cancer analysis of panoramic schema revealed that EPOR not only may play an important role in mediating EPO-induced erythroblast proliferation and differentiation but also has potential value in tumor immunity and is expected to be a prognostic marker for specific cancers.

Pan-Cancer Analysis Based on EPOR Expression With Potential Value in Prognosis and Tumor Immunity in 33 Tumors