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Abstract BACKGROUND Cell cycle protein-dependent kinase inhibitor protein 3 (CDKN3) is a member of the protein kinase family and has been shown to be oncogenic in several tumors. However, there are no pan-carcinogenic analyses for CDKN3. METHODS Using bioinformatics tools such as The Cancer Genome Atlas (TCGA) and the UCSC Xena database, we performed a pan-cancer analysis of CDKN3. We investigated the function of CDKN3 in 33 different kinds of tumor. And we explored the gene expression, survival prognosis status, clinical significance,DNA methylation, immune infiltration, and associated signal pathways of CDKN3. RESULTS CDKN3 was significantly upregulated in most of tumors and correlated with overall survival (OS) of patients. Methylation levels of CDKN3 differed significantly between tumors and normal tissues. In addition, infiltration of CD4 + T cells, cancer-associated fibroblasts, macrophages, and endothelial cells were associated with CDKN3 expression in various tumors. Mechanistically, CDKN3 was associated with P53, PI3K-AKT, cell cycle checkpoints, mitotic spindle checkpoint, and chromosome maintenance. CONCLUSION Our pan-cancer analysis provides a comprehensive understanding of the role of CDKN3 gene in tumorigenesis. Targeting CDKN3 may provide a new direction for future tumor therapy.
Chen et al. (Thu,) studied this question.