Abstract
Despite the increasing evidence supporting the association between KIF13A and cancer, pan-cancer analysis is currently limited. Therefore, we aimed to investigate the potential for KIF13A to contribute to oncogenesis in thirty-three different tumors using publicly accessible databases. Our research findings indicate that KIF13A has lower RNA tissue specificity and exhibits lower levels of expression compared to healthy tissue in most of tumor. However, we discovered distinct associations between KIF13A expression and the outcome of diverse tumor types. Genetic variation analysis revealed that cases of UCEC with genetic alterations in KIF13A exhibited a better prognosis compared to cases without genetic alterations in KIF13A. Analysis of differentially methylated genes (DMGs) in pan-cancer studies revealed that the promoter region of KIF13A exhibited significantly different methylation levels between tumor tissues and adjacent normal tissues across various cancer types. Furthermore, we observed differences in KIF13A (NP_017396.4) phosphorylation levels between normal tissues and primary tumor tissues at different phosphorylation sites across various tumor cases. Specifically, we noted an increased phosphorylation level of KIF13A at the S1698 site in HNSC and HCC, correlating with the early differentiation of human embryonic stem cells. Analysis of immune infiltration revealed a bidirectional regulatory pattern, suggesting that KIF13A may differentially shape the tumor microenvironment across cancer types, potentially influencing immunotherapy responses and stromal interactions. Gene enrichment analysis related to KIF13A indicates that it is involved pathways related to vesicle transport, pigment synthesis, and ubiquitination modification. The synergistic effects of these pathways may collectively contribute to the role of KIF13A in tumor pathogenesis. In conclusion, this pioneering pan-cancer study offers thorough comprehension of the role of KIF13A in various cancers. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12672-025-04327-9.