Background: KPNA2, a nuclear export protein that plays an important role in tumorigenesis, is an emerging hotspot target in oncology. Despite increasing supporting evidence of its importance, no pan-cancer analysis, across multiple databases, is available for in-depth data mining of the gene.
Methods: Tumor data from both The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) were explored to investigate the potential oncogenic roles of KPNA2. Diverse analytical methods were used to gain a full-scale understanding of KPNA2: gene expression, survival situations, genetic mutations, DNA methylation, sites of protein phosphorylation, immunocyte infiltration, and correlative cellular pathways.
Results: KPNA2 is highly expressed in many cancers, and different correlations exist between KPNA2 expression and prognosis of cancer patients. cBioPortal reported that a nonsense mutation of R285* was considered to be the primary tumorigenic genetic alteration to KPNA2 and was found in cases of LUSC, STAD, and CESC. Enhanced phosphorylation of S62 was found in several cancers and the level of infiltration of cancer-associated fibroblasts was found to be linearly correlated with KPNA2 expression levels in ACC, BRCA, MESO, TGCT, THCA, and THYM. Correlations between KPNA2 DNA methylation and the pathogenesis of various tumors in TCGA were further identified. KEGG and GO enrichment analysis identified cell cycle, microtubule binding, and tubulin binding functions for KPNA2.
Conclusion: This is the first pan-cancer analysis focusing on KPNA2. It provides a comprehensive understanding about the role of KPNA2 in tumorigenesis and highlights the potential targeted role of KPNA2 for cancer study.
Keywords: KPNA2; Molecular mechanism; Pan-cancer analysis; Phosphorylation; Prognosis.
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