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.

LINC00937 is a long non-coding RNA (lncRNA) up-regulated in multiple human carcinomas, such as oral squamous cell carcinoma (OSCC). However, the significance and potential mechanisms of LINC00937 in OSCC progression are still primarily need discussed. In our study, we first showed the part of LINC00937 in OSCC progress, and our data showed that LINC00937 has up-regulated in The Cancer Genome Atlas (TCGA) datasets and OSCC tissues. At the same time, LINC00937 is located in the cell nucleus. Up-regulate level of LINC00937 was correct with advanced clinical survival as well as HPV expression. Receiver operating curve (ROC) results showed the diagnostic ability of LINC00937 (AUC = 0.712) in OSCC patients. Meanwhile, LINC00937 is positively correct with FGR and IL10RA expression, downstream genes for LINC00937 in OSCC progress by PPI. In addition, pathway analysis showed LINC00937 was correlated with immune infiltrated cells relative-singling pathways. Finally, the silence of LINC00937 suppresses OSCC cell growth, induces apoptosis, inhibits migration, and invades in vitro. Our findings demonstrated that LINC00937 regulates expression of the downstream gene (FGR/IL10RA) and then regulates cell growth as well as metastasis in OSCC. Our data proved a piece of evidence that LINC00937 could serve as a prognostic biomarker for OSCC controlling immune infiltration.