A pan-cancer analysis of the oncogenic role of KIF13A in human tumors

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. 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 immune infiltration revealed an inverse association between KIF13A expression and CD8 + T-cell infiltration levels in HNSC, HNSC-HPV-, HNSC-HPV+, and LUSC, ‌but correlated positively with the abundance of cancer-associated fibroblasts in LUAD, PAAD, and STAD. 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. In conclusion, this pioneering pan-cancer study offers thorough comprehension of the role of KIF13A in various cancers.