Kinesin family member 14 (KIF14), a microtubule-based motor protein, plays an important role in chromosomal segregation, congression, and alignment. Considerable evidence indicates that KIF14 is involved in cytokinesis, although little is known about its role in oral squamous cell carcinomas (OSCCs). In the current study, we functionally and clinically investigated KIF14 expression in patients with OSCC. Quantitative reverse transcriptase-polymerase chain reaction and immunoblotting analyses were used to assess the KIF14 regulatory mechanism in OSCC. Immunohistochemistry (IHC) was performed to analyze the correlation between KIF14 expression and clinical behavior in 104 patients with OSCC. A KIF14 knockdown model of OSCC cells (shKIF14 cells) was used for functional experiments. KIF14 expression was up-regulated significantly (P<0.05) in OSCCs compared with normal counterparts in vitro and in vivo. In addition, shKIF14 cells inhibited cellular proliferation compared with control cells by cell-cycle arrest at the G2/M phase through up-regulation of G2 arrest-related proteins (p-Cdc2 and cyclin B1). As expected, IHC data from primary OSCCs showed that KIF14-positive patients exhibited significantly (P<0.05) more larger tumors compared with KIF14-negative patients. The current results suggest for the first time that KIF14 is an indicator of tumoral size in OSCCs and that KIF14 might be a potential therapeutic target for development of new treatments for OSCCs.
Keywords: Cell-cycle arrest; G2/M phase; Kinesin family member 14 (KIF14); Oral squamous cell carcinoma; Tumoral size.