Pan-cancer analysis of the prognostic and immunological role of Fanconi anemia complementation group E.

Fanconi anemia (FA) genes contribute to tumorigenesis by regulating DNA repair. Despite its importance for assembly and functionality of the FA core complex, no pan-cancer analysis of was performed. We aimed to provide a comprehensive understanding of the role of in cancers. Based on The Cancer Genome Atlas (TCGA), Cancer Cell Line Encyclopedia (CCLE), Genotype Tissue-Expression (GTEx), Human Protein Atlas (HPA), Gene Expression Omnibus (GEO), and Cancer Single-cell Atlas (CancerSEA) databases, we investigated the carcinogenicity of using various bioinformatics methods, including expression and prognosis, immune invasion, tumor mutation burden, microsatellite instability, and neoantigens. We monitored mutations in mice that caused tumorigenesis. expression and activity scores were upregulated in 15 and 21 cancers. High expression of affected shorter overall survival (OS) in seven cancers and longer overall survival in three cancers. It was correlated with shorter overall survival and progression-free interval (PFI) in endometrial cancer and longer overall survival and PFI in cervical cancer. expression negatively correlated with stromal/immune scores in 21 cancers including cervical cancer, endometrial cancer, and ovarian cancer. expression negatively correlated with CD8 T cells in endometrial cancer and positively correlated with M1 macrophages in cervical cancer, possibly related to cancer prognosis. positively correlated with immune checkpoint inhibitors PD-1, PD-L1, and CTLA4 in endometrial cancer and ovarian cancer. expression positively correlated with microsatellite instability, tumor mutational burden, and neoantigens in 7, 22, and five cancers, especially in endometrial cancer, potentially increasing the effectiveness of immunotherapy. Single-cell sequencing data showed was primarily expressed in cancer cells in cervical and ovarian cancer, and in fibroblasts in endometrial cancer. heterozygous mutant mice had increased tumor incidences and shorter overall survival and tumor-free survival (TFS) than homozygous mutant mice and wild-type mice. Conclusively, potential to serve as a biomarker for cancer prognosis and may predict cancer immunotherapy responses. heterozygous mutant resulted in increased tumorigenesis and poor prognosis in mice.