A pan-cancer analysis of the role of in human tumors.

WDFY2 is a protein that may provide valuable insights into the mechanisms underlying human tumors and aid in the development of novel therapies. Despite its potential importance, the role of WDFY2 in pan-cancer has not been systematically investigated. In this study, we comprehensively explored the expression pattern and function of WDFY2 across 33 cancers using various databases, including TCGA, CPTAC and GEO datasets. Our results indicate that WDFY2 is downregulated in most cancer types, including BRCA, KIRP, KICH, LUAD, KIRC, PCPG, PRAD, THCA, ACC, OV, TGCT and UCS, while it is upregulated in CESC, CHOL, COAD, HNSC, LUSC, READ, STAD and UCEC. Prognostic analyses showed that higher levels of WDFY2 were associated with worse disease outcomes in ACC, BLCA, COAD, READ, SARC, MESO and OV. WDFY2 mutations were most frequent in colorectal cancer but were not associated with disease prognosis. We also found that WDFY2 expression correlated with monocyte infiltration status in SKCM, endothelial cell infiltration in COAD, KIRC, MESO, OV and THCA, and cancer-associated fibroblast infiltration in COAD, LUAD and OV. Additionally, functional enrichment analysis revealed that WDFY2 is involved in metabolism. Overall, our comprehensive analysis sheds light on the role of WDFY2 in various cancers, providing a better understanding of its role in tumorigenesis.