Background: Kinesin family member 14 (KIF14) as an oncogene in many cancers. However, the clinical role and mechanism of KIF14 in oral squamous cell carcinomas (OSCC) is still largely unclear.
Methods: Gene Expression Omnibus (GEO) databases was used to screen differentially expressed genes (DEGs) between OSCC and non-cancer tissues. KEGG pathway, Gene Ontology, and Reactome pathway analyses were performed on the DEGs. Hub genes were identified via protein-protein interaction (PPI) network analysis. ssGSEA was employed to recognize tumor-infiltrating immune cells. The biological function of KIF14in OSCC was tested by CCK-8, Flow cytometry as well as western blotting.
Results: In this study, 7239 common DEGs were obtained from six datasets, with ten hub genes identified among the DEGs. Validation analyses revealed that KIF14 is a critical agent in the progress of OSCC. Knockdown KIF14 inhibits OSCC cells growth and induces apoptosis. And also, up-regulates cleaved-caspase-3 as well as Bax level and decreases Bcl-2 expression in OSCC cells. Gamma delta T cell and Monocyte were significantly correlated with overall survival for APOPA4 by ssGSEA assay. While, LCP2, and ITGAMN were up-regulated in OSCC with good prognostic efficacy and survival rate as well as positive correlate with APOA4 in OSCC. Meanwhile, knockdown KIF14 can suppress the expression of LCP2, and ITGAMN in OSCC cells. The ROC curve analysis was confirming the good survival status for LCP2, and ITGAMN with APOA4 in OSCC.
Conclusions: Therapeutic strategies or biomarker using KIF14 could contribute to better clinical management/research for patients with OSCC.